Christie Laura Grace Profile picture
Aug 18 104 tweets 53 min read Read on X
1/ A 🧵combining a bunch of 🧵s on cGAS STING and modRNA and LNP harms, including peer reviewed studies, specific injuries, with substack and podcast at the end.
"BREAKING STUDY PUBLISHED 10/17/2023: Foreign dsDNA can cause strokes via cGAS STING":

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2/ Length of the dsDNA plasmid drives strength of cGAs STING and the immune system. Cleaning it up and lowering amounts is a false statement.
Even in low amounts, longer pieces of dsDNA cause the most harm. 6/20
activatiohttps://x.com/_HeartofGrace_/status/1804274300255457685 Image
3/ T CELLS, have their OWN cGAS STING Pathway! DNA PLASMIDs can interact w/ cGAS STING OF T CELLS, causing FUNCTION of T CELLS to be: IMPAIRED, cause T CELL DEATH, IMPEDE T CELL PROLIFERATION, hindering an effective immune response, and CANCER.

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4/ STING Type III (R71H-G230A-R293Q) Common in European and Middle Eastern populations. this variation of STING has the highest prevalence of AUTOIMMUNE DYSFUNCTION AND AGRESSIVE CANCER RATES. Common in European and Middle Eastern populations.
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5/ A little map of injuries and image of a variation of STING and how that relates to mRNA NLP injuries

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6/ Another cGAS STING thread (this is not the spike protein)


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7/ CANCER: COMBINED" FEEDBACK LOOP of cGAS STING/ APOBEC: DNA plasmid in LNP +DS RNA triggers cGAS STING AND induction of DNA deaminase APOBEC3A + nuclear DNA damage: Dysregulation/feedback loops of cGAS STING meets APOBEC (DIFFERENT MULTI-HIT mechanism)

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8/ COVID JABS CAUSING MULTI SYSTEM ORGAN DAMAGE /FAILURE through (hyper) ACTIVATION/DYSREGULATION of cGAS STING pathway by interacting with DNA PLASMID contamination, SPIKE PROTEIN. (variants of STING and mutation of STING)

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9/ "Rapid Onset of Paralysis after COVID 19 Vaccination: potential cause: cGAS-STING "hyper" Activation a WITH INCREASED activation due to physiolgical differences in teenager compared to adult.
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11/ "p53 acts on the cGAS STING pathway in tumor suppression. cGAS STING has multiple roles in both driving cancer and stopping it."
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12/ There's a reason why hydroxychloroquine works with lupus and other autoimmune conditions (hydroxychloroquine works on the cGAS STING pathway).

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13/ "How plasmid DNA will track to the nucleus before it gets degraded in the cell. First it gets recognized by cGAS, ..., and actually PROTECT it from being broken down, and zip it right to the nucleus.:
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14/ cGAS STING DUOX2 and pancreatic cancer

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15/ berrant activation of cGAS STING pathway can cause neurodegeneration, leading to Alzheimer's and other neurological disorders. This is a complex process, and aggregation of proteins with amyloid structures forming is part of this pathway process.
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16/ cGAs STING during fetal development of lens


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17/ activation of the cGAS-STING pathway by POLE mutation likely contributes to advantageous survival of endometrial cancer patients with POLE mutations, as cGAS-STING pathway is associated with anti-tumor activity via stimulation of inflammatory genes

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18/ "Here is a list of many types of cells that are tied to cGAS STING. cGAS STING can be activated by pieces of DNA plasmid that exists currently as contamination in the current mRNA covid vaccines that utilizes plasmids. "

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19/ Now we tie cGAS STING to GSK-3, and the implications of disease, especially, amyloid (no spike needed!)

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20/ Our previous study found an increased accumulation of cytosolic dsDNA and expression of cGAS and STING in FLSs and synovial tissues from patients with RA. In addition, a positive correlation between the cGAS immunoreactive score"

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21/ More cgas sting interactions (like manganese)
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22/ cGAS STING pathway (DNA plasmid contamination can do this) activation and implications for prognosis, immune infiltration, and tumor metastasis in implications for prognosis, immune infiltration, and tumor metastasis

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23/ Lyme's disease and cgas sting (know anyone getting paid to do a study on this?

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24/ Brain injury, including seizures and strokes, have been recently found in studies this past year, to have involvement in activation by the cGAS STING pathway.

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25/ cGAS STING, dead box and cancer


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26/ I did this all to get sh1t on and used for a year, especially by people who pretended to be my friend and said they would help my dad. Scientists in THESE circles. Nice people.

cGAs STING injury and kidney injury link x.com/search?lang=en…
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27/ Pulmonary tumor after vaccination. cGAs STING and the lung

x.com/search?lang=en…
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28/ cGAS STING pathway: there are four different types of STING--This is dependent on race. European and Middle Eastern race share one distinct form. Africans another. Asians. And the indigenous. And within this pathway mutations exist.


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29/ impacts of the cGAS STING pathway activation with increased inflammation in hearing loss and tinnitus. The activation of the cGAS STING pathway by way of DNA plasmid contamination and the spike protein in Pfizer and Moderna MRNA vaccines...
x.com/search?lang=en…
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31/ cGAS STING, RA, and mod RNA injuries


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32/ cGAs STING T Cell Lymphoma after covid injection

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34/ "GAS STING engages in what is called a 2:2 binding stoichiometry with DNA... two cGAS molecules bind to two DNA molecules. This is crucial for the activation of cGAS, leading to the production of cGAMP, which subsequently activates the STING

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35/ around 40 bp can still activate cGAs STING, two strands of it. That is it

No volume needed


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36/ ANCA-Associated Vasculitis after Moderna COVID-19 Vaccination (case report):
cGAS STING

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37/
How Chronic inflammatory demyelinating polyneuropathy (CIDP) is caused by cGAS STING pathway interactions--Case Studies: patients experiencing AIDP after AstraZeneca COVID vaccine.


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38/ Covid injections can cause virus reactivation, by the cGAS STING pathway. cGAS STING pathway can be activated by: DNA plasmid contamination, the spike protein, bacteria, and positive charges in the covid vaccines.


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39/ manganese activates cGAS STINg, and researchers want to add it to LNP platform

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40/ f it hasn't become painfully clear yet, one would think it is imperative regardless of situation, to do everything possible, to keep inflammation down in the body, and to not trigger the cGAS STING pathway. Repeated activation of this pathway is tied cancer. The activation itself causes genomic instability and mutations.

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41/ Cerebral venous thrombosis after COVID-19 vaccines


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42/ Role of cGAS STINg in tumor environment


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43/ cgas sting, and tumor evasion without integration


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44/ DNA Plasmid/Spike activate cGAS STING pathway, and cause progression of Adenomyosis, and other harms. (STUDY):


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45/ not only did hydroxychloroquine interfere with the ACE2 receptor according to studies, HCQ and CQ block the binding of dsDNA (should do the same with spike) to cGAS, thus attenuating the underlying activation of the STING pathway mediated by cGAMP

46/ cGAS STING Path and Genetics Edition. TL;DR: Variations in cGAS STING pathway, immune system, hormones, and genes—XX versus XY--are the reasons.

47/cgas sting again at the molecular level
48/ The cGAS-STING pathway promotes the development of preeclampsia, in pregnancy, which is dangerous to the mother and baby. Preeclampsia can impair fetal growth, decreasing supply of oxygen and can lead to preterm birth, stillbirth, or infant death. DNA plasmid pieces and spike protein can activate the cGAS STING pathway.
49/ cGAS STING Pathway Activation in the BRAIN: "cGAS/STING signaling pathway-mediated microglial activation in the PFC underlies chronic ethanol exposure-induced anxiety-like behaviors in mice"


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50/ High cGAS and STING expression was associated with a higher incidence of NRAS/KRAS mutations, which are linked to poor prognosis in several cancers.


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51/ The Role of cGAS-STING Signalling in Metabolic Diseases: from Signalling Networks to Targeted Intervention"


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52/ NO SV40 NEEDED! WHAT about MODERNA? Exactly! HMMM? There is no sv40 there. Been posting about cGAS STING since last October causing Aortic dissection, myocarditis, autoimmune, and cancer involvement.
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53/ mRNA "vaccines" contain DNA plasmid, and spike protein, which can activate a pathway--cGAS STING, and drive ONCOGENE EXPRESSION and MUTATIONS W/OUT SV40!! "cGAS-STING pathway expression correlates with genomic instability and immune cell infiltration in BREAST CANCER"

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54/ countless hours, making these threads.
If I counted them up I would probably, i dont know what

GAS STING, IS the unifying mechanism for "vaccine" injury, not just for autoimmune and cancer, but CLOTS too! Platelets and Megakaryocytes have cGAS STING activation for CLOT formation!

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57/

PHYSICAL LAB TEST ASSAY: HOW to TEST the VACCINE INJURED and THOSE who have DIED from VACCINE INJURY if cGAS STING was part of the INJURY due to SPIKE protein, DNA PLASMID PIECES ETC from AUTOIMMUNE ATTACK resulting in MYOCARDITIS, Aortic Dissection, mulit organ system failure, Cancer progression at TUMOR SITE, AutoImmmune Neuropathy, AIDP, SFN, and more: BELLBROOK LABS Transcreener cGAMP cGAS Assay directly measures cyclic GMP-AMP (cGAMP) produced by cyclic GMP-AMP synthetase (cGAS, C6orf150, 2'3'-cGAMP Synthetase). These cGAMP measurements allow researchers to effectively determine the enzyme's activity.Image
58/ Layman's terms: The cGAS STING pathway is a very complex system in our bodies that protects us from infection. It is also a part of autoimmune disorders, neurodegeneration, organ injury and failure, myocarditis, AAD, and CANCER.


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59/ Protocol to induce and assess cGAS-STING pathway activation in vitro" Perhaps some of the scientists who are doing tests on the vaccine injured, or those who have died from injuries, due to multi organ failure, myocarditis, aortic dissection, auto immune attack on any organ, on the nerves, on the brain

some people are disgusting, immoral, liars, and thieves

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61/ MYOCARDITIS: Inflammation and damage to the heart by DNA plasmid contamination and spike--activation of the cGAS STING pathway causes damage including MYOCARDITIS after COVID "VACCINATION" Transfection of the cardiomyocyte (layman's explanation at the end)
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62/ GUT MICROBIOME, and COVID: The microbiota in your gut is responsible for peripheral cGAS-STING activation, promoting resistance to systemic viral infections like COVID. If you give an antibiotic during a viral infection, you risk inactivation of cGAS STING to deal with that viral infection, systemically. Your gut microbiome is not some lone ranger just hanging out. Drinking, smoking, AND specific antibiotic use, will knock down numbers of bifidobacteria (some antibiotics, even one course will reduce for A YEAR).

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63/ There's a lot of talk right now about P53 and cancer. This is a lot of science for 4 AM. P53 degrades DNA exonuclease TREX1 via TRIM24, causing cytosolic dsDNA accumulation thus, triggering cGAS STING. Loss of cGAS STNIG activation means loss of tumor suppression. Right now, there is a small molecule that should hit the market (probably in three years give or take), that has nothing to do with a gene, that goes right in, and acts on STING, regressing colon cancer tumors from 70-90%.
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64/ cGAS STING is the primary pathway for many of the harms caused by the 💉 (outside of the genomic integration concern)


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66/ GAS STING Pathway Activation by DNA Plasmid Contamination, SPIKE, and LPS in modRNA "vaccines": AIDP, Myocarditis, Stroke, Aortic Dissection, and More: Overview, and Biopsy Methods for Detection. When DNA integration testing fails to produce results, this pathway, should.

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67/ All the same pathway--myocarditis, stroke, rapid aortic dissection, neurodegenration, autoimmune demylenating polyneuropathy, fbirosis, RA, IBD, and other disorders: cGAS STING pathway. The DNA plasmid contamination and SPIKE can activate and send into a feedback loop. Image
68/ Super stack on how a positive feedback loop is generated by the 💉: cGAS STING Pathway activation by DNA Plasmid Contamination, SPIKE, and LPS in modRNA "vaccines": AIDP, Myocarditis, Stroke, Aortic Dissection, and More: Overview, and Biopsy Methods for Detection.
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69/

MEGA THREAD ON MULTIPLE PATHWAYS AFFECTED BY DNA PLASMID CONTAMINATION that exists as a CpG motif, and potential negative health outcomes, depending on exposure (dose amounts unknown/duration/frequency. cGAs STING included


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67/ Recognition of DNA by cGAS is dependent on DNA length. Double-stranded DNA (dsDNA) longer than 20 bp activates cGAS, inducing dimerization of cGAS and resulting in the formation of a 2:2 DNA/cGAS complex, whereas dsDNA less than 20 bp is not able to induce cGAS dimerization and activation"

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68/ Inhibition of cGAS in Paraventricular Nucleus Attenuates Hypertensive Heart Injury Via Regulating Microglial Autophagy" The cGAS STING pathway is activated by exogenous (from the outside) ds(double stranded) DNA.


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69/ going back to the new year time. Well before Valentines day anyways

treacherous


Autoimmune diseases can be triggered by abnormal activation of the cGAS STING pathway. There are options to inhibit the cGAS STING pathway. The cGAS STING pathway is activated by exogenous DNA. Plasmid DNA contamination in RNA "vaccines" is, considered to our cells, to be exogenous (from the outside) DNA. "Meloxicam inhibits STING phosphorylation and alleviates intracellular DNA-mediated autoimmune responses"Image
70/ nhibition of cGAS in Paraventricular Nucleus Attenuates Hypertensive Heart Injury Via Regulating Microglial Autophagy" The cGAS STING pathway is activated by exogenous (from the outside) ds(double stranded) DNA. DNA plasmid contamination is exogenous DNA.

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71/ Activin A alleviates neuronal injury through inhibiting cGAS-STING-mediated autophagy in mice with ischemic stroke dsDNA is exogenous DNA. Plasmid DNA contamination in covid RNA vaccines is exogenous DNA. Exogenous DNA activates the cGAS STING pathway in cells.

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72/ cGAS inhibition alleviates Alu RNA-induced immune responses and cytotoxicity in retinal pigmented epithelium"

degusting pigs


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73/ Inhibition of the cGAS-STING Pathway Attenuates Lung Ischemia/Reperfusion Injury via Regulating Endoplasmic Reticulum Stress in Alveolar Epithelial Type II Cells of Rats


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74/ nhibition of cGAS-STING by JQ1 alleviates oxidative stress-induced retina inflammation and degeneration"


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75/ Inhibition of cGAS–STING pathway alleviates neuroinflammation-induced retinal ganglion cell death after ischemia/reperfusion injury"


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76/
There is a clinical trial on cGAS STING with IBS in kids correlating exogenous DNA--right now. cGAS STING pathway activation by pieces of DNA that do not belong, Maybe for vaxx injured, target it as last resort?



dont you wish you could go back in time, and never ever interact or cross paths with some people, ever?

me tooImage
77/A lso, zeta potential with its impact on biodistribution, the specific molar ratio required to transfect the cardiomyocyte, the charge causing clots, remodeling the inside of the blood vessels, and the DNA plasmid causing activation of cGAS STING pathway and it's impact on so many organ systems, not to mention the cancer implications and how it satisfies the muti hit cancer theory, progressing cancer

78/ Spike protein activates the Sting pathway.


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79/

dna/rna hybrids, dna plasmid, spike, ssDNA and dsDNA, and some other things activate cGAS STING

Activation of cGAS-STING Pathway Is Associated with MSI-H Stage IV Colorectal Cancer (dsDNA activates the cGAS-STING. Plasmid DNA IS dsDNA)


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80/ Nerve pain, chronic peripheral neuropathic pain, chronic central neuropathic pain, and inflammation can be caused by exogenous dsDNA interacting with the cGAS-STING pathway, resulting in a chain reaction. Plasmid DNA contamination in the RNA vaccines IS dsDNA.

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81/ Happy new Year. Time to jump right in. Do or do not--there is no try. For the science folks: Read these two in tandem: 1: "Innate Immune Response to Cytoplasmic DNA: Mechanisms and Diseases" "Suppression of cGAS Activity" "Suppression of MITA Activity"



they all ignored this, including AMLOST everyone in these circles, with an exception of people who knew this was true, including a politician

two of the of the scientists even went on podcasts who knew of everything I was posting, called giradot an LNP expert, who are currently writing papers. about cgas sting while gutting me again, while another let them drag me, and watched with glee

What great peopleImage
82/ CLNICAL TRIALS ARE IN PROCESS ON THE HARMS OF EXOGENOUS DNA ON CHILDREN! "Exploration of the Activity of DNA Located Outside of Cellular Nucleus to Amplify Inflammation in Inflammatory Bowel Disease in Children Through Biological Pathway Cyclic GMP-AMP Synthase (cGAS)

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83/ dsDNA in💉activates "STING", and may cause: Subarachnoid haemorrhage, Hypoxia, injure mitochondria, neurodegeneration, MS, Lupus, ALS, PRION disease, brain cancer, AGS, SAVI, chronic neuroinflammation, increased tumor growth, impaired T-lymphocyte, and more.
Dec 2023
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85/ Background on cGAS–STING Pathway: Cancer cells contain high levels of cytosolic DNA. The cGAS–STING signaling axis is a major sensor of cytosolic DNA and triggers the innate immune response, leading to the production of pro-inflammatory cytokines, including type I interferons.

dec 5 Image
86/
December, 2023
Thyroid damage and auto immune is linked to dsDNA. dsDNA is found in the current plasmid DNA contamination. This is slightly different in the thyroid ( histone H2B)


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87/ Nov 26, 2023

cGAS STING pathway is activated by ds DNA ( plasmids) in cells (outside nucleus). It is complicated, and interacts with helicases, like DEAD box (DDX#) Proteins. Dysregulation in cGAS-STING pathway, like DDX41, can lead to tumor formation (cancer). cGAS STING can be mutated

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88/ DEAD BOX ! Dead box! and cGAS STING!

cGAS STING pathway is activated by ds DNA ( plasmids) in cells (outside nucleus). It is complicated, and interacts with helicases, like DEAD box (DDX#) Proteins. Dysregulation in cGAS-STING pathway, like DDX41, can lead to tumor formation (cancer). cGAS STING can be mutated


These same scientists, doc, etc told me I did not know what I was talking about here either.

THIS delayed science, actually delayed trying to warn people, by dragging me through the mud while focusing on sv40 and defamed me. I think some people do not owe just ME an apology, but to apologize to others for covering me up, slandering me, defaming me, and dragging me through the mud for over a year, it meant this info was sh1t on while they sh1t on me. How terrible!

Think about that
What great people.Image
89/his study comes in handy. The cGAS-STING pathway "sees" aberrant nucleic acids. The DNA plasmids are already aberrant in more than one way--it's bacterial, recombinant, has CpG motifs, AND, according to the study breakdown in the thread below, is being mutated inside the LNP!

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90/
The cGAS-STING pathway in humans, can detect and be activated by pieces of DNA, bacterial DNA, AND RNA (all are in the LNP!) If activated (which is outside of the nucleus), this can lead to multiple diseases, including autoimmune disease and cancer.


When these people sh1t on me, they sh1t on everything I was posting here, with malicious intent.
While people kept getting harmed, while articles were written about green monkey DNA.
Think about thatImage
91/
They all ignored it while people kept getting harmed.
DNA contamination found in c@vid vaccines IS dsDNA. Humans have a pathway called, cGAS–STING pathway. This pathway can be activated by dsDNA (PLASMID DNA), causing autoinflammatory, autoimmune, degenerative disease, and cancer.

we are now into november, 2023. The only thing being discussed was SV40 and DNA plasmids. Think about this.. dragged through media channels while people were harmed and died. I have no good words here.



What great people.Image
92/Npv 15 2023
DNA PLASMID CONTAMINATION in mod RNA "vaccines" does NOT have to enter the nucleus to cause cancer. Recent advances have now expanded the roles of cGAS-STING to cancer. Highly aggressive, unstable tumors have evolved to co-opt this program to drive tumorigenic behaviors. "The cytosolic DNA-sensing cGAS-STING pathway in cancer": can be activated by dsDNA outside of the nucleus, which can be in the form of DNA plasmid contamination, which was recently found by multiple scientists in the c@vid "vaccines", thus, causing aggressive, unstable cancer.

I was told I did not now what i was talking about, by scientists i these circles, and that I was a piece of sh1t

By doing this, that buried everything I was talking about, for a YEAR, all for the pleasure of beating someone up online

what great people

93/ oo. SAME PATHWAY (cGAS) Acute myocardial infarction is accompanied by massive cardiomyocyte necrosis and tissue inflammation. In multiple studies, it was reported this extensive cardiomyocyte necrosis is also associated with elevated circulating mtDNA

Right there. November 2023--I talked about mtDNA and myocarditis

94/
nov 15 2023


DNA PLASMID CONTAMINATION in modRNA vaccines can cause STROKES Same pathway as CANCER. IT does NOT need to enter the nucleus. cGAS-STING pathway is mediator in response to dsDNA. DNA plasmid contamination is dsDNA.

(I was told everything that was said by CR. Receipts)Image
95/ dsDNA [PLASMID CONTAMINATION IN LNP/modRNA ] CAN CAUSE STROKES via cGAS STING


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96/ rumble cgas sting (I was supposed to record something similar MONTHS ago but my friend /podcaster had a baby, which is more important,

rumble.com/v58fgjp-the-pa…
97/ cGAS STING Pathway activation by DNA Plasmid Contamination, SPIKE, and LPS in modRNA "vaccines": AIDP, Myocarditis, Stroke, Aortic Dissection, and More: Overview, and Biopsy Methods for Detection.

christiegrace.substack.com/p/cgas-sting-p…
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98/ CANCER: "COMBINED" FEEDBACK LOOP of cGAS STING AND APOBEC: DNA plasmid in LNP +DS RNA triggers cGAS STING AND induction of DNA deaminase APOBEC3A + nuclear DNA damage:

christiegrace.substack.com/p/cancer-combi…
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99/ Hydroxychloroquine! But, it's not just antiviral. Look what it is doing to cGAS!


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100/ this actually occurs via cgas sting, apobec, a couple of other things, and one mechanism I a waiting to finish writing and submit on.


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More from @_HeartofGrace_

Aug 20
1/If you haven't been paying attention, MANY social security numbers and full info were hacked and released. Everyone that I know had their social security number and information breached and their info landed on this list. Instructions on how to place a freeze on your credit👇🏻 Image
2/ I've been helping my parents check and place freezes on their credit to protect what they have.

fortune.com/2024/08/19/soc…
3/🚨 It looks like for some people it's not easily accessed without creating an account.

This is the website that is linked in that article where you enter your first name, your last name, the state, and the year of your birth. It scans quickly and if you're on this list you're going to see some horrifying data including probably every single place you've lived. It does not ask for your social security number. This just tells you if your information is leaked to the public right now and it shows you exactly what is leaked.

These hackers stole full information.

If you were married at one point and you changed names be sure to check maiden name.

npd.pentester.com
Read 4 tweets
Aug 7
🚨🚨💉💉Here's how lipid nanoparticles and the spike protein should theoretically cause birth defects and other harms, even if they never even tough the baby growing in the womb if the mother got a modRNA/LNP injection, with no DNA plasmid present:

Below is a screen shot from a Rumble presentation from the late Dr. Arne Burkhardt (rumble link and citations below). In this screenshot of Dr. Burkhardt's presentation, he obtained this tissue and saw that it contained spike protein expressed in the placenta, and this mother, had received at least one modRNA injection.

We know from multiple LNP studies that the LNP is indeed going to the placenta.

The trophoblast is part of the placenta and it is made up of layers contribute to the formation of the placental barrier, which separates maternal and fetal blood while allowing the transfer of nutrients, gases, and waste products.

This is important because many nutrients and hormones cross the placenta that are involved in fetal development.

The trophoblast also produces several hormones needed for pregnancy, including hCG, to maintain the corpus luteum for progesterone production, and hPL, which regulates maternal glucose metabolism. It also modulates the immune system to stop the mother's immune system form thinking that the placenta is foreign tissue to be attacked by her immune system.

If any abnormalities form in this area, this can impact trophoblast function and cause complications like preeclampsia, placental abruption, birth defects, and still birth.

Blood flow could also be disrupted.

Regarding the placenta there is a transporter "system" that regulates the passage of nutrients and hormones, among other things, and this transporter system can be compromised.

There are important hormones that need to cross the placenta to reach the growing baby that are vital to the development of a healthy baby.

The size and charge of the LNP may interact with this system, and compete for certain aspects of this transport system or simply block it.

The following are important hormones, glucose, amino acids, and other nutrients that are vital to fetal development:

Glucose transporter (SLC2A1 AKA GLUT1) transports glucose from the mother to the growing baby.
If LNPs accumulate in the placenta, they could obstruct or alter the function of GLUT1, reducing glucose supply to the fetus, causing intrauterine growth restriction and developmental delays in the baby in the womb.

There are a couple of amino acid transporters involved in getting amino acids to the growing baby.

SLC22A4 transports amino acids and other small molecules. LNPs could interfere with the transport of amino acids that could be detrimental to protein synthesis in the baby and could negatively impact fetal growth.

LC38A1 and SLC38A2 transport what are called neutral amino acids, and if these are disrupted this could also negatively impact fetal development and growth.

Thyroid Hormones

A BIG FACTOR is thyroid hormones.
SLC16A2 is paramount for of the thyroid hormones T3 and T4 into fetal tissues. LNPs blocking this could theoretically result in inadequate thyroid hormone delivery to the fetus, causing not only birth defects but concerns with the cognitive function of the baby.

Iron transport:
SLC11A2 regulates iron uptake and if this was impacted, it could cause anemia in the growing baby.
TFRC--this is the transferrin receptor which mediates uptake of the transferrin-bound iron, and if this is impacted we would see iron deficiency, impacting fetal brain development and overall growth.

Calcium channels:
CACNA1S and CACNA1C are what are called L-type calcium channels, and they are in charge of calcium transport from the mother and these are essential for bone development and other physiological processes, and if there are calcium imbalances as a result of LNP imbalances, we might see fetal bone growth and development impacted in the womb.

Water channels!
Yes, the placenta has what are called water channels. Water channels are pretty cool, these are called aquaporins--AQP1 and AQP3 and these are responsible for the transport of water across the placenta to the growing baby. If there was a pregnant mother who received a modRNA injection, and she suffered from oligohydramnios (low amniotic fluid), one might wonder if this was correlated.

Oligohydramnios can cause compression of the umbilical cord, promoting decreased oxygen, nutrient supply to the fetus, preterm labor, or what is called "potter's sequence," which includes limb deformities and facial deformities due to compression of the fetus.

**************************************************************************
If we tie this all together, then we might see LNP causing a disruption in the placenta without ever touching the growing baby, and interference with glucose, amino acid, and iron transport can result in nutrient deficiencies, impacting fetal growth, development, and health.

Insufficient thyroid hormones, glucose, or amino acids can lead to developmental delays, cognitive disabilities, and other congenital conditions.

Disruption in nutrient and hormone transport can cause intrauterine growth restriction, causing low birth weight and potential long-term health issues.

Disruption of calcium and water transport can result in metabolic imbalances, affecting bone health and fluid regulation.

Has anyone heard of any issues with pregnancies after modRNA injection with LNPs?

Asking for a friend.Image
@drcole12
@DrJBhattacharya
@drdrew
@mottomeneki
@SenatorRennick
@ABridgen
@FLSurgeonGen
Read 5 tweets
Jul 28
🚨🚨🚨💉For those who lost loved ones, who never got a reason why, did you loved one experience the following? Septic like symptoms but no sepsis? (they could not figure it out?) Fever, chills, low blood pressure, rapid heart rate (Tachycardia), rapid breathing (Tachypnea), weakness, lactic acidosis, multiple organ dysfunction, darkening of skin under the eyes, and confusion? Did this happen before the death of your loved one but no doctor could explain why? Septic like symptoms but no bacteria present?

If this is you, YOUR LAWYER contacts me in full name on X only, and we have a call. If it was Pfizer or Moderna, I am almost certain can explain the EXACT mechanism in laymans terms and technical.

Anonymous accounts in DMs will be not be answered.
@drcole12
@AaronSiriSG

I know why this happened if they had Pfizer or Moderna. I will not post it in some tweet. I will represent your client in court. I will bring in my evidence of where I worked, what i did, and I will explain this fully.

@Answers4Sean
I know how this happened. I am so sorry.

Have you docs who say they can explain it explain all of that?

I can.
I swear on everything good and holy I can explain why.

It hit me like a mac truck when I was prepping to go on the podcast I did this week, I just didn't mention it because it is different mechanism.
Read 5 tweets
Jul 27
🚨🚨💉Nice chronological list below. Lawyers you might be interested.
I would like to submit the date of August 17th, 2018.
(b. Elimination of roles of the RAC in HGT and biosafety.)
And it was taken over by the FDA, OSP, and IBC. This is very important!

"In a Federal Register notice issued on August 17, 2018 (83 FR 41082), the NIH proposed a series of actions to the NIH Guidelines for Research Involving Recombinant or Synthetic Nucleic Acid Molecules (NIH Guidelines) to streamline oversight of human gene transfer research (HGT), and to focus the NIH Guidelines more specifically on biosafety issues associated with research involving recombinant or synthetic nucleic acid molecules."

This is what was decided:

"Elimination of HGT protocol submission and reporting requirements to the NIH, and individual HGT protocol review by the Recombinant DNA Advisory Committee (RAC)."

The recombinant advisory committee was the group that was in charge of biosafety and ethics for the use of things like RNA with lipids. They were the one thing we had standing in the way (if they were doing what they were supposed to do).

"Modification of roles and responsibilities of investigators, institutions, Institutional Biosafety Committees (IBCs), the RAC, and the NIH to be consistent with these goals including:

a. Modification of roles of IBCs in reviewing HGT to be consistent with review of other covered research.

b. Elimination of roles of the RAC in HGT and biosafety."

Do you know what they did here, and who was in charge?

"After careful consideration of public comments, the NIH is amending the NIH Guidelines in the following areas:

1. Elimination of HGT protocol submission and reporting requirements to the NIH, and individual HGT protocol review by the Recombinant DNA Advisory Committee (RAC).

2. Modification of roles and responsibilities of investigators, institutions, Institutional Biosafety Committees (IBCs), the RAC, and the NIH to be consistent with these goals including:

a. Modification of roles of IBCs in reviewing HGT to be consistent with review of other covered research.

b. Elimination of roles of the RAC in HGT and biosafety."

what this means is that the RAC will no longer review individual HGT protocols. This function will be fully transitioned to Institutional Biosafety Committees (IBCs) and the Food and Drug Administration (FDA).
But also the NIH Office of Science Policy (OSP), and in 2018, that was David T. L. Lee, PhD.

Also, the IBC does not have the experience to work with pediatric populations.

Experiments categorized as Major Actions under Section III-A-1-a must be submitted to the Office of Science Policy (OSP), NIH
These proposals must be published in the Federal Register for a minimum of 15 days to allow for public comment and must receive specific approval from NIH before initiation.

"The deliberate transfer of drug resistance traits to microorganisms that are not naturally known to acquire these traits will require NIH Director approval. This is to ensure that such transfers do not undermine the ability to control disease agents in human, veterinary medicine, or agriculture contexts."

The DNA plasmids that have contaminated the Pfizer and Moderna RNA injections contain an antibiotic resistance part to them--that is standard issues when you use plasmids to make RNA. That is plasmid biotech 101.

Before initiating experiments involving the deliberate transfer of recombinant or synthetic nucleic acid molecules into human research participants, researchers must obtain approval from their IBC and all other applicable institutional and regulatory authorities.

The criteria for synthetic nucleic acids that require IBC approval now include:

Length:
Nucleic acids containing more than 100 nucleotides.
Biological Properties:

Nucleic acids with properties enabling integration into the genome, such as cis elements.

Replication Potential:
Nucleic acids that have the potential to replicate within a cell.

Transcription/Translation Potential:
Nucleic acids that can be transcribed or translated.
Now, according to the NIH Guidelines for Research Involving Recombinant or Synthetic Nucleic Acid Molecules, the COVID-19 injections, which contain synthetic nucleic acid molecules (mRNA), would require Institutional Biosafety Committee (IBC) approval prior to initiation.
Specifically, these injections fall under the category of experiments involving the deliberate transfer of synthetic nucleic acid molecules into humans, as outlined in Section III-C-1.

The mRNA in the COVID-19 injections qualifies as synthetic nucleic acid molecules.

As per Section III-C-1, any experiment involving the deliberate transfer of recombinant or synthetic nucleic acid molecules into human research participants requires approval from the IBC before initiation.

Now the thing to look up, is who were the people involved with the IBC for PFizer and Moderna?Image
In 2020, the Director of the NIH Office of Science Policy (OSP) was Nina F. Schor, MD, PhD. Dr. Schor took over the role in 2019. Neurologist. Zero biotech experience. Nina F. Schor, MD, PhD, is primarily known for her work in pediatric neurology and neuroscience. Zero experience with nucleic acids.
Read 4 tweets
Jul 26
🚨 Infections and Cancer: CDC states a current increase n bacterial infections. Some share on social media they've had covid many times, more bacterial infections, and some people (common denominator?) keep getting prolonged infection. Drug resistance is one thing. However, Multiple injections of lipids?

Our immune system needs to SEE things that are there to clear or deal with what is called a pathogen. A pathogen can be bacteria, a virus, but another thing it sees as a pathogen is a pharmaceutical lipid.

We have things in our body called Pattern Recognition Receptors (PRRs).

PRRs can detect PAMPs (pathogen-associated molecular patterns)

PRRs detect the PAMPs. PRRs also detect DAMPs

PAMPs are common structures found on pathogens, such as bacterial cell wall components, like that of listeria. DAMPs are parts of us that are released when our cells are damaged.

Our cells that are part of our immune system can recognize things that are not us, like pharmaceutical liposomes that are part of the lipid nanoparticle that is being used to not only deliver the RNA for the covid injections, but now, it appears the word is spreading, that traditional attenuated vaccines are now going to switch over to the lipid component.

Not only is this bad from the cGAS STING aspect (the change over) but lets look at what is called the MPS--mononuclear phagocyte system (read about the MPS below).

The body need to first MARK the pathogen for clearance. It recognizes a pathogen, but it has to MARK it, like placing a flag on something, or if your car was stranded at night, and maybe you have a flare to put out--a signal to say "This is where I am!"

Our immune systems MAKES proteins that are there to help MARK bad things that enter us, like viruses, bacteria, and pharmaceutical lipids (there are 4 kinds of lipids in the lipid nanoparticle: cholesterol, DSPC, ionizable lipids that can be charged (and some that already have a charge), and the PEG on the outside of the lipid nanoparticle.

The PEG was placed on the outside of the lipid nanoparticle to essentially cloak it from our immune system so our PRRs could not see it right away. It is like a cloaking shield a Romulan ship would use, and studies have shown this can last for a day or up to over 50 hours of cloaking time. It does not guarantee the shielding from our immune system detecting it, but it gets in the way.

Once the immune system sees the lipids that are there, it wants to attach proteins to the surface of it.

We have different proteins in our body that attach to things to mark them for removal (destruction). These are called Opsonins.

We also have things called macrophages. Some of you might have seen cool videos of macrophages chasing a bacteria, engulfing it, and digesting it. These are not an opsonin. These surround the bad guy, envelop it, and digest it.

Here are the types of flags, and the list of what is usually going to mark which thing.

There is overlap on which opsonins can bind to what things. The immune system usually wants to launch a hefty response and get a few things in the area to deal with what is going on (comprehensive).

The lipids in the RNA injections are detected by our immune system, once the cloaking time is up.

Then our body goes in to mark all of those things (there are a LOT of them in the injections!!!!)

1st opsonin protein: C3B
This is something that "sticks" to the outside of that pathogen, and the lipid. C3B also binds to some bacteria and viruses!

Then we have the opsonin C4B. This also binds to bacteria, virus, and pharmaceutical lipids! Same with iC3b but it does not bind with all the viruses. C3B is one of the main markers of those pharma lipids.

Then we have our immunoglobulins.
IgG!
IgG can bind to viruses, bacteria, and pharma lipids

IgM can also bind to all three.

Then we get into things like C-Reactive Protein, lactoferrin and MBL, but those are not the main players here.

Studies have shown (the time frame varies by person, current infection state, health, etc) that if you inject pharma lipids like DSPC and PEG in vivo, that if you repeat injections of those lipids, depending on time frame, they can take longer for the immune system to clear because the POOL of our PROTEINS to MARK the INVADERS gets DEPLETED!
This means that in these studies, it now took the immune system LONGER to clear the lipids out, because there were imply not enough opsonins to mark them all. So they just hung out. And we know these in themselves can cause inflammation.

So in the beginning of 2021, if you all remember, people, starting with the frontline workers, and THEN the doctors hit the immune compromised who have/had current autoimmune conditions and other immuno comprised states like CANCER. And this was really bad, considering spike protein came in, DNA plasmids came in (no level is safe!! I do not care what FDA says on this! They've been compromised anyways by pharma and their own malfeasance), but also a HUGE NUMBER of PHARMA GRADE LIPIDS were injected to people ONCE and then what did they tell people? When were people getting the next dose again? (Insert profanities here)
Those doctors ta the FDA, those scientists, docs at hospitals--they injected people again 3 weeks later, during COVID! They injected people with something that depletes the opsonin system, twice in three weeks. (insert profanities)

Consider this, if you deplete your protein pool, your opsonin pool, what if you get strep? What if you get the flu? What if you get a urinary tract infection? What if you get covid?

This system can replenish itself, but, some things CAN occur here, including impacts on cancer.

We do not have this unlimited supply of opsonins.

So not only if you keep getting injected with these lipids can harm occur from inflammation, they can also reduce the number of opsonins you have because remember, they were injected all over the body, head to toe.

Not only can the pool of these proteins be depleted, they can be ALTERED.

If repeated exposure to liposomes alters opsonin levels or immune function, the immune system might adapt by changing the types of antibodies it produces.

Antibody
class
switch

Does a paper need to be written for this stuff too for it to be taken seriously? Is it only true if it is peer reviewed?
I linked it below for you.

So, if we have a depleted pool of opsonins meant to flag the bad guys in our body that do not belong, the immune system might have a tougher time, and in this process, the body can class switch, it can change what is coming in, because certain opsonins (proteins) have been depleted fighting one thing, and might change.

CANCER:
Cancer cells can be marked by complement proteins. Opsonins!
For instance, complement components like C3b can bind to cancer cells, leading to their recognition and uptake. This is called complement-mediated cytotoxicity.

C3b marks cancer cells for phagocytosis (engulf--eat them).
Depletion of the complement system reduces the opsonization of tumor cells, leading to decreased recognition and clearance by phagocytes like macrophages and neutrophils.
If you have depleted opsonins, and you do not have enough or less to mark cancer cells, that can cause tumor progression. This can lead to not only tumor growth, but mestasis.

Did you hear of anyone who had their cancer advance after ....?

They knowingly gave a blast of lipid pharmaceuticals to people who had/have cancer.

This depletion can also impact the effectiveness of monoclonal antibodies (cannot mark the cells, antibodies cannot SEE them!)

This might also impact immune checkpoint inhibitors and CAR T therapy.

And now, scientists (do not just blame the FDA) want to use RNA and lipids going forward.

This is bad news bears, and might be a big piece of the puzzle beyond the spike protein and other factors, why people this past year or so, some people, have been getting sick with multiple infections.Image
@drdrew
@DrJBhattacharya
@AaronKheriatyMD
@SenatorRennick
@RepThomasMassie
Read 4 tweets
Jul 7
🚨 How plasmid DNA will track to the nucleus (with extra steps) before it gets degraded in the cell. First it gets recognized by cGAS, but that is not the only thing that will recognize it, and actually PROTECT it from being broken down, and zip it right to the nucleus.

DNA plasmid will be recognized by the cGAS STING pathway immediately upon cell entry. This is the first part of the cell that recognizes it with rapid speed. cGAS is the cell's main "smoke detector" that recognizes things that do not belong, like viruses, bacteria, double stranded RNA and DNA.

But here's the thing--DNA will cause the strongest response, and it is also LENGTH dependent--longer pieces of DNA plasmid will cause cGAS STING to cause the strongest response of all, even at lower amounts.

You can have a mixture of different lengths of DNA. Small pieces will activate the immune system in a mold to moderate way. Medium sized pieces of DNA will trigger a stronger response--the small pieces will actually act as "pass interference" (US football term here) and stop the larger pieces from binding.

The longer pieces of DNA will cause a very strong immune system response--one that can be dangerous, and cause a hyperactivation of our immune systems and cause it to attack us, destroy tissue, and cause us injury, including but not limited to autoimmune concerns.

There is also an order to the organs in our body (eyes, brain, bladder, heart, etc) with how other things will impact the cellular damage (I am explaining on podcasts coming up, and why myocarditis (heart damage) aside from immune issues and clots, are the highest injuries seen (followed by bladder, etc).

Back to what is happening in the cell. There is an order of operations in our cells for how things are taken care of regarding foreign entry of plasmid DNA. Right now we will just speak to entering the nucleus.

There are multiple proteins inside the cell that can bind to plasmid DNA, and some do not care what kind of DNA, they see it as "bad" because DNA does not belong free floating around in our cells.

The proteins:
✅cGAS (cyclic GMP-AMP synthase)
✅IFI16 (Interferon Gamma Inducible Protein 16)
✅Other DNA-Binding Proteins (like HMGB1 (High Mobility Group Box 1) and DDB2 (Damage-Specific DNA Binding Protein 2)
✅Motor Proteins (DYNEIN!!!!!)

And then we have the thing that breaks down the DNA plasmid:
✅TREX1

☑️1. DNA plasmid has now entered the cell vis a lipid nanoparticle

☑️2. Initial Interactions with cGAS

cGAS-STING Pathway (IFI16 as well):

cGAS STING and IF116 rapidly detect cytoplasmic DNA, particularly double stranded DNA (like plasmid DNA).

IFI16 specifically senses foreign DNA and activates immune responses similar to cGAS-STING.

The cGAS-STING pathway is known for its rapid response to foreign DNA, triggering signaling cascades within minutes of detection. cGAS STING, the smoke detector for our cells, is coming in fast and hard, and is the first on the scene.

cGAS (the smoke detector) has the evolutionary advantage in binding to newly arrived cytoplasmic DNA to trigger an immune response quickly.

☑️3. Dynein time!

Dynein is going to come in with rapid speed too--about the same time cGAS does, or just behind it. Dynein is what is called a MOTOR PROTEIN!
It looks like this little ball with feet, and it can attach to plasmid DNA, it will bind to it! It will attach to the DNA plasmid, and carry it on its back like Luke Skywalker carrying Yoda (except on a tight rope to the nucleus, it is now walking it to the nucleus).

(see video below of Kinesin protein walking on a little rope thing we call microtubules, it will look like it is walking on a tight rope. It is simlar to Dynein).

However, when Dynein binds to plasmid DNA it is now protected from being broken down! It is now shielded, like Luke Skywalker shielding Yoda from harm.

☑️4. Size of DNA plasmid matters!
Size Variation and Transport Efficiency:

Small Plasmids (20-120 base pairs):

Smaller plasmid fragments diffuse more readily and are easily transported by dynein-microtubule interactions. T
Their smaller size allow them to move through the nuclear pore complex more easily.

Medium Plasmids (120-2000 base pairs):

Medium-sized plasmids benefit significantly from active transport mechanisms.
Their interaction with dynein and microtubules ensures they reach the nucleus without being degraded or immobilized within the cytoplasm.

Large Plasmids (2000-4000 base pairs):

Larger plasmids might face more difficulty due to their size but are still effectively transported by the cytoskeletal network.

☑️5. Dynein can bind to plasmid DNA either directly or via adaptor proteins that recognize the DNA.
Dynein moves the DNA towards the cell center (minus end of microtubules), directing it towards the nucleus.

☑️ NO SV40 needed to get it into the nucleus, there are CHARGE MEDIATED localization reactions here--meaning the CHARGE is driving it into the nucleus!

The negative charge of DNA, due to its phosphate backbone, can interact with positively charged molecules or proteins within the cell.

☑️6. Another way DNA plasmid can enter the nucleus During Telophase

Our cells are dividing, and when this happens, DNA plasmids can enter the nucleus.

Cell Division Phases
Prophase: Chromosomes condense, and the nuclear envelope begins to break down.
Metaphase: Chromosomes align at the cell's equatorial plane.
Anaphase: Chromatids separate and move to opposite poles of the cell.
Telophase: Nuclear envelopes re-form around each set of chromosomes, and the cell begins to split into two daughter cells.

The nuclear envelope is more permeable during reformation, allowing easier entry of exogenous DNA.
The temporary absence or incomplete formation of the nuclear envelope reduces physical barriers to DNA entry.

☑️ 7. So now, we have cGAS that has bound to DNA plasmid, and we have DYNEIN that has walked the DNA plasmid pieces right to the nucleus, carrying it like a snuggie on its back.

☑️ 8. TREX 1 comes into the picture. TREX 1 is the thing that is going to break down DNA plasmid, but Dynein-bound DNA is likely less accessible to nucleases because it is associated with a large protein complex. TREX has a difficult time interacting with the motor protein carrying the DNA plasmid on its back.

☑️9. Association with other proteins!
In addition to dynein, plasmid DNA can associate with other cellular proteins that shields it from degradation. These proteins can form complexes that obscure the DNA from nucleases like TREX 1.

HMGB1 (High Mobility Group Box 1)
Can bind DNA and influence its stability and interaction with other cellular components.
Acts as a DNA chaperone and can also participate in the immune response.

IFI16 (Interferon Gamma Inducible Protein 16)
A DNA sensor that can detect foreign DNA in the cytoplasm.
Activates immune responses, similar to the cGAS-STING pathway.

DDB2 (Damage-Specific DNA Binding Protein 2)
Involved in DNA repair and can bind damaged DNA.
Participates in recognizing and responding to DNA damage.

☑️10. Limitations of cGAS-STING Pathway
The cGAS-STING pathway can become saturated if there is an overwhelming amount of dsDNA in the cytoplasm. Saturation occurs when the amount of DNA exceeds the pathway's capacity to process and respond effectively.
The response of the cGAS-STING pathway is dose-dependent, meaning that higher concentrations or continuous exposure to dsDNA can lead to prolonged or sustained immune activation. This can potentially lead to chronic inflammation or immune dysregulation, and damage to organs causing injury to people, and autoimmune disease.

The ability of cells to handle dsDNA can vary between different cell types and under different physiological conditions. Some cells may have higher tolerance thresholds for dsDNA, while others may be more sensitive (I will explain this on the podcast coming up!)

☑️11. cGAS can have altered functionality for a few reasons. This has been discussed in other threads, including by RACE (your RACE determines what kind of cGAS you have, er smoke detector in your body! There are also what are called HLA mutations (DR) that can cause a dysregulation in immune response.

Genetic Mutations: Mutations in genes encoding cGAS, STING, or associated proteins can impair the pathway's ability to detect or respond to dsDNA properly.

Certain diseases or conditions may interfere with cGAS-STING signaling, either enhancing or dampening its response to dsDNA. For example, viruses may encode proteins that inhibit or exploit cGAS-STING signaling to evade immune detection.

Drugs or therapies that modulate immune responses, including those targeting cGAS-STING pathway components, can also alter immune responses in desired or undesired ways.

☑️12. So lastly, TREX 1 comes in and this is the thing that cleans up DNA, and it is the last thing to arrive on the scene in your cell, after cGAS has already had its way with it, after the immune system has already been activated, and after the plasmid DNA has already been transported to the nucleus. It is the slowest moving part of your cell's defense mechanism.Image
2/ Here is what a motor protein looks like walking along a microtubule, this is Kinesin, not Dynein, but it will carry that DNA plasmid like Luke carrying Yoda on its back, and it will walk it right to the nucleus

3/ The DNA can also get in via diffusion, it can just transfer right into the nucleus via charge mediated transport, meaning the DNA has an ATTRACTION to things in the nucleus it wants to join with, it wants to be with. Image
Read 5 tweets

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