SOCS3 antibody (70R-14244)
Affinity purified Mouse polyclonal Human SOCS3 antibody
Overview
Overview
| Synonyms | Polyclonal SOCS3 antibody, Anti-SOCS3 antibody, ATOD4 antibody, CIS3 antibody, SOCS 3, SOCS 3 antibody, STAT-induced STAT inhibitor 3 antibody, Cytokine-inducible SH2 protein 3 antibody, SOCS-3, SOCS-3 antibody, SOCS3 |
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| Applications | IHC-P, WB |
| Immunogen | SOCS3 antibody was raised in Rabbit using a synthetic peptide corresponding to a sequence in the middle region of human SOCS3, identical to the related Rabbit sequence, different from the related rat sequence by one amino acid, as the immunogen |
Images
Western Blot analysis using SOCS3 antibody (70R-14244)
Lane 1:Jurkat cells Lysate; Lane 2: CEM cells Lysate; Lane 3:Raji cells Lysate
Specifications
| Host | Rabbit |
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| Isotype | IgG |
| Method of Purification | SOCS3 antibody was purified by affinity chromatography |
| Form & Buffer | Supplied in lyophilized form |
Usage & Assay Information
| Usage Recommendations | Optimal conditions to be determined by the end user |
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Storage & Safety
| Storage | Store at 4 deg C for short term storage. For long term storage aliquot and store at -20 deg C, avoid repeated freeze/thaw cycles. |
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General Information
| Biological Significance | The Janus family of protein tyrosine kinases (JAKs) and STAT transcription factors regulate cellular processes involved in cell growth, differentiation, and transformation through their association with cytokine receptors. The CIS family of proteins (also referred as the SOCS or SSI family) has been implicated in the regulation of signal transduction by a variety of cytokines. The cytokine-inducible SH2 protein 3 (CIS3/SOCS3/SSI3) has been shown to inhibit the JAK/STAT pathway and act as a negative regulator of fetal liver erythropoiesis. Recently, it is reported that CIS3 regulates the erythropoietin (EPO) receptor (EPOR) signaling in erythroid progenitors and Ba/F3 cells expressing the EPOR (BFER). CIS3 binds directly to the EPOR as well as JAK2 and inhibits EPOdependent proliferation and STAT5 activation. It is reported that JAB/SOCS1 is strongly induced by interferongamma and forced expression of JAB/SOCS1 conferred cells interferon resistance. This resistance was caused by inhibition of JAK1 and JAK2 activation in response to IFN gamma. Moreover, recent detailed analysis of JAB/SOCS1 knockout mice revealed that JAB/SOCS1 is indeed a "negative feedback regulator" that determines the sensitivity of cells to IFN gamma. |
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