Recombinant Rat Suppressor of cytokine signaling 3 (Socs3)

1. These results suggest that SOCS3 might be a key molecular involved in the development of complicated cancer pain and that overexpression of SOCS3 might be an important strategy for treatment for mechanical allodynia associated with bone cancer. PMID: 28326931
2. SOCS3 induces neurite differentiation and promotes neuronal cell survival.SOCS3-induced neurite differentiation was mediated via the PI3 kinase pathway. PMID: 27118613
3. Using cultured primary neurons, JEV efficiently replicated in embryonic neurons rather than adult neurons, and the preference was accompanied by higher SOCS3 expression and protein tyrosine phosphatase activity. PMID: 28111888
4. results suggest that knocking down of SOCS3 enhances dendritic regeneration and prevents demyelination after SCI PMID: 26384335
5. alveolar macrophages can secrete SOCS1 and -3 in exosomes and microparticles, respectively, for uptake by alveolar epithelial cells and subsequent inhibition of STAT activation. PMID: 25847945
6. SOCS-3 expression levels increased rapidly within 12 h after SAH, more slowly after 12 h, and did not reach a peak within 48 h. SOCS-3 was involved in cerebral vasospasm after subarachnoid hemorrhage via an IL-6- and IL-10-related mechanism. PMID: 24463741
7. The TNF/SOCS3 pathways work through insulin receptor resistance to trigger apoptosis. PMID: 25086044
8. The results of study suggest that the STAT3/SOCS3 signaling pathway plays an important role in regulating neuronal death after spinal cord injury. PMID: 24959867
9. Data in vitro indicate that suppressor of cytokine signaling 3 (SOCS3) may play a negatively regulatory role in development and progression of vein graft failure. PMID: 24142708
10. SOCS3 is a crucial physiological negative regulator for vein graft failure. PMID: 24685947
11. SOCS3 expression accompanied the severity of inflammation and the expression of proinflammatory cytokines, as well as the activation status of STAT3 and p38 MAPK PMID: 24078776
12. SOCS3-induced pro-inflammatory effects were due, at least in part, to its role in controlling activation and nuclear accumulation of nuclear factor-kappaB and activity of phosphatidylinositol 3-kinase. PMID: 24088176
13. Prolactin stimulates normal liver growth, promotes survival, and regulates liver regeneration by mechanisms that may include hepatic downregulation of IL-6 and upregulation of SOCS-3, increased hepatocyte proliferation, and angiogenesis. PMID: 23948778
14. IL-1b alone did not significantly increase SOCS-3 levels but when coincubated with insulin, prevented the downregulation of SOCS-3 expression. XOMA 052 neutralized the antagonistic effect of IL-1b on insulin-induced downregulation of SOCS-3. PMID: 23401297
15. The expressions of C/EBPalpha and PPARgamma were significantly reduced after gene silencing of SOCS-1 or SOCS-3 in adipocytes. PMID: 23222907
16. Vagal afferent neurons of diet-induced obese rats become leptin resistant; LPS and SOCS-3 may play a role in the development of leptin resistance. PMID: 21521717
17. Data suggest that down-regulation of SOCS-1 and SOCS-3 ameliorates the capacity of glucose transport and provides a potential gene therapy approach to managing metabolic syndrome. PMID: 21364493
18. With respect to neurite outgrowth SOCS3 alone is (as expected) strongly inhibitory, but it can also enhance the growth-promoting activity of mitogen-activated protein kinase 8 interacting protein 1 (JIP1). PMID: 20816823
19. Chronic central leptin infusion increases the association of insulin receptor with SOCS3. PMID: 21255014
20. Our data demonstrate the negative impact of enhanced SOCS3 expression on the regenerative potential of mature central nervous system neurons. PMID: 21145973
21. postnatal overnutrition induced higher SOCS3 expression in adult animals,indicating central leptin resistance in adulthood. PMID: 20303731
22. SOCS-3 knockdown may have increased the leptin-mediated in situ fatty acid oxidation in the DIO adipocytes, and therefore, SOCS-3 might be an excellent target for therapeutic intervention for obesity. PMID: 19862646
23. AngII response in spontaneouly hypertensive rats associated with increased hypothalamic JAK-2/SOCS-3 expression may suggest that abnormal regulation of the central angiotensin pathways may contribute to dysfunction of water-electrolyte homeostasis. PMID: 20848345
24. role of SOCS3 expressed in the mediobasal hypothalamus (MBH) in development of diet-induced obesity; data suggest knockdown of Socs3 mRNA limited to the MBH increases Npy mRNA levels, which decreases locomotor activity and alters feeding patterns PMID: 20819948
25. SOCS3 of retina may play an important role in mitigating pathogenic effects of proinflammatory cytokines during different stages of experimental autoimmune uveoretinitis. PMID: 19176113
26. High leptin concentration could induce the expressions of SOCS-3 mRNA and protein in mature adipocytes. PMID: 19408656
27. SOCS3 knock-down does not influence the growth and adipogenic differentiation feature of adipose-derived stromal cells. PMID: 19693688
28. Noradrenaline acting at central beta-adrenoceptors induces Socs3 expression in rat brain. PMID: 20193756
29. increased expression in diabetes PMID: 20185635
30. Results suggest that SOCS-3 may be a mediator of hypothalamic leptin resistance in aged rats, and that increased SOCS-3 expression may be due to age-related hyperleptinemia. PMID: 12163036
31. Antisense knockdown of ischemia-induced SOCS-3 protein expression exacerbated transient MCAO-induced infarct volume, assigning a neuroprotective role to SOCS-3 PMID: 12437578
32. induced by Ang II in rat heart and neonatal rat ventricular myocytes and participates in the modulation of the signal generated by this hormone PMID: 12960061
33. SOCS-3 exhibits a rapid, robust, and transient induction in hippocampus after seizure, first in glia, followed by a robust induction in pyramidal and granule neurons, peaking at approximately 24 hr. PMID: 14614901
34. SOCS-3 participates, as a late event, in the negative cross-talk between angiotensin II and insulin, producing an inhibitory effect on insulin-induced glucose transporter-4 translocation. PMID: 15514089
35. Cross-talk between the SOCS/interferon and the IL-1beta pathways of signalling in pancreatic beta cells. PMID: 15578154
36. Socs3 overexpression leads to neuroblastoma cell death and, on the other hand, leads to primary cell differentiation, indicating the involvement of SOCS-3 in neuronal cell survival and differentiation. PMID: 15998644
37. Promoter deletion analysis revealed that the STAT response element (SRE) in the SOCS3 promoter is necessary for the promoter activity. PMID: 16300827
38. involvement of SOCS3 in a direct gene regulatory pathway downstream of leptin-activated JAK-STAT signaling in pancreatic beta-cells PMID: 16306356
39. These data suggest that training-induced elevations in SOCS-3 expression in skeletal muscle may contribute to the exercise-induced increase in IL-6 expression. PMID: 16484300
40. Leptin induced SOCS-3 expression and its association with the insulin receptor in rat skeletal muscle cells but functional significance of this increase was not apparent upon measuring glucose uptake. PMID: 17223256
41. SOCS-3 might have a defensive role in H. pylori-infected gastric mucosal cells PMID: 17405912
42. increased glomerular IL-4 in nephrotoxic nephritis inhibits infiltrating macrophages from expressing SOCS3 and was associated with attenuated glomerular injury PMID: 18424750
43. These results demonstrate SOCS-3 induction occurs in reactive astrocytes of the post-ischemic hippocampus, suggesting that SOCS-3 is involved in regulating the astroglial reaction to an ischemic insult. PMID: 18586073
44. The up-regulation of SOCS1 and SOCS3 gene expression may be one of the possible mechanisms responsible for endotoxin tolerance. PMID: 19080716
45. The objective of this study was to investigate the effect of SOCS-3 on TNFalpha-induced signalling in beta cells. PMID: 19643162

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KEGG: rno:89829

STRING: 10116.ENSRNOP00000003940

UniGene: Rn.127801