IndraLab
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"Because Pten deletion promoted mTOR signaling and axon growth rostral to injury irrespective of age in both the rubrospinal and corticospinal systems, we hypothesized that differences in environmental influences at and around the lesion site could be responsible for the age dependent decline in axon regeneration beyond the injury site."
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"Transfection of PTEN into the PC3 cells decreased the activation of Akt and the downstream mTOR regulated 70-kDa S6 (p70 (s6k)) kinase and reversed the resistance to doxorubicin in these cells, indicating that changes in PTEN status and Akt activation modulate the cellular response to doxorubicin."
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"A mechanistic study further reveals that downregulation of hepatic Me1 expression is largely mediated by the phosphatase and tensin homologue (PTEN)-dependent suppression of the mechanistic target of rapamycin/sterol regulatory element-binding protein 1 (mTOR/SREBP1) signaling pathway in hepatic I/R model."
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"We therefore decided to compare the primary effects of altered mTOR signaling on synaptic transmission in both glutamatergic and GABAergic neurons by characterizing autaptic cultures of neurons in which mTOR activity was increased by loss of the negative regulator Pten or decreased by treatment with the mTOR inhibitor rapamycin."
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"Phosphatase and tensin homolog (PTEN) activation inhibits AKT and mTOR signaling, and current studies have confirmed that microRNA (miRNA) -21 targets PTEN to activate the AKT and mTOR pathway, which plays an important role in the key pathological damage observed in DN [XREF_BIBR, XREF_BIBR]."
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"Phosphatase and tensin homolog (PTEN) mutation in glioblastoma multiforme (GBM) patients causes abnormally high activity of the pathways of Phosphatidylinositide 3-kinases (PI3K), Protein Kinase B (AKT), and the mammalian target of rapamycin (mTOR) and is associated with unfavorable prognosis."
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"Specifically, genomic profiling based on clinical-grade NGS could identify whether PTEN loss or other GAs activating the mTOR pathway are present alongside the BRAF fusion in a pilocytic astrocytoma of patient, thus suggesting a potential responsiveness to combined sorafenib and mTOR targeted therapy."
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"Here we demonstrate that mTOR activity in Ehrlich Lettre ascites (ELA) cells is transiently increased within minutes following osmotic cell swelling and that inhibition of phosphatidylinositol-3-phosphatase (PTEN) counteracts the upstream phosphatidylinositol kinase and potentiates mTOR activity."
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"Since PTEN negatively regulates the mTOR signaling pathway, we then investigated whether there was interaction between the MTOR rs2295080 and PTEN rs701848 in influencing RCC risk, however, as shown in XREF_TABLE, no significant interaction was observed (P interaction = 0.118), although individuals with both risk genotypes (rs2295080 TT and rs701848 CC) had a significantly increased RCC risk of 1.72."
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"This indicated that loss of Pten activates Akt and that there might be a complex mechanism, through which Pten regulates the expression of Sox2 at different stages during ESCs differentiation.Mouse ESCs are maintained by using the cytokine LIF to activate Stat3 signaling , and PTEN negatively regulates PI3K/mammalian target of rapamycin (mTOR) , which promotes STAT3 activity ."
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"We have previously shown that mTORC1 activity, detected as phosphorylation of 4E‐BP1, is transiently increased in mouse fibroblasts following hypoosmotic exposure, that is, mTOR activity is significantly increased and boosted by PTEN inhibition within minutes following osmotic cell swelling but reduced following prolonged (4 h/24 h) hypotonic adaptation (Lambert et al. 2014)."
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"In addition to FXS and RTT, a number of genetic susceptibilities have been linked to elevated autism risk including maternal 15q11-13 chromosomal duplications, anomalies in the tumor suppressor genes NF1, TSC1 and TSC2, and PTEN that activate mammalian target of rapamycin (mTOR)/phosphatidylinositol 3-kinase (PI3K) signaling pathways, and mutations in a range of synaptic genes such as the neurexins, neuroligins, SHANK3 and CNTNAP2."
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"7 EGFR, which belongs to the erbB family, activates the same downstream signaling pathways, including the Ras-Raf-MAPK signaling pathway and the phosphoinositide-3-kinase (PI3K)/AKT signaling pathway, involving other key effectors such as nuclear factor-kappaB and mammalian target of rapamycin (mTOR), which could be inhibited by phosphatase and tensin homolog (PTEN)."
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"The PTEN and TSC2 tumor suppressors function to antagonize mTOR (mammalian target of rapamycin) activation by Akt; hence, compound heterozygous inactivation of Pten and Tsc2 in the mouse may in principle exacerbate the tumor phenotypes observed in the single mutants in a reciprocal manner."
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"A protein positioned downstream of PTEN, namely, PRAS40, does not inhibit the mTOR pathway in its phosphorylated form (discussed in Section 2.1), and it can therefore be assumed that upon activation of the mTOR pathway, these proteins are linked and correlate in terms of phosphorylation status."
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"The same group revealed that concurrent activation of mTOR and Janus kinase and signal transducers and activators of transcription (JAK and STAT3) pathways, by double inhibition of PTEN and suppressor of cytokine signaling 3 (SOCS3), are necessary for sustaining long distance axon regeneration in the adult CNS."
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"Interestingly, it has been shown recently that loss of Pten induces ER UDPase ectonucleoside triphosphate diphosphohydrolase 5 (ENTPD5), and activation of the AKT and mTOR pathway leads to induction of pyruvate kinase isoenzyme type M2 (PKM2), which contribute to aerobic glycolysis, also known as the Warburg effect, and tumor growth in a xenograft model of prostate cancer."
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"MTOR can be inhibited by rapamycin via interaction with its receptor FK506-binding protein 12, and is activated by PI3K and PTEN loss; eventually this initiates carcinogenesis and subsequent progression via the oxygen and nutrient supply through the upregulation of HIF1α expression and promotion of angiogenesis (63,64)."
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"However, Magee et al. elegantly demonstrated that after PTEN deletion, which activates the mTOR-signalling pathway, deletion of Rictor abrogates leukaemogenesis and HSC depletion in adult, but not neonatal, mice [53], highlighting that the PTEN-mTORC2 signalling axis has a role in activating these processes in a temporally dependent manner."
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"Similar effects of ezetimibe have been noted in other tumor bearing models if mice are fed a low-fat, low-cholesterol diet.30 Although PTEN deficiency can increase cholesterol synthesis by activating the mammalian target of rapamycin and its downstream targets PPAR-gamma, srebp-1 and srebp-2,31 the increase in serum cholesterol levels was mild in Pten Deltahep mice."
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"Alternatively, it is possible that the effects on the PI3K and mTOR pathway mediated by PTEN loss are not reflected in steady-state levels of these various phosphorylated proteins or that PTEN loss results in effects on prostate cancer in addition to the PI3K and mTOR pathway (eg, c-Jun N-terminal kinase [JNK] signaling and/or enhancer of zeste homolog 2 [EZH2] overexpression)."
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"The physical microenvironment can be transformed into pathological tumours, fibrosis and inflammatory microenvironments, inducing age-related diseases, such as cancer, degenerative diseases and inflammation However, in a special type of senescence, PTEN loss-induced senescence (PICS), mammalian target of rapamycin complexes 1 and 2 (mTORC1 and mTORC2) can directly stabilize p53 and initiate the p21-associated senescent pathway through PI3K/AKT activation and MDM2 inhibition without triggering the DDR (Jung et al., 2019) ."
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"Mutations or deletions of phosphatase and tensin homolog (PTEN) and the heterodimeric complex of tuberous sclerosis proteins 1 and 2 (TSC1 and hamartin, TSC2 and tuberin) can dramatically upregulate mTOR signaling and contribute to a class of human neurological diseases characterized as " TORopathies "."