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Isoform b of DDR1 is responsible for collagen I-induced up-regulation of N-cadherin (show CDH2 ELISA Kits) and tyrosine 513 of DDR1b is necessary.
NIC (show NCSTN ELISA Kits) exacerbated AZA-dependent injury via augmenting p66shc transcription. While RES suppressed NIC (show NCSTN ELISA Kits)+AZA-mediated injury, -surprisingly-it further enhanced activity of the p66shc promoter. RES protected cells via the cytoplasmic p66shc/Nrf2 (show GABPA ELISA Kits)/heme oxygenase-1 (HO-1 (show HMOX1 ELISA Kits)) axis
The results show that the interaction between STS-1 (show STS1 ELISA Kits) and ShcA is regulated in response to EGF receptor (show EGFR ELISA Kits) activation.
Nox4 (show NOX4 ELISA Kits)-derived H2O2 in part activates Nox2 (show CYBB ELISA Kits) to increase mitochondrial ROS (show ROS1 ELISA Kits) via pSer36-p66Shc, thereby enhancing VEGFR2 (show KDR ELISA Kits) signaling and angiogenesis in endothelial cells.
Taken together, these data argue for a complex mechanism of PKC-beta-dependent regulation of SH (show POLD3 ELISA Kits)CA (p66) activation invol (show SIGLEC1 ELISA Kits)ving Ser(139) and a motif surroun (show SIGLEC1 ELISA Kits)ding Ser(213).
Data identify, for the first time, a novel non-canonical dynamic mode of interaction between Met and the p66 (show POLD3 ELISA Kits) protein isoform of Shc and its effects on rewiring binding effector complexes according to the activation state of the receptor.
regulates the alternative splicing of XAF1 (show XAF1 ELISA Kits) in extracellular matrix-detachment induced autophagy to coordinate with the anoikic cell death
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 (show CASP3 ELISA Kits), caspase-9 (show CASP9 ELISA Kits), Bax (show BAX ELISA Kits) was enhanced and the expression of anti-apoptotic protein Bcl-2 (show BCL2 ELISA Kits) was declined.
In mice and humans, reduced p66Shc levels protect from obesity, but not from ectopic fat accumulation, glucose intolerance and insulin (show INS ELISA Kits) resistance.
Data suggest SHC1 (SH2 domain protein C1) expression down-regulates epithelial-mesenchymal transition by repressing TGFB (show TGFB1 ELISA Kits)-induced SMAD2 (show SMAD2 ELISA Kits)/3 activation through differential partitioning of receptors at cell surface of mammocytes/keratinocytes.
Data show that adaptor protein Shc is required for angiogenesis in zebrafish (accession number LOC563639), mice, and human vascular endothelial cell-culture models.
ShcA is required for Wnt-5a (show WNT5A ELISA Kits)/Ror2 (show ROR2 ELISA Kits) mediated upregulation of xPAPC (show PCDH8 ELISA Kits), which demonstrates the functional relevance of this interaction.
Studied p66Shc levels, redox state, and developmental potential in early bovine embryos. p66Shc content was increased by either high (20%) O(2) culture or H(2)O(2) treatment, and significantly dec'd by antioxidant polyethylene glycol-conjugated catalase (show CAT ELISA Kits).
p66shc, but not p53 (show TP53 ELISA Kits), is significantly more abundant in an embryo population that exhibits higher frequencies of embryo arrest.
p66Shc is involved in the regulation of embryo development specifically in mediating early cleavage arrest and facilitating development to the blastocyst stage for in vitro produced bovine embryos
These results support a model in which Shc orchestrates signals from cell-cell and cell-matrix adhesions to elicit flow-induced inflammatory signaling.
The results indicate that Shc proteins should be considered as potential targets for developing interventions to mitigate weight gain on high-fat diet by stimulating energy expenditure.
Hyperglycemia and elevated free fatty acids in the diabetic milieu recruit p66Shc to upregulate endothelial miR (show MLXIP ELISA Kits)-34a via an oxidant-sensitive mechanism, which leads to endothelial dysfunction by targeting Sirt1 (show SIRT1 ELISA Kits).
p66SHC-mediated oxidative stress and telomere shortening synergize in some tissues (including testes) to accelerate aging.
Taken together, these data argue for a complex mechanism of PKCbeta-dependent regulation of p66 (show POLD3 ELISA Kits) activation involving Ser (show SIGLEC1 ELISA Kits)(139) and a motif surrounding Ser (show SIGLEC1 ELISA Kits)(213).
JNK1 (show MAPK8 ELISA Kits)/2-dependent regulation of p66ShcS36 phosphorylation, is reported.
Data show that the major mitochondrial partner of Shc adaptor protein p46Shc is the lipid oxidation enzyme 3-ketoacylCoA thiolase (show HADHB ELISA Kits) ACAA2 (show ACAA2 ELISA Kits), to which p46Shc binds directly and with a strong affinity.
p53 (show TP53 ELISA Kits)-dependent augmentation of p66(Shc) expression and function represents a key signalling response contributing to beta cell apoptosis under conditions of lipotoxicity
Silencing of p66(Shc) restored insulin (show INS ELISA Kits) response via IRS-1 (show IRS1 ELISA Kits)/Akt (show AKT1 ELISA Kits)/eNOS (show NOS3 ELISA Kits) pathway. Its knockdown in endothelial cells from Ob/Ob mice lessened ROS (show ROS1 ELISA Kits) production, FFA oxidation, and dysregulation of redox-sensitive pathways.
These data identify multiple modes by which ShcA can fine-tune the development of early thymocytes, including a previously unappreciated ShcA-c-Abl axis that regulates thymocyte proliferation.
This gene encodes three main isoforms that differ in activities and subcellular location. While all three are adapter proteins in signal transduction pathways, the longest (p66Shc) may be involved in regulating life span and the effects of reactive oxygen species. The other two isoforms, p52Shc and p46Shc, link activated receptor tyrosine kinases to the Ras pathway by recruitment of the GRB2/SOS complex. p66Shc is not involved in Ras activation. Unlike the other two isoforms, p46Shc is targeted to the mitochondrial matrix. Several transcript variants encoding different isoforms have been found for this gene.
SHC (Src homology 2 domain containing) transforming protein 1
, Sporulation-specific activator of Chs3p (chitin synthase III), required for the synthesis of the chitosan layer of ascospores; has similarity to Skt5p, which activates Chs3p during vegetative growth; transcriptionally induced at alkaline pH
, squalene--hopene cyclase
, SH2 domain protein C1
, SHC-transforming protein 1
, src homology 2 domain-containing-transforming protein C1
, SHC-transforming protein 1-like
, SHC (Src homology 2 domain-containing) transforming protein 1
, SHC-transforming protein 3
, SHC-transforming protein A
, src homology 2 domain-containing transforming protein C1
, src homology collagen
, adaptor protein SHC