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Signaling adapter that couples activated growth factor receptors to signaling pathways.
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Hyperglycemia and elevated free fatty acids in the diabetic milieu recruit p66Shc to upregulate endothelial miR (Montrer MLXIP Anticorps)-34a via an oxidant-sensitive mechanism, which leads to endothelial dysfunction by targeting Sirt1 (Montrer SIRT1 Anticorps).
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 (Montrer POLD3 Anticorps) activation involving Ser (Montrer SIGLEC1 Anticorps)(139) and a motif surrounding Ser (Montrer SIGLEC1 Anticorps)(213).
JNK1 (Montrer MAPK8 Anticorps)/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 (Montrer HADHB Anticorps) ACAA2 (Montrer ACAA2 Anticorps), to which p46Shc binds directly and with a strong affinity.
In mice and humans, reduced p66Shc levels protect from obesity, but not from ectopic fat accumulation, glucose intolerance and insulin (Montrer INS Anticorps) resistance.
p53 (Montrer TP53 Anticorps)-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 (Montrer INS Anticorps) response via IRS-1 (Montrer IRS1 Anticorps)/Akt (Montrer AKT1 Anticorps)/eNOS (Montrer NOS3 Anticorps) pathway. Its knockdown in endothelial cells from Ob/Ob mice lessened ROS (Montrer ROS1 Anticorps) 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.
PKCbeta2 inhibition protects mice from gut (Montrer GUSB Anticorps) ischemia-reperfusion injury by suppressing the adaptor p66(Shc)-mediated oxidative stress and subsequent apoptosis.
Signaling adapter that couples activated growth factor receptors to signaling pathways. Participates in signaling downstream of the angiopoietin receptor TEK/TIE2, and plays a role in the regulation of endothelial cell migration and sprouting angiogenesis (By similarity). Participates in a signaling cascade initiated by activated KIT and KITLG/SCF. Isoform p47Shc and isoform p52Shc, once phosphorylated, couple activated receptor kinases to Ras via the recruitment of the GRB2/SOS complex and are implicated in the cytoplasmic propagation of mitogenic signals. Isoform p47Shc and isoform p52 may thus function as initiators of the Ras signaling cascade in various non-neuronal systems. Isoform p66Shc does not mediate Ras activation, but is involved in signal transduction pathways that regulate the cellular response to oxidative stress and life span. Isoform p66Shc acts as a downstream target of the tumor suppressor p53 and is indispensable for the ability of stress-activated p53 to induce elevation of intracellular oxidants, cytochrome c release and apoptosis. The expression of isoform p66Shc has been correlated with life span.
SH2 domain protein C1
, SHC-transforming protein 1
, SHC-transforming protein A
, src homology 2 domain-containing-transforming protein C1