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Socs1a transgenic zebrafish have liver steatosis and insulin (show INS Proteins) resistance.
Studies demonstrate a conserved role for SOCS1 in T cell development and suggest a novel T cell-independent function in embryonic myelopoiesis mediated, at least in part, via its effects on receptors using the Jak2 (show JAK2 Proteins)-Stat5 (show STAT5B Proteins) pathway.
in homozygotes, GH signaling is reduced by the action of the SOCS1 and SOCS3 (show SOCS3 Proteins) proteins.
SOCS1 alleviates RhTRIM5alpha-mediated regulation in the late phase of HIV-1 life cycle probably due to the destabilization of RhTRIM5alpha.
The upregulation of SOCS-1 and SOCS-2 (show SOCS2 Proteins) by cortisol may be playing a key role in suppressing cytokine signaling and the associated inflammatory response.
Our findings support the tumor suppressor role of SOCS1 in PCa (show FLVCR1 Proteins) and suggest that attenuation of MET signaling is one of the underlying mechanisms. SOCS1 in PCa (show FLVCR1 Proteins) cells also appears to prevent the tumor-promoting functions of cancer-associated fibroblasts.
Findings indicate that miR (show MLXIP Proteins)-21 and miR (show MLXIP Proteins)-155 promote the development of non-small cell lung carcinoma (NSCLC) in part by downregulating three tumor suppressor genes suppressor of cytokine signaling 1 protein (SOCS1), SOCS6 (show SOCS6 Proteins), and PTEN.
Evaluating SOCS1 and p21 protein (show NRAS Proteins) expression in prostatectomy specimens may have a prognostic value in identifying the aggressive prostate cancer. Inverse correlation between SOCS1 expression and disease severity was observed. However, SOCS1 expression did not correlate with that of p53 (show TP53 Proteins), MET or p21 (show CDKN1A Proteins) in the whole study cohort.
In this study, the authors report that JOSD1 (show JOSD1 Proteins) plays an important role in regulating type-I interferon (show IFNA Proteins) (IFN-I)-mediated antiviral activity. JOSD1 (show JOSD1 Proteins) physically interacts with SOCS1, which is an essential negative regulator of many cytokines signaling, and enhances SOCS1 stability by deubiquitinating K48-linked polyubiquitination of SOCS1.
Co-immunoprecipitation experiments showed that SOCS1 mutations abolished JAK3 (show JAK3 Proteins) binding, revealing a key role for SOCS1 in regulating JAK3 (show JAK3 Proteins)/STAT5 (show STAT5A Proteins) signaling
C/EBPbeta (show CEBPB Proteins) overexpression or knockdown did not change the levels of IL-1beta (show IL1B Proteins)-induced SOCS1. SOCS1 regulated the levels of C/EBPbeta (show CEBPB Proteins) mRNA by ubiquitination of C/EBPbeta (show CEBPB Proteins) as well as transcriptional regulation in human chondrocytes.
patients with renal graft rejection expressed lower levels of SOCS1
Inhibiting the STAT3 (show STAT3 Proteins)-Mcl-1 (show MCL1 Proteins) signaling axis by ectopic SOCS1 improved radiosensitivity by inducing apoptosis and enhancing DNA damage after radiotherapy, offering a mechanistic rationale for a new esophageal squamous cell carcinoma treatment.
an overview of the mechanisms underlying SOCS1 function as a tumor suppressor and discuss the emerging evidences of SOCS1 activity as an oncogene (show RAB1A Proteins).
MiRNA sponges against miR (show MLXIP Proteins)-19 or miR (show MLXIP Proteins)-155 inhibit the functions of these miRNAs and potentiate the induction of SOCS1 and p53 (show TP53 Proteins) in mouse leukemia cells and in human myeloma cells.
these findings suggest that SOCS-1 may exert its protective effect in acute lung injury by rescuing epithelial sodium channel alpha-subunit (show SCNN1A Proteins) expression via suppression of ASK-1 (show MAP3K5 Proteins).
loss of SOCS1 in CD11c (show ITGAX Proteins)+ cells skewed the balance of immune response to infection by increasing innate responses while decreasing antigen-specific adaptive responses to infectious antigens
IFN-lambda signaling is regulated by SOCS1 but not by SOCS3 (show SOCS3 Proteins) or USP18 (show USP18 Proteins).
Study conclude that under pro-proliferative cytokine stimulation at the onset of myeloproliferative diseases SOCS1 acts as a tumor suppressor, while under anti-proliferative conditions it exerts oncogenic function.
results indicate that SOCS1 is one of the essential molecules that maintain regulatory T cell stability, particularly under the inflammatory conditions in which APCs (show APCS Proteins) are highly activated
The Stat3 (show STAT3 Proteins) exerts its activity through the induction of miR (show MLXIP Proteins)- 155, which suppresses suppressor of cytokine signaling (SOCS (show CISH Proteins))1.
Cell type-specific, different roles for viral immediate early (show JUN Proteins) or early gene expression and/or viral tegument proteins in the early stimulation of SOCS1 and SOCS3 (show SOCS3 Proteins) during murine cytomegalovirus infection.
Loss of SOCS3 (show SOCS3 Proteins) significantly accelerated the pathology and inflammatory disease characteristic of SOCS1 deficiency. We propose a model in which SOCS1 and SOCS3 (show SOCS3 Proteins) operate independently to control specific cytokine responses and together modulate the proliferation and activation of lymphoid and myeloid cells to prevent rapid inflammatory disease
miR (show MLXIP Proteins)-155 not only directly inhibited SOCS1 expression, but also increased the expression of p-STAT (show STAT1 Proteins) and PDCD4 (show PDCD4 Proteins), as well as the production of proinflammation mediators IL-6 (show IL6 Proteins) and TNF-alpha (show TNF Proteins) in atherogenesis.
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 IL2, IL3 erythropoietin (EPO), CSF2/GM-CSF, and interferon (IFN)-gamma. The protein encoded by this gene functions downstream of cytokine receptors, and takes part in a negative feedback loop to attenuate cytokine signaling. Knockout studies in mice suggested the role of this gene as a modulator of IFN-gamma action, which is required for normal postnatal growth and survival.
suppressor of cytokine signaling 1
, suppressor of cytokine signalling
, suppressor of cytokine signaling 1b
, suppressor of cytokine signaling 1-like protein
, JAK binding protein
, JAK-binding protein
, STAT induced SH3 protein 1
, STAT-induced STAT inhibitor 1
, Tec-interacting protein 3
, cytokine-inducible SH2 protein 1
, JAK2-binding protein
, cytokine inducible SH2-containing protein 1
, cytokine inducible SH2-containing protein 7