Browse our anti-SHC1 (SHC1) Antibodies

Human SHC (Src Homology 2 Domain Containing) Transforming Protein 1 (SHC1) interaction partners

1. In B cell lymphoma cells, reactive oxygen species production promoted p66shc expression, induced DNA damage, and facilitated cell apoptosis.

2. p66SHC is a novel regulator of autophagy and mitophagy in B cells and mediates coordination of autophagy and apoptosis in B cell survival and differentiation.

3. These data demonstrate that metabolic reprogramming is a key component of ShcA signaling and serves an unappreciated yet vital role during breast cancer initiation and progression. These data further unravel a novel interplay between ShcA and PGC-1alpha in the coordination of metabolic reprogramming and demonstrate the sensitivity of breast tumors to drugs targeting oxidative phosphorylation

4. p66Shc increases prostate cancer migratory activity through generation of ROS for activation or inhibition of ROS-sensitive proteins.

5. Our results suggest that increases in ShcA perturb nephrin phosphosignaling dynamics, leading to aberrant nephrin turnover and slit diaphragm disassembly.

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

7. 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.

8. 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.

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

10. 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.

11. 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.

12. 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.

13. 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.

14. 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

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

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

17. 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

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

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

20. 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).

Zebrafish SHC (Src Homology 2 Domain Containing) Transforming Protein 1 (SHC1) interaction partners

1. Data show that adaptor protein Shc is required for angiogenesis in zebrafish (accession number LOC563639), mice, and human vascular endothelial cell-culture models.

Xenopus laevis SHC (Src Homology 2 Domain Containing) Transforming Protein 1 (SHC1) interaction partners

1. ShcA is required for Wnt-5a/Ror2 mediated upregulation of xPAPC, which demonstrates the functional relevance of this interaction.

Cow (Bovine) SHC (Src Homology 2 Domain Containing) Transforming Protein 1 (SHC1) interaction partners

1. The p66(Shc) adaptor protein controls oxidative stress response in early bovine embryos.

2. 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.

3. p66shc, but not p53, is significantly more abundant in an embryo population that exhibits higher frequencies of embryo arrest.

4. 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

5. These results support a model in which Shc orchestrates signals from cell-cell and cell-matrix adhesions to elicit flow-induced inflammatory signaling.

Mouse (Murine) SHC (Src Homology 2 Domain Containing) Transforming Protein 1 (SHC1) interaction partners

1. This study postulates a p66Shc-mediated inflammatory cascade leading to oxidative stress as a causative pathogenic mechanism in diabetes-associated cognitive impairment that is at least partially mediated through an AD-pathology-independent mechanism.

2. These results suggest that p66Shc may regulate the relative abundance and timing of lineage-associated transcription factor expression in the blastocyst inner cell mass .

3. Genetic inhibition of ShcA signaling in the Polyoma virus middle T (MT) breast cancer mouse model sensitized mammary tumors to biguanides during the earliest stages of breast cancer progression.

4. Document a genetic link between the p66ShcA locus and accelerated aging phenotype(s) in kidneys of diabetic mice.

5. oncogenic BRAF renders cells refractory to p66ShcS36 phosphorylation, which is essential for p66Shc activation and mitochondrial reactive oxygen species production.

6. A complex epigenetic mechanism linking miRNAs and chromatin modifying enzymes drive persistent p66 Shc transcription and reactive oxygen species generation.

7. p66Shc-/- mice gained less weight than WT mice when on a high-fat diet. p66Shc deletion significantly modified the composition of gut microbiota and their modification after an HFD.

8. Study in MMTV/MT6 and MMTV/NIC breast cancer mouse models show that ShcA phosphotyrosine motifs potentiate immune suppression by limiting signal transducer and activator of transcription (STAT)-1-driven anti-tumour immunity, while simultaneously increasing STAT3 immunosuppressive signals.

9. Sirt3 modulates age-associated mitochondrial biology and function via lysine deacetylation of target proteins, and authors show that its regulation depends on its nitration status and is benefited by the improved NAD(+)/NADH ratio in aged p66(Shc(-/-)) brain mitochondria.

10. miR-200c might be responsible for muscle wasting and myotube loss, most probably via a p66Shc-dependent mechanism in a pathological disease such as Duchenne muscular dystrophy.

11. Data show that 66-kDa Src homology 2 domain-containing protein (p66Shc) is acetylated under high glucose conditions and is deacetylated by Sirtuin1 lysine deacetylase (Sirt1) on lysine 81.

12. a pivotal role for p66(shc) -induced vascular dysfunction in a common pathogenic cascade shared by noise-induced and age-related hearing loss, is reported.

13. P66Shc, a key regulator of metabolism and mitochondrial ROS production, is dysregulated by mouse embryo culture

14. 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.

15. Hyperglycemia and elevated free fatty acids in the diabetic milieu recruit p66Shc to upregulate endothelial miR-34a via an oxidant-sensitive mechanism, which leads to endothelial dysfunction by targeting Sirt1.

16. p66SHC-mediated oxidative stress and telomere shortening synergize in some tissues (including testes) to accelerate aging.

17. Taken together, these data argue for a complex mechanism of PKCbeta-dependent regulation of p66 activation involving Ser(139) and a motif surrounding Ser(213).

18. JNK1/2-dependent regulation of p66ShcS36 phosphorylation, is reported.

19. Data show that the major mitochondrial partner of Shc adaptor protein p46Shc is the lipid oxidation enzyme 3-ketoacylCoA thiolase ACAA2, to which p46Shc binds directly and with a strong affinity.

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