π¨π¨π¨πcGAS 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!
(if you are new here--there are many tweet threads with over 200 studies backing mechanisms for injury, including positive and negative charges to cause clots and injury, and other ways the LNP, the charges (zeta), spike, RNA itself with mis fold and frame shift happening with ANY RNA, with explanations, and of course there are some "side" mechanisms that are happening, but cGAS STING is the primary pathway. This is ALSO the pathway that was being activated during delta wave. And yes, lots of cross talk and other side "conversations", but this should be the unifier.)
A megakaryocyte is a large, specialized cell found in the bone marrow that is primarily responsible for the production of platelets, which are essential components of blood clotting.
Megakaryocytes are among the largest cells in the bone marrow. They have a large, lobulated nucleus and abundant cytoplasm.
The primary function of megakaryocytes is to produce platelets. Platelets are small, anucleate cell fragments that play a crucial role in hemostasis, the process that stops bleeding by forming blood clots.
Megakaryocytes extend long cytoplasmic projections called proplatelets into the blood vessels of the bone marrow. These proplatelets fragment into thousands of platelets.
π¨ππOrder of operations for Clot formation via cGAS STING activation with platelets and Megakaryocytes:
1. Exogenous DNA, which is PLASMID DNA pieces which exists as contamination in the "vaccines"(bacteria can do this too, and spike!) enters a cell and is detected in the cytoplasm.
2. cyclic GMP-AMP synthase (cGAS) protein binds to the plasmid DNA in the cytoplasm of the cell (that is the area outside the nucleus).
3. this activates cGAS, which catalyzes the synthesis of cyclic GMP-AMP (cGAMP).
4. cGAMP binds to stimulator of interferon genes (STING) protein located on the endoplasmic reticulum (ER) membrane and causes a conformational change (dimerization) in STING, initiating activation.
5. STING recruits and activates TANK-binding kinase 1 (TBK1) and IKKΞ΅, and this phosphorylates transcription factors such as IRF3 and NF-ΞΊB.
6. Phosphorylated IRF3 and NF-ΞΊB translocate to the nucleus, where they induce the expression of type-I interferons (IFN-I) and other pro-inflammatory cytokines.
It's the same pathway, and this is how it happens with our cells responsible for making clots, and how this pathway engaged the clotting process:
7. Megakaryocytes, the large bone marrow cells responsible for producing platelets, possess functional cGAS and STING proteins.
When PLASMID DNA activates cGAS-STING pathway in megakaryocytes, it leads to the production of type-I interferons and other cytokines.
8. in maturation process, megakaryocytes extend proplatelets into bone marrow sinusoids.
The cGAS and STING proteins are transferred to these developing proplatelets, which will become platelets.
uh oh
π¨π¨ππ9. Mature platelets contain cGAS and STING proteins inherited from megakaryocytes, and although platelets are anucleate and have limited translational capacity, they can still respond to cGAS-STING activation.
10. Upon encountering exogenous DNA or cGAMP, STING in platelets becomes activated, leading to platelet activation and aggregation, thus, forming clots.
11. Activated STING in platelets enhances their responsiveness to activation signals.
Platelets aggregate more readily, forming clots faster.
12. I have said this phrase over and over again: POsitive Feedback Loops: the smoke detector system is now engaging in a cycle:
The production of cytokines and interferons from STING activation can further amplify the immune response.
Chronic activation of the cGAS-STING pathway by persistent exogenous or self-DNA can lead to sustained inflammation. Self DNA, our DNA, is getting released by cells and detected AGANI by cGAS because, the cells are going through damage by the first round of immune system activation, so it hits the cGAS TWICE. You also have cross talk between cells, and NEGHBOR cells getting their cGAs activated, thus, starting a cascade (paracrine)
Shorter summary:
Plasmid DNA enters the cell, activating cGAS, which produces cGAMP.
cGAMP activates STING, leading to cytokine production and immune response.
STING activation in megakaryocytes influences platelet production and cytokine response.
Platelets inherit cGAS-STING machinery, enhancing their activation and aggregation.
Activated platelets form clots more efficiently, contributing to hemostasis and, in chronic cases, to hypercoagulation.
Feedback Loop: Chronic activation by self-DNA can cause sustained inflammation and autoimmune clotting disorders.
Sources:
Megakaryocytes possess a STING pathway that is transferred to platelets to potentiate activation
ncbi.nlm.nih.gov
STING activation in platelets aggravates septic thrombosis by enhancing platelet activation and granule secretion
sciencedirect.com
Oh no, got liver injury via cGAS STING? Got liver clots? Cancer? That's no bueno:
Activation of cGAS-STING signaling pathway promotes liver fibrosis and hepatic sinusoidal microthrombosis
sciencedirect.com
Innate immune signaling and immunothrombosis: New insights and therapeutic opportunities
onlinelibrary.wiley.com
(if you are new here--there are many tweet threads with over 200 studies backing mechanisms for injury, including positive and negative charges to cause clots and injury, and other ways the LNP, the charges (zeta), spike, RNA itself with mis fold and frame shift happening with ANY RNA, with explanations, and of course there are some "side" mechanisms that are happening, but cGAS STING is the primary pathway. This is ALSO the pathway that was being activated during delta wave. And yes, lots of cross talk and other side "conversations", but this should be the unifier.)
A megakaryocyte is a large, specialized cell found in the bone marrow that is primarily responsible for the production of platelets, which are essential components of blood clotting.
Megakaryocytes are among the largest cells in the bone marrow. They have a large, lobulated nucleus and abundant cytoplasm.
The primary function of megakaryocytes is to produce platelets. Platelets are small, anucleate cell fragments that play a crucial role in hemostasis, the process that stops bleeding by forming blood clots.
Megakaryocytes extend long cytoplasmic projections called proplatelets into the blood vessels of the bone marrow. These proplatelets fragment into thousands of platelets.
π¨ππOrder of operations for Clot formation via cGAS STING activation with platelets and Megakaryocytes:
1. Exogenous DNA, which is PLASMID DNA pieces which exists as contamination in the "vaccines"(bacteria can do this too, and spike!) enters a cell and is detected in the cytoplasm.
2. cyclic GMP-AMP synthase (cGAS) protein binds to the plasmid DNA in the cytoplasm of the cell (that is the area outside the nucleus).
3. this activates cGAS, which catalyzes the synthesis of cyclic GMP-AMP (cGAMP).
4. cGAMP binds to stimulator of interferon genes (STING) protein located on the endoplasmic reticulum (ER) membrane and causes a conformational change (dimerization) in STING, initiating activation.
5. STING recruits and activates TANK-binding kinase 1 (TBK1) and IKKΞ΅, and this phosphorylates transcription factors such as IRF3 and NF-ΞΊB.
6. Phosphorylated IRF3 and NF-ΞΊB translocate to the nucleus, where they induce the expression of type-I interferons (IFN-I) and other pro-inflammatory cytokines.
It's the same pathway, and this is how it happens with our cells responsible for making clots, and how this pathway engaged the clotting process:
7. Megakaryocytes, the large bone marrow cells responsible for producing platelets, possess functional cGAS and STING proteins.
When PLASMID DNA activates cGAS-STING pathway in megakaryocytes, it leads to the production of type-I interferons and other cytokines.
8. in maturation process, megakaryocytes extend proplatelets into bone marrow sinusoids.
The cGAS and STING proteins are transferred to these developing proplatelets, which will become platelets.
uh oh
π¨π¨ππ9. Mature platelets contain cGAS and STING proteins inherited from megakaryocytes, and although platelets are anucleate and have limited translational capacity, they can still respond to cGAS-STING activation.
10. Upon encountering exogenous DNA or cGAMP, STING in platelets becomes activated, leading to platelet activation and aggregation, thus, forming clots.
11. Activated STING in platelets enhances their responsiveness to activation signals.
Platelets aggregate more readily, forming clots faster.
12. I have said this phrase over and over again: POsitive Feedback Loops: the smoke detector system is now engaging in a cycle:
The production of cytokines and interferons from STING activation can further amplify the immune response.
Chronic activation of the cGAS-STING pathway by persistent exogenous or self-DNA can lead to sustained inflammation. Self DNA, our DNA, is getting released by cells and detected AGANI by cGAS because, the cells are going through damage by the first round of immune system activation, so it hits the cGAS TWICE. You also have cross talk between cells, and NEGHBOR cells getting their cGAs activated, thus, starting a cascade (paracrine)
Shorter summary:
Plasmid DNA enters the cell, activating cGAS, which produces cGAMP.
cGAMP activates STING, leading to cytokine production and immune response.
STING activation in megakaryocytes influences platelet production and cytokine response.
Platelets inherit cGAS-STING machinery, enhancing their activation and aggregation.
Activated platelets form clots more efficiently, contributing to hemostasis and, in chronic cases, to hypercoagulation.
Feedback Loop: Chronic activation by self-DNA can cause sustained inflammation and autoimmune clotting disorders.
Sources:
Megakaryocytes possess a STING pathway that is transferred to platelets to potentiate activation
ncbi.nlm.nih.gov
STING activation in platelets aggravates septic thrombosis by enhancing platelet activation and granule secretion
sciencedirect.com
Oh no, got liver injury via cGAS STING? Got liver clots? Cancer? That's no bueno:
Activation of cGAS-STING signaling pathway promotes liver fibrosis and hepatic sinusoidal microthrombosis
sciencedirect.com
Innate immune signaling and immunothrombosis: New insights and therapeutic opportunities
onlinelibrary.wiley.com
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