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Validated All-in-One™ qPCR Primer for SHC1(NM_183001.4) Search again
Product ID:
HQP017081
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
SHC, SHCA
Gene Description:
SHC adaptor protein 1
Target Gene Accession:
NM_183001.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Gene References into function
- Tyrosine phosphorylation of the beta-amyloid precursor protein cytoplasmic tail promotes interaction with Shc.
- Isoform-specific knockdown and expression of adaptor protein ShcA using small interfering RNA
- The p66Shc longevity gene is silenced through epigenetic modifications of an alternative promoter
- Among ten hepatocellular carcinoma cases with amplicon 1q21-q22, significant gene expression level of JTB, SHC1, CCT3 and COPA in the tumors than the paired adjacent non-malignant liver tissues.
- shc phosphorylation is regulated by protein kinase C-dependent phosphorylations of Lck in T-lymphocytes
- Single nucleotide polymorphisms in SHC1 have no impact on longevity for Japanese centenarians.
- there is a novel interaction between Tie2 with the adapter molecule ShcA that may play a role in the regulation of migration and three-dimensional organization of endothelial cells induced by angiopoietin-1
- novel interplay between p66Shc and p52Shc in the control of T-cell fate
- Shc and IGF-1R serve as key elements in the translocation of ERalpha to the cell membrane and in the facilitation of ERalpha-mediated rapid E2 action
- Shc is a critical angiogenic switch for VEGF production downstream from the HGF and ErbB2 RTKs.
- Y317 of p52(Shc) serves as an important regulatory site that allows tyrosine phosphorylation pathways to moderate androgen sensitivity in human prostate cancer cells.
- MK2 is activated with p66(ShcA) co-expression and p66(ShcA) is an in vitro substrate for MK2, further demonstrating their association and suggesting a biological role for p66(Shc) in MK2 activation
- CD9 activates the p46 Shc isoform in tumor cells and leads to apoptosis
- polymorphisms in SHC1 is associated with breast cancer
- insulin receptor substrate-4 and ShcA have roles in signaling by the fibroblast growth factor receptor
- NCAM activates FGFR signaling in a manner distinct from FGF2 stimulation, and regulates ShcA phosphorylation by the concerted efforts of the NCAM/FGFR as well as the NCAM/Fyn signaling pathway.
- Type 2 diabetes induces p66(shc) gene expression in circulating peripheral blood mononuclear cells.
- p52Shc couples tyrosine kinase receptors to Ras by recruiting Grb2.
- conclude that the expression of p66Shc protein is regulated by signaling through the thyrotropin receptor in proliferating thyroid cells
- p46 Shc expressed in the nucleus may play an important role in gastric carcinogenesis
- SHPS-1 functions as an anchor protein that recruits both Shc and SHP-2, whose recruitment is necessary for IGF-I-dependent Shc phosphorylation
- p66shc may have a complex role in mammalian longevity: it is highly expressed in fibroblasts from centenarians
- Expression of p66SHC protein correlates with proliferation of prostate cancer cells.
- DDR2 autophosphorylation generates cytosolic domain phosphotyrosines that promote the formation of DDR2 cytosolic domain-Shc signaling complexes.
- The data show that Shc is connected to the activated TCR via direct interaction with Lck.
- p66(shc) regulates mitochondrial oxidative capacity and may extend life span by repartitioning metabolic energy conversion away from oxidative and toward glycolytic pathways
- p66Shc overexpression plays a pro-apoptotic role in human cell lines that is independent from the presence of a functional form of p53.
- Important variations in the p66Shc gene may be extremely rare and probably this gene is not involved in the genetic susceptibility to coronary artery disease.
- present study identifies ShcA as a mediator of the anti-apoptotic activity of venous malformation -mutant Tie2
- Upon IGF-I stimulation, a complex assembles on SHPS-1 that contains SHP-2, c-Src, and Shc wherein Src phosphorylates Shc, a signaling step that is necessary for an optimal mitogenic response
- CpG methylation has a role in the control of p66Shc gene expression and Ca2+ signaling may lead to epigenetic modifications in nondividing cells
- report novel investigations into the role of the mitochondrial import machinery on p66(Shc) activation, which highlight the energetic status of mitochondria as a crucial determinant of p66(Shc) function
- Since p66Shc is an aging-regulating gene, we envision that these data may help in understanding the relationship among aging, cancer, and stem cells.
- p66Shc may play an important role in downstream hypoxic signaling, involving HIF-1alpha protein accumulation and cell death in T lymphocytes.
- PTX3 and p66((ShcA)) mRNA levels are significantly more elevated in WBCs and in adipose tissue samples of patients with high levels of LDL compared to those with low levels.
- the adaptors Nck and ShcA influenced adherence of S. Typhimurium to non-phagocytic cells.
- p66 Shc may have a role in progression of colon cancer
- IL-15 but not IL-21 caused an increased phosphorylation of Shc and ERK1/2.
- Up-regulation of muscle p66(ShcA) relates to proteolysis rate, suggesting an involvement of this gene in muscle catabolic response in hypercatabolic traumatized patients.
- Suggest new pathway for the induction of oxidative stress by AGEs involving FKHRL1 inactivation and MnSOD suppression via Ser-36 phosphorylation of p66(shc) in human kidney cells.
- demonstrated that 8-isoprostane has a significant influence on p66Shc promoter methylation. In the control group and in patients with ESRD, increasing 8-isoprostane levels were linked to an elevated promoter methylation
- Protein-tyrosine phosphatase epsilon regulates Shc signaling in a kinase-specific manner: increasing coherence in tyrosine phosphatase signaling
- Shc has an intrinsic phosphorylation-dependent gating mechanism where the SH2 domain adopts an open conformation only when tyrosine phosphorylation has occurred.
- These results identify p66Shc and FOXO3a as novel partners of beta(1)Pix and represent the first direct evidence of beta(1)Pix in cell proliferation via Erk/p66Shc-dependent and Akt-independent mechanisms.
- in VSMCs exposed to hyperglycemia, IGF-I stimulation of Shc facilitates the transfer of Grb2 to p85 resulting in enhanced PI3K activation and AKT phosphorylation leading to enhanced cell proliferation and migration
- A novel role for p66Shc-ROS pathway in androgen-induced prostate cancer cell proliferation and a role in early prostate carcinogenesis.
- The recruitment of Shc protein to FGFR2 via an indirect mechanism provides new insight into the regulation of protein assembly and activation of various signalling pathways.
- In human endometriosis, the PI3K-Akt and MAPK signaling pathways may be activated via overexpression of AXL and SHC1, respectively.