IndraLab
Statements
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"Abnormal signaling and metabolic dysregulation in pulmonary vascular cells may contribute to the development of PAH, alongside several currently investigated pathways, including the nitric oxide pathway, prostacyclin pathway, endothelin-1 pathway, transforming growth factor pathway, renin–angiotensin–aldosterone system pathway, RhoA/ROCK signaling pathway, platelet-derived growth factor pathway, peroxisome proliferator-activated receptors pathway, HIF1 pathway, protein kinase B pathway, mitochondrial phosphatase and tensin homolog-induced kinase 1 pathway, and the HIPPO and p53 signaling pathways [36, 63]."
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"Several studies have demonstrated that PTEN can activate p53 through direct and indirect protein–protein interactions, including phosphatase-dependent and phosphatase-independent mechanisms. xref , xref With all of these observations, we propose a model for the action of progesterone in ER/PR-positive breast cancer via PR in a time- and concentration-dependent manner by modulating signaling pathways that include tumor suppressor pathways ( xref )."
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"PTEN is expressed in vascular smooth muscle cells and induces p53 activity to suppress tumor-induced angiogenesis.15 16 Therefore, mutations in the PTEN leading to the loss of its mediating effect on the pathway result in abnormal angiogenesis, which might, in turn, explain the incidence of AVMs.17A small group of patients with BRRS exhibit vascular malformations, including arteriovenous shunts, anomalies, and fistulas."
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"Prolonged stable disease (SD) was defined as lasting ≥+ 6 months.Genetic analysis was performed to analyze phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA), phosphatase and tensin homolog (PTEN), rapidly accelerated fibrosarcoma (RAF), rat sarcoma virus (RAS), and tumor protein p53 (TP53) aberrations for patients who had archival tissue samples available."
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"AKT inhibition suppresses cumulus cell expansion, xref and in pancreatic islet β-cells, it results in a dysfunction that leads to apoptosis through PTEN activation. xref PTEN is a tumour suppressor that induces apoptosis by activating caspase-3 and caspase-8, xref inhibiting cell proliferation, xref and increasing apoptosis. xref The activation of PTEN activates p53 and their interactions induce apoptosis through the Bax and caspase 3 pathways. xref PTEN and p53 also form a complex in the nucleus and induce the expression of tumour suppressors, resulting in apoptosis xref and the induction of cell cycle arrest at the G1 phase to inhibit cell proliferation. xref "
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"While dapagliflozin did not synergize with paclitaxel in mice with p53-driven M6, MYC-driven M158 tumors, or MEK1-driven EpH4 1424 tumors with Brca1-driven tumors, it prolonged survival in mice with Pten-driven EMT6 tumors and HRAS-driven Ac711 tumors (Fig. 6a–e), in addition to ERBB2-driven MMTV-PyMT, and p53 and Pik3ca-driven 4T1 tumors (Fig. 4b, d)."
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"Accumulating evidence is beginning to suggest that, in certain circumstances, PTEN (phosphatase and tensin homologue deleted on chromosome 10)/PI3K/Akt also promotes p53 translation and protein stability, suggesting that additional mechanisms may be involved in the Akt mediated regulation of p53 in tumours."
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"Moreover, because Casein Kinase I (CKI) family members have been shown to phosphorylate N-terminal sites of p53 and to decrease p53 affinity to Mdm2, and because phosphorylation of Mdm2 by CKIδ leads to Mdm2 degradation and p53 expression (Knippschild et al., 2014), we determined their transcript levels in PTEN-deficient PINs at various time points."