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anti-Human SOCS6 Antibodies:
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Low SOCS6 expression is associated with Prostate Cancer.
Together, our data provide important evidence for miR-19 mediated SOCS6 in OS growth and revealed miR-19/SOCS6/JAK2/STAT3 pathway as a potential therapeutic strategy for OS patients.
Results indicate that similar to PTEN pseudogene (PTENP1), suppressor of cytokine signaling 6 protein (SOCS6) expression was also significantly lower in esophageal squamous cell carcinoma (ESCC) samples.
our results describe for the first time the role of miR-494-3p during normal hematopoietic stem/progenitor cells differentiation and suggest that its increased expression, and the subsequent downregulation of its target SOCS6, might contribute to the megakaryocyte hyperplasia commonly observed in primary myelofibrosis patients.
miR-142-3p regulates NPC development by down-regulating SOCS6 expression and suggest that modulation of miR-142-3p expression could be a therapeutic strategy for NPC
Stage-independent downregulation of SOCS2 and SOCS6 correlate with disease-free survival in colorectal cancer.
Studied both the function of upregulated miR-424-5p in pancreatic cancer and how downstream suppressor of cytokine-induced signaling 6 (SOCS6) is negatively regulated by miR-424-5p.
miR-17-5p might function as a pro-proliferative factor by repressing SOCS6 in gastric cancer
SOCS2 and SOCS6 expression are remarkably reduced in hepatocellular carcinoma and correlate with aggressive tumor progression and poor prognosis
Results show that SOCS6 forms complex with DRP1 and the mitochondrial phosphatase PGAM5, attenuates DRP1 phosphorylation, and promotes DRP1 mitochondrial translocation.
SOCS6 negatively regulates Flt3 activation, the downstream Erk signaling pathway, and cell proliferation.
Reduced copy number and mRNA expression of SOCS6 are associated with disease recurrence in primary lung squamous cell carcinoma and may be useful prognostic biomarkers.
The results may contribute to understanding SOCS5 and SOCS6 expression regulation in various cancer tissues, and show that these two factors may be used for diagnosing cancer.
SOCS6 has ubiquitin ligase activity toward c-KIT
These results establish that SOCS-6 acts as a negative regulator of T cell activation by promoting ubiquitin-dependent proteolysis of p56(lck).
Data support the importance of loss-of-function of SOCS6 as a frequent event in gastric tumorigenesis.
HOIL-1 expression stabilizes SOCS6 and induces the ubiquitination and degradation of proteins associated with SOCS6
These observations suggest that Erk activation may be correlated in the cells with high expression of SOCS6.
These observations suggest that SOCS6 is composed of at least two functional domains required for its biological role in localizing and degrading Stat3 in the nucleus.
Study demonstrated that hypermethylation of the SOCS6 promoter is one of the mechanisms for the epigenetic regulation of SOCS6 expression.
Four new members of the SOCS family of molecules in rainbow trout (Oncorhynchus mykiss), CISH and SOCS6, 7 and 9, are described for the first time in this species
Results suggest: 1) SOCS6 and SOCS7 bind tyrosine-phosphorylated DAB1 and commit it to ubiquitination and proteasomal degradation. 2) Removal of phosphorylated DAB1 by SOCS6 and SOCS7 terminates reelin signaling and allows a new cycle of reelin signaling to commence. 3) Repeated cycles of reelin signaling "ON" and "OFF" drive the fundamentally cyclic process of cell migration in the cortex.
Our results show that endogenous Cul5 suppresses epithelial cell transformation by several pathways, including inhibition of Src-Cas-induced ruffling through SOCS6
SOCS-6 binds to insulin receptor substrate 4, and mice lacking the SOCS-6 gene exhibit mild growth retardation(SOCS-6)
SOCS4 expression, in contrast, does not appear to be EPO inducible.SOCS4 is ineffective at counteracting EPO-mediated events.
SOCS6 has a role as a negative regulator of receptor tyrosine kinases
SOCS-6 expression is induced by insulin, which regulates its binding to the p85 monomer of phosphoinositide 3-kinase
TH1-specific chromatin structure is created by early recruitment of Swi-SNF complexes and nucleosome remodeling dependent on Stat4.
The protein encoded by this gene contains a SH2 domain and a CIS homolog domain. The protein thus belongs to the cytokine-induced STAT inhibitor (CIS), also known as suppressor of cytokine signaling (SOCS) or STAT-induced STAT inhibitor (SSI), protein family. CIS family members are known to be cytokine-inducible negative regulators of cytokine signaling. The expression of this gene can be induced by GM-CSF and EPO in hematopoietic cells. A high expression level of this gene was found in factor-independent chronic myelogenous leukemia (CML) and erythroleukemia (HEL) cell lines.
STAT induced STAT inhibitor-4
, cytokine-inducible SH2 protein 4
, suppressor of cytokine signaling 4
, suppressor of cytokine signaling 6
, suppressor of cytokine signaling
, hypothetical protein LOC100124796
, SH2 domain containing SOCS box protein SOCS6
, cytokine inducible SH2-containing protein 4
, cytokine inducible SH2-containing protein CIS4
, suppressor of cytokine signaling 6 protein
, suppressor of cytokine signaling 6, like