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The upregulation of SOCS-1 (show SOCS1 ELISA Kits) and SOCS-2 by cortisol may be playing a key role in suppressing cytokine signaling and the associated inflammatory response.
The induction of a tolerogenic phenotype in DCs by NPs (show NPS ELISA Kits) was mediated by the AhR (show AHR ELISA Kits)-dependent induction of Socs2, which resulted in inhibition of nuclear factor kappaB activation and proinflammatory cytokine production (properties of tolerogenic DCs).
Long-term palmitate treatment up-regulates SOCS2 and reduces PI3K (show PIK3CA ELISA Kits) activity, thereby impairing glucose stimulated insulin (show INS ELISA Kits) secretion.
Targeting of SOCS2 by miR (show MLXIP ELISA Kits)-194 resulted in derepression of the oncogenic kinases FLT3 (show FLT3 ELISA Kits) and JAK2 (show JAK2 ELISA Kits), leading to enhanced ERK (show EPHB2 ELISA Kits) and STAT3 (show STAT3 ELISA Kits) signaling.
Single-cell RNA sequencing reveals enrichment of homeostatic modules in monocytes and dendritic cells from human metastatic melanoma. Suppressor-of-cytokine-2 (SOCS2) protein, a conserved program transcript, is expressed by mononuclear phagocytes infiltrating primary melanoma and is induced by IFNgamma.
this study shows that IL-7 (show IL7 ELISA Kits) induces the expression of SOCS2 through the JAK (show JAK3 ELISA Kits)/STAT-5 (show STAT5A ELISA Kits) pathway and that SOCS2 interacts with CD127 (show IL7R ELISA Kits) in early endosomes and direct the receptor complex to the proteasome for degradation
Overexpression of SOCS2 inverted these phenotypes generated by hsv2-miR (show MLXIP ELISA Kits)-H9-5p, indicating the potential roles of SOCS2 in Hsv2-miR (show MLXIP ELISA Kits)-H9-5p-driven metastasis in lung cancers. The results highlighted that Hsv2-miR (show MLXIP ELISA Kits)-H9-5p regulated and contributed to bone metastasis of lung cancers. We proposed that Hsv2-miR (show MLXIP ELISA Kits)-H9-5p could be used as a potential target in lung cancer therapy
Overexpression of SOCS-2 is associated with hepatocellular carcinoma.
focus on SOCS2 and review its biological function as well as its implication in pathological processes
SOCS2 may improve outcome of TBI in mice by regulating aspects of the neuroinflammatory response
This study showed that there was significantly increased levels of SOCS-2 mRNA in elderly and Alzheimer's disease brains.
Upon deletion of the STAT5 (show STAT5A ELISA Kits) response elements from the Socs2 promoter in mice, cytokine induction was abrogated, while basal activity remained intact. Our data suggest that promoter-bound STAT5 (show STAT5A ELISA Kits) modulates cytokine responses and enhancer-bound STAT5 (show STAT5A ELISA Kits) is mandatory for gene activation.
In a knockout mouse model, deficiency of SOCS2 was associated with decreased neuroinflammation and increased survival following HSV-1 infection, without significant effect on viral load. This result indicates that SOCS2 plays a major role in driving neuroinflammation and subsequent brain damage during HSV-1 encephalitis.
Our data show that absence of SOCS2 turns cardiomyocytes unresponsive to LIF (show LIF ELISA Kits)-induced [Ca(2 (show CA2 ELISA Kits)+)] raise, indicating that endogenous levels of SOCS2 are crucial for full activation of LIF (show LIF ELISA Kits) signaling in the heart.
Knockdown of SOCS2 makes mice less sensitive to multiple low dose streptozotocin.
Study provides an insight into the role of SOCS2 in modulating the immune response to Bovine herpesvirus 5 [BoHV-5]infection.
Data (including data from studies in knockout mice) suggest Socs2 regulates liver regeneration rate after partial hepatectomy, Ghr (growth hormone receptor (show GHR ELISA Kits)) level via ubiquitination/proteolysis, and serum Igf1 (insulin-like growth factor-1 (show IGF1 ELISA Kits)) level.
GH appears to act directly on the metatarsals of Socs2(-/-) mice, promoting growth via a mechanism that is independent of IGF-1 (show IGF1 ELISA Kits).
comparison of murine wt and Socs2(-/-) HSC (show FUT1 ELISA Kits) gene expression in response to 5-FU revealed a significant overlap with the molecular programs that correlate with SOCS2 expression in leukemias, particularly with the oncogenic pathways
Studies indicate the critical role of suppressor of cytokine signaling 2 (SOCS2) in ontrolling the local growth hormone (GH (show GH1 ELISA Kits)) anabolic bone effects.
hepatic growth hormone receptor (show GHR ELISA Kits) and suppressor of cytokine signaling (SOCS (show CISH ELISA Kits))2 messenger RNA expression appeared to be promptly and sensitively regulated by increased estradiol levels before ovulation of dairy heifers
relative amount of suppressors of cytokine signaling-2 (SOCS-2)messenger RNA increased after parturition
This gene encodes a member of the suppressor of cytokine signaling (SOCS) family. SOCS family members are cytokine-inducible negative regulators of cytokine receptor signaling via the Janus kinase/signal transducer and activation of transcription pathway (the JAK/STAT pathway). SOCS family proteins interact with major molecules of signaling complexes to block further signal transduction, in part, by proteasomal depletion of receptors or signal-transducing proteins via ubiquitination. The expression of this gene can be induced by a subset of cytokines, including erythropoietin, GM-CSF, IL10, interferon (IFN)-gamma and by cytokine receptors such as growth horomone receptor. The protein encoded by this gene interacts with the cytoplasmic domain of insulin-like growth factor-1 receptor (IGF1R) and is thought to be involved in the regulation of IGF1R mediated cell signaling. This gene has pseudogenes on chromosomes 20 and 22. Alternative splicing results in multiple transcript variants.
suppressor of cytokine signaling-2
, suppressor of cytokine signaling 2
, suppressor of cytokine signaling 2 variant 1
, STAT induced STAT inhibitor-2
, STAT-induced STAT inhibitor 2
, STAT-induced STAT inhibitor-2
, cytokine-inducible SH2 protein 2
, cytokine inducible SH2-containing protein 2
, suppressor of cytokine signalling 2