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Validated All-in-One™ qPCR Primer for SOCS2(NM_001270471.2) Search again
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.
Summary
This gene encodes a member of the STAT-induced STAT inhibitor (SSI), also known as suppressor of cytokine signaling (SOCS), family. SSI family members are cytokine-inducible negative regulators of cytokine signaling. The expression of this gene can be induced by a subset of cytokines, including erythropoietin, GM-CSF, IL10 and interferon (IFN)-gamma. The protein encoded by this gene is found to interact with the cytoplasmic domain of insulin-like growth factor-1 receptor (IGF1R), and thus is thought to be involved in the regulation of IGF1R mediated cell signaling.
Gene References into function
- SOCS-2 is overexpressed in advanced stages of chronic myeloid leukemia. It may be a component of a negative feedback mechanism that is functioning inadequately, induced by Bcr-Abl but unable to reverse its growth-promoting effects.
- SOCS2 mediates the suppression of JAK2 phosphorylation by estrogen, which inhibits growth hormone signaling
- SOCS1 and SOCS2 but not SOCS3 suppressed the growth of ovarian and breast cancer cells.
- Association of single-nucleotide polymorphisms in the SOCS2 gene with type 2 diabetes in the Japanese was studied.
- Results describe the 1.9-A crystal structure of the ternary complex of SOCS2 with elongin C and elongin B.
- SOCS2 only interacts with the Y1077 motif, but with higher binding affinity and can interfere with CIS and STAT5a prey recruitment at this site.
- SOCS2 expression is regulated by STAT5.
- Using RT-PCR, we demonstrated for the first time that neutrophils express mRNA for SOCS-2.
- A defect in expression of SOCS-2 and SOCS-3 genes may be crucial for the IGF-I hypersensitivity and progressive increase in erythroid cell population size characteristic of Polycythemia vera.
- Favorable prognostic value of high SOCS2 expression in primary mammary carcinomas.
- analysis of STAT5, CIS, and SOCS2 interactions with the growth hormone receptor
- SOCS2 epigenetic downregulation might be an important second step in the genesis of cytokine-independent myeloproliferative disorder clones
- difference in SOCS1, SOCS2 and SOCS3 transcript levels between normal individuals and SLE patients is not statistically significant
