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https://www.mdpi.com/2076-393X/9/1/36/htm

It is generally thought that the sole function of viral membrane fusion proteins is to allow the viruses to bind to the host cells for the purpose of viral entry into the cells, so that the genetic materials can be released and the viral replication and amplification can take place.

However, recent observations suggest that the SARS-CoV-2 spike protein can by itself trigger cell signaling that can lead to various biological processes. It is reasonable to assume that such events, in some cases, result in the pathogenesis of certain diseases.

Our laboratory only tested the effects of the SARS-CoV-2 spike protein in lung vascular cells and those implicated in the development of PAH. However, this protein may also affect the cells of systemic and coronary vasculatures, eliciting other cardiovascular diseases such as coronary artery disease, systemic hypertension, and stroke. In addition to cardiovascular cells, other cells that express ACE2 have the potential to be affected by the SARS-CoV-2 spike protein, which may cause adverse pathological events.

Thus, it is important to consider the possibility that the SARS-CoV-2 spike protein produced by the new COVID-19 vaccines triggers cell signaling events that promote PAH, other cardiovascular complications, and/or complications in other tissues/organs in certain individuals (Figure 3). We will need to monitor carefully the long-term consequences of COVID-19 vaccines that introduce the spike protein into the human body.

Furthermore, while human data on the possible long-term consequences of spike protein-based COVID-19 vaccines will not be available soon, it is imperative that appropriate experimental animal models are employed as soon as possible to ensure that the SARS-CoV-2 spike protein does not elicit any signs of the pathogenesis of PAH or any other chronic pathological conditions.

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Well, lookie here. Might be a coincidence, might be misunderstanding on my part.

But, following up on this old post from FReeper Cathi --

"The SARS-CoV-2 spike protein without the rest of the viral components has also been shown to activate cell signaling by Patra et al. [29]. The authors reported that the full-length SARS-CoV-2 spike protein expressed by the means of transient transfection, either in the human lung alveolar epithelial cell line A549 or in the human liver epithelial cell line Huh7.5, activated NF-κB and AP-1 transcription factors as well as p38 and ERK mitogen-activated protein kinases, releasing interleukin-6. This cell signaling cascade was found to be triggered by the SARS-CoV-2 spike protein downregulating the ACE2 protein expression, subsequently activating the angiotensin II type 1 receptor [29]. These experiments using transient transfection may reflect the intracellular effects of the spike protein that could be triggered by the RNA- and viral vector-based vaccines.

These results collectively reinforce the idea that human cells are sensitively affected by the extracellular and/or intracellular spike proteins though the activation of cell signal transduction."

I replied:

OK, so what proteins are preferentially (or increasingly) synthesized by the cell upon binding by the spike protein? What are their systemic downstream effects, in those not suffering insult to the lungs by a real c00f infection?

...activated NF-κB and AP-1 transcription factors as well as p38 and ERK mitogen-activated protein kinases,...

Well, The NF-κB transcription factor was discovered 30 years ago and has since emerged as the master regulator of inflammation and immune homeostasis. It achieves this status by means of the large number of important pro- and antiinflammatory factors under its transcriptional control.

So I tried Goolaging for "NF-κB transcription factor clotting" and found this old paper:

NF-κB Transcription Factor p50 Critically Regulates Tissue Factor in Deep Vein Thrombosis*

NF-κB transcription factors regulate the expression of tissue factor (TF), a principal initiator of the coagulation cascade. Dominant among them is the p50/p65 heterodimer.

Now, I fully admit, I notice this is an old paper and might have been superseded, or disproven. The paper was working on Mice, and not people; and had a disclaimer as such in its own discussion section. And, for all I know, I misread it and got it ass-backwards. But the fact there seems to be an association, between a protein produced, when you ring the doorbell of the ACE2 receptor, and Deep Vein Thrombosis; and that both the Coof and mRNA jabs produce spike protein which interact with the ACE2 receptor; and that both the Coof and mRNA jabs cause clotting issues (and DVT has been presented in the literature as an occult ("hidden" not "demonic") symptom of Coof infection, is enough to make me ask if we have any cardiologists / hematologists / thrombologists here, who can comment from a more informed perspective?