癌症的基本特征包括细胞增殖、血管生成、迁移、凋亡逃避机制和细胞永生等。找到癌症发生过程中这些通路的关键标记物和对应的抗体用于检测至关重要。
为您推荐一个泛素化位点预测神器——泛素化分析工具，可以为您的蛋白的泛素化位点作出预测和评分。
细胞自噬受体图形绘图工具为你的蛋白的细胞受体结合位点作出预测和评分，识别结合到自噬通路中的蛋白是非常重要的，便于让我们理解自噬在正常生理、病理过程中的作用，如发育、细胞分化、神经退化性疾病、压力条件下、感染和癌症。
Mouse Shc1 Antibody(Center)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
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Application 
| WB, E |
|---|---|
| Primary Accession | P98083 |
| Other Accession | NP_001106802.1 |
| Reactivity | Mouse |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 62608 Da |
| Antigen Region | 378-405 aa |
| Gene ID | 20416 |
|---|---|
| Other Names | SHC-transforming protein 1, SHC-transforming protein A, Src homology 2 domain-containing-transforming protein C1, SH2 domain protein C1, Shc1, Shc, ShcA |
| Target/Specificity | This Mouse Shc1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 378-405 amino acids from the Central region of mouse Shc1. |
| Dilution | WB~~1:1000 E~~Use at an assay dependent concentration. |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | Mouse Shc1 Antibody(Center) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | Shc1 |
|---|---|
| Synonyms | Shc, ShcA |
| Function | 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. |
| Cellular Location | Cytoplasm. Cell junction, focal adhesion {ECO:0000250|UniProtKB:P29353} [Isoform p66Shc]: Mitochondrion. Note=In case of oxidative conditions, phosphorylation at 'Ser-36' of isoform p66Shc, leads to mitochondrial accumulation |
| Tissue Location | Widely expressed. Expressed in neural stem cells but absent in mature neurons |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Signaling adapter that couples activated growth factor receptors to signaling pathway. 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.
REFERENCES
Ursini-Siegel, J., et al. Cancer Res. 70(20):7776-7787(2010)
Ma, Z., et al. Oncogene 29(41):5559-5567(2010)
Fadini, G.P., et al. Diabetes 59(9):2306-2314(2010)
Ranieri, S.C., et al. Proc. Natl. Acad. Sci. U.S.A. 107(30):13420-13425(2010)
Gines, S., et al. J. Biol. Chem. 285(28):21537-21548(2010)
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