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SOCS3 impacts on IEC turnover following T. muris infection, potentially through enhancement of IDO. IDO may dampen the immune response which can drive intestinal epithelial cell hyperproliferation in the absence of SOCS3, demonstrating the intricate interplay of immune signals regulating mucosal homeostasis, and suggesting a novel tumour suppressor role of SOCS3.
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The findings of this indicated that co-deletion of PTEN and SOCS3 results in modest but measureable enhancement of early regeneration of DRG axons following crush injury.
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Our findings suggest a role for murine cytomegalovirus (MCMV)-related stimulation of SOCS1 and SOCS3 in the progression of retinal disease during ocular, but not systemic, MCMV infection.
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Lentivirusmediated overexpression of SOCS3 was revealed to ameliorate neutrophilic airway inflammation by inhibiting pulmonary Th17 responses in mice with chronic Pseudomonas aeruginosa lung infections.
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These data demonstrate that loss of SOCS3 in cardiomyocytes promotes deoxycorticosterone-acetate -salt-induced cardiac remodeling and inflammation.
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In the present study, we investigated the hypothesis that SOCS3 expression in the VMH could exert an important role regulating the metabolic changes typically observed during pregnancy and lactation.
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SOCS3 was targeted by miR30a- 5p in allergic rhinitis
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SOCS3 was upregulated in lung CD4+ T cells in a mouse model of chronic PA lung infection and exogenous SOCS3 suppressed Th17-mediated neutrophil recruitment in vitro.
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findings show SOCS3 does not appear to mediate the early inflammatory or leucine-induced changes in protein synthesis in skeletal muscle
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The strength of long bones is determined by coalescence of trabeculae during corticalization.This process is regulated by SOCS3 via a mechanism dependent on IL-6 and expression of sex hormones.
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High SOCS3 expression is associated with glioma.
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Mechanistic analysis indicated that E47 activated expression of the transcription factor Spi-B and the suppressor of cytokine signaling 3 (SOCS3), which both downregulated Foxp3 expression. These findings demonstrate that the balance of Id3 and E47 controls the maintenance of Foxp3 expression in Treg cells and, thus, contributes to Treg cell plasticity.
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Our results show, for the first time, that SOCS-3 regulates leptin-induced responses in cartilage
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Loss of suppressor of cytokine (SOCS3) expression in mature muscle fibers increased the inflammatory response to myotoxic injury but did not impair muscle regeneration in either adult or old mice. Therefore, reduced SOCS3 expression in muscle fibers is unlikely to underlie impaired muscle regeneration.
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Findings revealed a novel participation of SOCS3 regulating several endocrine and metabolic aspects.
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Findings indicate that inactivation of the Rb family proteins (Rb, p107, and p130) in hematopoietic stem cells (HSCs) progressively impairs their homeostasis, which is rescued upon repression of suppressor of cytokine signaling 3 protein (Socs3) expression in triple knockout (TKO) HSCs.
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Data suggest that, in B cell lymphoma, expression of MIRN30 is up-regulated in both granulocytic myeloid-derived suppressor cells and monocytic myeloid-derived suppressor cells; in B cell lymphoma, 3prime untranslated region of Socs3 appears to be direct target of MIRN30 in myeloid-derived suppressor cell differentiation. (MIRN30 = microRNA 30; Socs3 = suppressor of cytokine signaling 3 protein)
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Cell type-specific, different roles for viral immediate early or early gene expression and/or viral tegument proteins in the early stimulation of SOCS1 and SOCS3 during murine cytomegalovirus infection.
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oncostatin M mitigated the proliferation of Th17 cells and decreased the expression of IL-17 and IL-21; it promoted the activation of suppressor of cytokine signaling 3 (SOCS3), STAT3, and STAT5; observations suggest that OSM can inhibit Th17 differentiation by reciprocally controlling SOCS3, STAT3, and STAT5
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Results demonstrate a novel tunable form of cross-talk in which alveolar epithelial cells use Prostaglandin E2 (PGE2) as a signal to request SOCS3 from alveolar macrophages to dampen their endogenous inflammatory responses during infection.