No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species and application
anti-Human SOCS2 Antibodies:
anti-Mouse (Murine) SOCS2 Antibodies:
anti-Rat (Rattus) SOCS2 Antibodies:
Go to our pre-filtered search.
Human Polyclonal SOCS2 Primary Antibody for WB - ABIN967065
Greenhalgh, Bertolino, Asa, Metcalf, Corbin, Adams, Davey, Nicola, Hilton, Alexander: Growth enhancement in suppressor of cytokine signaling 2 (SOCS-2)-deficient mice is dependent on signal transducer and activator of transcription 5b (STAT5b). in Molecular endocrinology (Baltimore, Md.) 2002
Show all 4 Pubmed References
Human Polyclonal SOCS2 Primary Antibody for IF (p), IHC (p) - ABIN736028
Zhu, Dai, Han, He, Mo, Chen, Chen, Wu, Yang, Jiang, Chen, Sun, Zhong: Expression of SOCSs in human prostate cancer and their association in prognosis. in Molecular and cellular biochemistry 2013
Show all 3 Pubmed References
Human Polyclonal SOCS2 Primary Antibody for ELISA, WB - ABIN563827
Hamilton, Lin, Wang, Knowlton: Effect of ovariectomy on cardiac gene expression: inflammation and changes in SOCS gene expression. in Physiological genomics 2008
The upregulation of SOCS-1 and SOCS-2 by cortisol may be playing a key role in suppressing cytokine signaling and the associated inflammatory response.
SOCS2 expression was heterogeneously upregulated in some human colon cancers. Thus, SOCS2 was upregulated by p53 dysfunction and seemed to be associated with the tumorigenic potential of colon cancer.
SOCS2 impairs IFN/JAK/STAT signaling through reducing the stability of tyrosine kinase 2 (TYK2), downregulating the expression of type I and III IFN receptors, attenuating the phosphorylation and nucleus translocation of STAT1.
High SOCS2 expression is associated with higher grade breast cancer.
Study provides evidence for an inhibitory role of SOCS2 in TNFalpha induced NF-kappa B activation, identifies NDR1 as a novel substrate of SOCS2, and demonstrates that SOCS2 and TNFalpha induced NF-kappa B signaling are linked through NDR1.
Overexpression of miR-196b suppresses SOCS2 in human laryngeal squamous cell carcinoma resulting in tumor progression and poor prognosis.
Methyltransferase-like 3 represses SOCS2 expression in hepatocellular carcinoma through an m6A-YTHDF2-dependent mechanism. Our findings suggest an important mechanism of epigenetic alteration in liver carcinogenesis
Study in lung cancer BEAS-2B cells shows that SOCS2 binding to the growth hormone receptor (GHR) is impaired by a GHR threonine substitution at Pro 495. This results in decreased internalisation and degradation of the receptor.
SOCS-1, SOCS-2, and SOCS-3 proteins may directly or indirectly, have important roles in development and pathogenesis of papillary thyroid cancer
Despite of the key role of SOCS2 in the regulation of GH receptor signaling, study did not find any significant association between SOCS2 polymorphisms and acromegaly.
The induction of a tolerogenic phenotype in DCs by NPs was mediated by the AhR-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 activity, thereby impairing glucose stimulated insulin secretion.
Targeting of SOCS2 by miR-194 resulted in derepression of the oncogenic kinases FLT3 and JAK2, leading to enhanced ERK and STAT3 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 induces the expression of SOCS2 through the JAK/STAT-5 pathway and that SOCS2 interacts with CD127 in early endosomes and direct the receptor complex to the proteasome for degradation
Overexpression of SOCS2 inverted these phenotypes generated by hsv2-miR-H9-5p, indicating the potential roles of SOCS2 in Hsv2-miR-H9-5p-driven metastasis in lung cancers. The results highlighted that Hsv2-miR-H9-5p regulated and contributed to bone metastasis of lung cancers. We proposed that Hsv2-miR-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.
crystals of SOCS2 in complex with its adaptor proteins, Elongin C and Elongin B, underwent a change in crystallographic parameters when treated with dimethyl sulfoxide during soaking experiments.
our data suggest a novel role for SOCS2 in interacting with and regulating the trafficking of TrkB, leading to increased neurite outgrowth in hippocampus neurons.
SOCS2 negatively regulates the development of natural killer cells by inhibiting JAK2 activity via direct interaction.
the absence of SOCS2 is protective against bone loss typical of inflammatory bowel disease.
SOCS2 deletion had no effect on total dendrite length, number of dendritic segments, number of branch points or total dendritic spine density but increased the number of mature "mushroom" spines.
Upon deletion of the STAT5 response elements from the Socs2 promoter in mice, cytokine induction was abrogated, while basal activity remained intact. Our data suggest that promoter-bound STAT5 modulates cytokine responses and enhancer-bound STAT5 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-induced [Ca(2+)] raise, indicating that endogenous levels of SOCS2 are crucial for full activation of LIF 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) level via ubiquitination/proteolysis, and serum Igf1 (insulin-like growth factor-1) level.
GH appears to act directly on the metatarsals of Socs2(-/-) mice, promoting growth via a mechanism that is independent of IGF-1.
comparison of murine wt and Socs2(-/-) HSC 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) anabolic bone effects.
Taken together, our observations indicated that SOCS2 could suppress myotube formation, act as an anti-regulator of mitochondria biogenesis via inhibiting p38 MAPK signal pathway.
SOCS2 immunoprecipitates with TrkA and a juxtamembrane motif of TrkA is required for this interaction. Over-expression of SOCS2 in PC12 Tet-On cells increased total and surface TrkA expression. SOCS2 regulates neurite outgrowth.
Results show that CISH has no non-redundant functions in beta cell proliferation or glucose homeostasis during pregnancy in mice. Socs2 might compensate for the loss of Cish during pregnancy.
SOCS2-mediated feedback regulation of the JAK/STAT pathway is deficient in BCR/ABL1-induced chronic myeloid leukemia.
SOCS2 plays a role in modulating heart damage and function in a murine model of acute Chagas disease.
This study identified SOCS2 as an important regulator of hepatic homeostasis under conditions of high-fat dietary stress.
upregulated in intestinal epithelium in response to parasitic infections
Mapping of this negative regulator of cytokine-induced signal transduction
hepatic growth hormone receptor and suppressor of cytokine signaling (SOCS)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