Browse our anti-SHC3 (SHC3) Antibodies

Human SHC (Src Homology 2 Domain Containing) Transforming Protein 3 (SHC3) interaction partners

1. our results indicate the importance of Shc3 in HCC progression and identify Shc3 as a novel biomarker and potential therapeutic target in HCC.Significance: Ectopic expression of Shc3 forms a complex with MVP/MEK/ERK to potentiate ERK activation and plays an important role in sorafinib resistance in HCC.

2. We may conclude that RAI plays an important role in hypoxic signaling in Neuroblastoma (NB)cells and the interplay between RAI and HIF-1alpha may be relevant in the protection of NB cells against hypoxia. Our results may contribute to a further understanding the physiology of NB cells and the molecular mechanisms involved in their survival, with important implications in NB progression

3. High SHC3 expression is associated with glioblastoma.

4. Rai (ShcC/N-Shc), a member of the family of Shc-like adaptor proteins, as a new regulator of migration of normal and cancer stem/progenitor cells.

5. Polymorphism in RAI and CD3EAP are associated with outcome of myeloma patients treated with high dose treatment.

6. amplification of SHC3 and EDG3 genes suggests that the two proteins co-operate and are important for ependymomas in vivo.

7. Tyrosine phosphorylation of the beta-amyloid precursor protein cytoplasmic tail promotes interaction with Shc.

8. ALK-ShcC signal activation, possibly caused by co-amplification with the N-myc gene, might give additional effects on malignant tumor progression of neuroblastoma.ShcC is a potent substrate of the activated ALK kinase.

9. The neuron-specific Rai (ShcC) adaptor protein inhibits apoptosis by coupling Ret to the phosphatidylinositol 3-kinase/Akt signaling pathway.

10. ShcC has phosphotyrosine-dependent and -independent functions in neuroblastoma cells

11. The inappropriate in vivo expression of Shc3 in high-grade glioma may contribute to the survival of the cancer cells.

12. data suggest that RAI (ShcC/H-Shc)is a critical substrate for RET oncoproteins in thyroid carcinomas

13. 11 SNPs within SHC3 were examined to determine the association with nicotine dependence (ND) in either African-Americans (AA) or European-Americans (EA); three SNPs for AAs and one for EAs were significantly associated with at least one ND.

14. shcc is expressed in the human gut, especially in the enteric glial cells

15. ShcC is a therapeutic target that might induce differentiation in the aggressive type of neuroblastomas.

Mouse (Murine) SHC (Src Homology 2 Domain Containing) Transforming Protein 3 (SHC3) interaction partners

1. The results provide evidence that Rai/ShcC plays opposite roles in Th17 cell differentiation and astrocyte activation

2. Deficit of p66ShcA restores redox-sensitive stress response program in cisplatin-induced acute kidney injury.

3. Rai (ShcC/N-Shc), a member of the family of Shc-like adaptor proteins, as a new regulator of migration of normal and cancer stem/progenitor cells.

4. Rai interferes with the TCR signaling cascade one of the earliest steps--recruitment of the initiating kinase ZAP-70 to the phosphorylated subunit of the TCR/CD3 complex.

5. TrkB-mediated ERK1/2 activation is impaired in huntingtin knock-in striatal cells involves reduced p52/p46 Shc expression

6. role in phosphotyrosine-mediated signalings and neuronal plasticities

7. Tyrosine phosphorylation of the beta-amyloid precursor protein cytoplasmic tail promotes interaction with Shc.

8. binds the Trk receptors in a phosphotyrosine-dependent manner via their N-terminal phosphotyrosine binding domain

9. Rai has a functional neuroprotective role in brain injury, with possible implications in the treatment of stroke

10. ShcC mediates TrkB-Ras/MAPK signaling & regulates NMDA receptor function in the hippocampus via interaction with phosphotyrosines on the receptor subunits. It serves as a modulator of hippocampal synaptic plasticity underlying learning & memory.

11. ShcC has phosphotyrosine-dependent and -independent functions in neuroblastoma cells

12. Expressed in T and B cells; loss of Rai results in breaking of immunological tolerance and development of systemic autoimmunity.

13. study reports co-localization of adaptor proteins nShc & Grb10, with Kv1.3 channel in the olfactory bulb neural lamina; BDNF-induced current suppression of the Kv1.3 channel was prevented by both nShc and Grb10