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Using multiple -omics approach, study validated key molecules, such as CAP1, SHC1 and PRCP, that might play a significant role in IgA nephropathy pathogenesis.
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miR-5582-5p induced apoptosis and cell cycle arrest in cancer cells, but not in normal cells. GAB1, SHC1, and CDK2 were identified as direct targets of miR-5582-5p.
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Identification of p66Shc as a regulator of CXCR4/CCR7 recycling in B cells; this underscores the relevance of its deficiency to Chronic lymphocytic leukemia pathogenesis and provides new clues to the mechanisms underlying the therapeutic effects of ibrutinib.
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p66Shc expression in peripheral blood mononuclear cells was not associated with prevalent diabetic complications but predicted new onset of complications, especially macroangiopathy.
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The positive rate of ShcA was significantly higher in lupus nephritis (LN) class V, while it was negative in primary membranous nephropathy (MN) and other secondary MN, suggesting that ShcA might be used to distinguish membranous LN from primary and other secondary MN.
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Data suggest that up-regulation of SHC threonine phosphorylation is responsible for elevated Akt-signaling and Erk-signaling in triple-negative breast cancer cell lines.
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Characterization of bioenergetic parameters and reactive oxygen species production showed that the cellular model of Leigh syndrome is described by increased intracellular oxidative stress and oxidative damage to DNA and proteins, which correlate with increased p66Shc phosphorylation at Ser36.
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A positive relationship between the p66Shc expression and oxidative stress was found. p66Shc and oxidative stress were significant predictors of the degree of tubular damage.
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Adeno-X Adenoviral System 3 can be used to efficiently construct recombinant adenovirus containing p66Shc gene, and the Adeno-X can inhibit the proliferation of MCF-7 cells by inducing cell cycle arrest at the G2/M phase
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STAT4 is a novel transcriptional regulator of p66Shc in normal and chronic lymphocytic leukemia B cells
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Isoform b of DDR1 is responsible for collagen I-induced up-regulation of N-cadherin and tyrosine 513 of DDR1b is necessary.
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NIC exacerbated AZA-dependent injury via augmenting p66shc transcription. While RES suppressed NIC+AZA-mediated injury, -surprisingly-it further enhanced activity of the p66shc promoter. RES protected cells via the cytoplasmic p66shc/Nrf2/heme oxygenase-1 (HO-1) axis
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The results show that the interaction between STS-1 and ShcA is regulated in response to EGF receptor activation.
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Nox4-derived H2O2 in part activates Nox2 to increase mitochondrial ROS via pSer36-p66Shc, thereby enhancing VEGFR2 signaling and angiogenesis in endothelial cells.
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Taken together, these data argue for a complex mechanism of PKC-beta-dependent regulation of SHCA (p66) activation involving Ser(139) and a motif surrounding Ser(213).
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Data identify, for the first time, a novel non-canonical dynamic mode of interaction between Met and the p66 protein isoform of Shc and its effects on rewiring binding effector complexes according to the activation state of the receptor.
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regulates the alternative splicing of XAF1 in extracellular matrix-detachment induced autophagy to coordinate with the anoikic cell death
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The silence of p66(Shc) in HCT8 cells reduced the proliferation and accelerated the apoptosis, in addition, the expression of pro-apoptotic proteins caspase-3, caspase-9, Bax was enhanced and the expression of anti-apoptotic protein Bcl-2 was declined.
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In mice and humans, reduced p66Shc levels protect from obesity, but not from ectopic fat accumulation, glucose intolerance and insulin resistance.
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Data suggest SHC1 (SH2 domain protein C1) expression down-regulates epithelial-mesenchymal transition by repressing TGFB-induced SMAD2/3 activation through differential partitioning of receptors at cell surface of mammocytes/keratinocytes.
