Spike protein (inc vax) induced immunodeficiency & carcinogenesis megathread #16: Pl3K and mTOR inhibition.
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Any extracts used in the following article are for non commercial research and educational purposes only and may be subject to copyright from their respective owners.
Mechanistically, SCV-2-S inhibited the PI3K/AKT/mTOR pathway by upregulating intracellular reactive oxygen species (ROS) levels, thus promoting the autophagic response.
Next question is how long the ROS induced inhibition lasts for, and by implication how long spike protein binds to ACE2? Extremely concerning.
SARS-CoV-2 spike promotes inflammation and apoptosis through autophagy by ROS-suppressed PI3K/AKT/mTOR signaling (2021)
PI3K and mTOR signaling pathways in cancer: new data on targeted therapies
Lise Willems et al. Curr Oncol Rep. 2012 Apr.
Abstract
The mammalian target of rapamycin (mTOR) and the phosphoinositide 3-kinase (PI3K) signaling pathways are commonly deregulated in cancers and promote cellular growth, proliferation, and survival. mTOR is part of two complexes, mTORC1 and mTORC2, with different biochemical structures and substrates specificity. PI3K/AKT activation may result from genetic hits affecting different components of the pathway, whereas the mechanisms leading to constitutive mTORC1 activation remain globally unknown. The connections between the PI3K and mTOR kinases are multiple and complex, including common substrates, negative feedback loops, or direct activation mechanisms. First-generation allosteric mTOR inhibitors (eg, rapamycin) are mainly active on mTORC1 and mostly display cytostatic anti-tumor activity. Recently, second-generation catalytic mTOR inhibitors targeting both mTOR complexes 1 and 2 have been developed. Some of them also inhibit class IA PI3K. Here, we highlight recent data generated with these new inhibitors against cancer cells and their potential as anti-cancer drugs.
Spike protein (inc vax) induced immunodeficiency & carcinogenesis megathread #16: Pl3K and mTOR inhibition.
Spike protein (inc vax) induced immunodeficiency & carcinogenesis megathread #16: Pl3K and mTOR inhibition.
Spike protein (inc vax) induced immunodeficiency & carcinogenesis megathread #16: Pl3K and mTOR inhibition.
Any extracts used in the following article are for non commercial research and educational purposes only and may be subject to copyright from their respective owners.
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Background/relevance:
Mechanistically, SCV-2-S inhibited the PI3K/AKT/mTOR pathway by upregulating intracellular reactive oxygen species (ROS) levels, thus promoting the autophagic response.
Next question is how long the ROS induced inhibition lasts for, and by implication how long spike protein binds to ACE2? Extremely concerning.
SARS-CoV-2 spike promotes inflammation and apoptosis through autophagy by ROS-suppressed PI3K/AKT/mTOR signaling (2021)
https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC8390448/
* * *
PI3K and mTOR signaling pathways in cancer: new data on targeted therapies
Lise Willems et al. Curr Oncol Rep. 2012 Apr.
Abstract
The mammalian target of rapamycin (mTOR) and the phosphoinositide 3-kinase (PI3K) signaling pathways are commonly deregulated in cancers and promote cellular growth, proliferation, and survival. mTOR is part of two complexes, mTORC1 and mTORC2, with different biochemical structures and substrates specificity. PI3K/AKT activation may result from genetic hits affecting different components of the pathway, whereas the mechanisms leading to constitutive mTORC1 activation remain globally unknown. The connections between the PI3K and mTOR kinases are multiple and complex, including common substrates, negative feedback loops, or direct activation mechanisms. First-generation allosteric mTOR inhibitors (eg, rapamycin) are mainly active on mTORC1 and mostly display cytostatic anti-tumor activity. Recently, second-generation catalytic mTOR inhibitors targeting both mTOR complexes 1 and 2 have been developed. Some of them also inhibit class IA PI3K. Here, we highlight recent data generated with these new inhibitors against cancer cells and their potential as anti-cancer drugs.
https://pubmed.ncbi.nlm.nih.gov/22350330/
Link to full PDF (organisations or purchase):
https://link.springer.com/article/10.1007/s11912-012-0227-y
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