Send to:

Choose Destination
    • Showing Current items.

    SHC1 SHC adaptor protein 1 [ Homo sapiens (human) ]

    Gene ID: 6464, updated on 15-Apr-2019

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Using multiple -omics approach, study validated key molecules, such as CAP1, SHC1 and PRCP, that might play a significant role in IgA nephropathy pathogenesis.

    Identification of novel molecular signatures of IgA nephropathy through an integrative -omics analysis.
    Krochmal M, Cisek K, Filip S, Markoska K, Orange C, Zoidakis J, Gakiopoulou C, Spasovski G, Mischak H, Delles C, Vlahou A, Jankowski J., Free PMC Article

    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.

    Novel miR-5582-5p functions as a tumor suppressor by inducing apoptosis and cell cycle arrest in cancer cells through direct targeting of GAB1, SHC1, and CDK2.
    An HJ, Kwak SY, Yoo JO, Kim JS, Bae IH, Park MJ, Cho MY, Kim J, Han YH.

    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.

    p66Shc deficiency enhances CXCR4 and CCR7 recycling in CLL B cells by facilitating their dephosphorylation-dependent release from β-arrestin at early endosomes.
    Patrussi L, Capitani N, Cattaneo F, Manganaro N, Gamberucci A, Frezzato F, Martini V, Visentin A, Pelicci PG, D'Elios MM, Trentin L, Semenzato G, Baldari CT.

    p66Shc expression in peripheral blood mononuclear cells was not associated with prevalent diabetic complications but predicted new onset of complications, especially macroangiopathy.

    p66Shc gene expression in peripheral blood mononuclear cells and progression of diabetic complications.
    Fadini GP, Albiero M, Bonora BM, Poncina N, Vigili de Kreutzenberg S, Avogaro A., Free PMC Article

    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.

    The Src homology and collagen A (ShcA) adaptor protein may participate in the pathogenesis of membranous lupus nephritis.
    Cao W, Liu X, Xu X, Zeng M, Sun B, Yu X, Wang N, Mao H, Zhang B, Yuan Y, Xing C.

    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.

    Phosphorylation of threonine residues on Shc promotes ligand binding and mediates crosstalk between MAPK and Akt pathways in breast cancer cells.
    Suen KM, Lin CC, Seiler C, George R, Poncet-Montange G, Biter AB, Ahmed Z, Arold ST, Ladbury JE.

    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.

    Modulation of mitochondrial dysfunction-related oxidative stress in fibroblasts of patients with Leigh syndrome by inhibition of prooxidative p66Shc pathway.
    Wojtala A, Karkucinska-Wieckowska A, Sardao VA, Szczepanowska J, Kowalski P, Pronicki M, Duszynski J, Wieckowski MR.

    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.

    p66Shc: A novel biomarker of tubular oxidative injury in patients with diabetic nephropathy.
    Xu X, Zhu X, Ma M, Han Y, Hu C, Yuan S, Yang Y, Xiao L, Liu F, Kanwar YS, Sun L., Free PMC Article

    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

    Recombinant adenovirus of human p66Shc inhibits MCF-7 cell proliferation.
    Yang X, Xu R, Lin Y, Zhen Y, Wei J, Hu G, Sun H., Free PMC Article

    STAT4 is a novel transcriptional regulator of p66Shc in normal and chronic lymphocytic leukemia B cells

    Expression of the p66Shc protein adaptor is regulated by the activator of transcription STAT4 in normal and chronic lymphocytic leukemia B cells.
    Cattaneo F, Patrussi L, Capitani N, Frezzato F, D'Elios MM, Trentin L, Semenzato G, Baldari CT., Free PMC Article

    Isoform b of DDR1 is responsible for collagen I-induced up-regulation of N-cadherin and tyrosine 513 of DDR1b is necessary.

    Up-regulation of N-cadherin by Collagen I-activated Discoidin Domain Receptor 1 in Pancreatic Cancer Requires the Adaptor Molecule Shc1.
    Huang H, Svoboda RA, Lazenby AJ, Saowapa J, Chaika N, Ding K, Wheelock MJ, Johnson KR., Free PMC Article

    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

    Nicotine Exposure Augments Renal Toxicity of 5-aza-cytidine Through p66shc: Prevention by Resveratrol.
    Arany I, Hall S, Faisal A, Dixit M.

    The results show that the interaction between STS-1 and ShcA is regulated in response to EGF receptor activation.

    Identification of STS-1 as a novel ShcA-binding protein.
    van der Meulen T, Swarts S, Fischer W, van der Geer P.

    Nox4-derived H2O2 in part activates Nox2 to increase mitochondrial ROS via pSer36-p66Shc, thereby enhancing VEGFR2 signaling and angiogenesis in endothelial cells.

    ROS-induced ROS release orchestrated by Nox4, Nox2, and mitochondria in VEGF signaling and angiogenesis.
    Kim YM, Kim SJ, Tatsunami R, Yamamura H, Fukai T, Ushio-Fukai M., Free PMC Article

    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).

    Novel Insights into the PKCβ-dependent Regulation of the Oxidoreductase p66Shc.
    Haller M, Khalid S, Kremser L, Fresser F, Furlan T, Hermann M, Guenther J, Drasche A, Leitges M, Giorgio M, Baier G, Lindner H, Troppmair J., Free PMC Article

    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.

    Non-canonical dynamic mechanisms of interaction between the p66Shc protein and Met receptor.
    Landry M, Pomerleau V, Saucier C., Free PMC Article

    regulates the alternative splicing of XAF1 in extracellular matrix-detachment induced autophagy to coordinate with the anoikic cell death

    Detachment-Based Equilibrium of Anoikic Cell Death and Autophagic Cell Survival Through Adaptor Protein p66(Shc).
    Cai Z, Zhao D, Sun Y, Gao D, Li X, Yang J, Ma Z.

    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.

    The silence of p66(Shc) in HCT8 cells inhibits the viability via PI3K/AKT/Mdm-2/p53 signaling pathway.
    Zhang L, Zhu S, Shi X, Sha W., Free PMC Article

    In mice and humans, reduced p66Shc levels protect from obesity, but not from ectopic fat accumulation, glucose intolerance and insulin resistance.

    p66Shc deletion or deficiency protects from obesity but not metabolic dysfunction in mice and humans.
    Ciciliot S, Albiero M, Menegazzo L, Poncina N, Scattolini V, Danesi A, Pagnin E, Marabita M, Blaauw B, Giorgio M, Trinei M, Foletto M, Prevedello L, Nitti D, Avogaro A, Fadini GP.

    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.

    ShcA Protects against Epithelial-Mesenchymal Transition through Compartmentalized Inhibition of TGF-β-Induced Smad Activation.
    Muthusamy BP, Budi EH, Katsuno Y, Lee MK, Smith SM, Mirza AM, Akhurst RJ, Derynck R., Free PMC Article

    p66shc expression in coronary heart disease patients was significantly higher compared with the control group

    The expression of p66shc in peripheral blood monocytes is increased in patients with coronary heart disease and correlated with endothelium-dependent vasodilatation.
    Miao Q, Wang Q, Dong L, Wang Y, Tan Y, Zhang X.

    Finally, a crystal structure of EGFR in complex with a primed Shc1 peptide reveals the structural basis for EGFR substrate specificity.

    EGF-receptor specificity for phosphotyrosine-primed substrates provides signal integration with Src.
    Begley MJ, Yun CH, Gewinner CA, Asara JM, Johnson JL, Coyle AJ, Eck MJ, Apostolou I, Cantley LC., Free PMC Article

    p53-dependent augmentation of p66(Shc) expression and function represents a key signalling response contributing to beta cell apoptosis under conditions of lipotoxicity

    The p66(Shc) redox adaptor protein is induced by saturated fatty acids and mediates lipotoxicity-induced apoptosis in pancreatic beta cells.
    Natalicchio A, Tortosa F, Labarbuta R, Biondi G, Marrano N, Carchia E, Leonardini A, Cignarelli A, Bugliani M, Marchetti P, Fadini GP, Giorgio M, Avogaro A, Perrini S, Laviola L, Giorgino F.

    Data show that ouabain-induced glioblastoma cells apoptosis and increased reactive oxygen species (ROS) generation in extracellular signal-related kinases ERK1/2-Shc signaling adaptor protein p66SHC-dependent pathway.

    Ouabain elicits human glioblastoma cells apoptosis by generating reactive oxygen species in ERK-p66SHC-dependent pathway.
    Yan X, Liang F, Li D, Zheng J.

    Results show elevated level of p66Shc protein reveal in ovarian cancer cells (OCa) indicating a functional role of the protein in regulating the proliferation of OCa cells.

    p66Shc longevity protein regulates the proliferation of human ovarian cancer cells.
    Muniyan S, Chou YW, Tsai TJ, Thomes P, Veeramani S, Benigno BB, Walker LD, McDonald JF, Khan SA, Lin FF, Lele SM, Lin MF., Free PMC Article

    firstprevious page of 6 nextlast
    Support Center