ライフサイエンスコーパス: SOCS3

1 gnaling, suppressor of cytokine signaling 3 (SOCS3).

2 called suppressor of cytokine signalling 3 (SOCS3).

3 y is the suppressor of cytokine signaling 3 (SOCS3).

4 TEN) and suppressor of cytokine signaling 3 (SOCS3).

5 pathway [suppressor of cytokine signaling 3 (SOCS3)].

6 L-6-induced STAT3-regulated genes, including SOCS3.

7 ary hepatocytes via deregulation of TNFalpha/SOCS3.

8 inflammatory cytokine production mediated by SOCS3.

9 ogated gemfibrozil-mediated up-regulation of SOCS3.

10 siologic vascularization is not regulated by SOCS3.

11 let survival, and this protection depends on SOCS3.

12 ogated gemfibrozil-mediated up-regulation of SOCS3.

13 sed in part by the leptin signaling molecule SOCS3.

14 ignaling and shows its counter-regulation by SOCS3.

15 back to WT levels by exogenously expressing SOCS3.

16 pression of the LIF/STAT3 negative regulator SOCS3.

17 L)-6 and suppressor of cytokine signaling-3 (SOCS3), 2 key factors of the JAK/STAT pathway that induc

18 tion of suppressors of cytokine signaling 3 (SOCS3), a critical negative regulator of inflammation.

19 ssion of Suppressor of cytokine signaling 3 (Socs3), a feedback inhibitor of the Jak-Stat pathway tha

20 cortical suppressor of cytokine signaling 3 (SOCS3), a negative regulator of cytokine-activated pathw

21 Suppressor of cytokine signaling 3 (SOCS3), a protein suppressor of the JAK-STAT pathway, wa

22 ssion of suppressor of cytokine signaling-3 (Socs3), a target of resistin and hepcidin implicated in

23 nit of the IL-10 receptor (IL-10R), and also SOCS3, a negative regulator of proinflammatory cytokine

24 progressive E2f-mediated transactivation of Socs3, a potent inhibitor of Jak2 signaling, in cycling

25 Inhibition of SOCS3 abolished the antiinflammatory and vasoprotective

26 pha) and suppressor of cytokine signaling 3 (SOCS3) activities in whole retina and retinal endothelia

27 ing family members and provide evidence that SOCS3 acts as a potent feedback inhibitor of IL-31-induc

28 ction of suppressor of cytokine signaling 3 (SOCS3), an effect mediated by soluble egg Ag (SEA) obtai

29 As STAT target genes include SOCS3, an inhibitor of insulin receptor, holo-RBP suppre

30 Lentiviral delivery of SOCS3, an inhibitor of STAT3 signaling, into primary neu

31 e STAT signalling inhibitory proteins SOCS1, SOCS3 and CISH were marked by m(6)A, exhibited slower mR

32 This was mediated through suppression of SOCS3 and induction of vitamin D receptor binding with t

33 miR-221 directly inhibits the expression of SOCS3 and IRF2, two oncogenes that negatively regulate t

34 TNF-alpha induced both SOCS3 and PCSK9 in a concentration-dependent manner.

35 This suggests that SOCS3 and phospho-STAT3 act in an inversely dependent ma

36 ic nerve injury stimulated the expression of Socs3 and Sfpq (splicing factor, proline/glutamine rich)

37 In vivo, the injury-dependent induction of Socs3 and Sfpq inhibits optic nerve regeneration but doe

38 ing via direct transcriptional repression of SOCS3 and SOCS4 and this is essential for cancer cell gr

39 ated tumor suppressor genes such as TNFAIP3, SOCS3 and TNFRSF14.

40 We also identified a key pathway, stat3/socs3, and demonstrated its role in promoting hair cell

41 d by upregulation of fkbp5, irg1l, gilz, and socs3, and development genes, matrix metalloproteinases

42 ion of STAT3, increased protein abundance of SOCS3, and development of insulin resistance in L6 myotu

43 ate the effects of pioglitazone on TNFalpha, SOCS3, and downstream insulin signal transduction protei

44 and IL-2-stimulated ALK(-) TCL cells, CD25, SOCS3, and Irf-4 genes were activated predominantly by t

45 cted genes-CD25 (IL-2Ralpha), Egr-1, Fosl-1, SOCS3, and Irf-4-was confirmed at the protein level.

46 resulted in transcriptional upregulation of SOCS3, and treatment with RNA interference against SOCS3

47 suppressor of cytokine signaling 1 (SOCS1), SOCS3, and ubiquitin-specific peptidase 18 (USP18).

48 , including the proapoptotic protein Bim and SOCS3, are expressed at higher levels among activated CD

49 Here, we identify the adapter-encoding gene SOCS3 as a critical transcriptional target of PPARgamma.

50 that Ebola virus VLPs stimulate induction of SOCS3 as well as proinflammatory cytokines, and that exp

51 sIL-6R from IL-6R and downregulation of the SOCS3 autoinhibitory pathway.

52 sion of suppresor of cytokine signaling 1 or SOCS3 between liver samples from patients with AHC and t

53 Immunoprecipitation analyses revealed that SOCS3 bound p53 and subsequently increased the expressio

54 hanisms likely involve the downregulation of SOCS3 by JNK inhibition.

55 , the induction of STAT3 target genes (e.g., SOCS3) by IL-6 was also abolished, indicating that MCMV

56 hat host suppressor of cytokine signaling 3 (SOCS3) can also bind to EBOV VP40, leading to enhanced u

57 and adult mice, we show that either PTEN and SOCS3 co-deletion, or co-overexpression of osteopontin (

58 back regulators of the JAK/STAT pathway, and SOCS3 contributes to host immunity by regulating the int

59 pression of regenerative inhibitors, such as Socs3, contributes to the robust regenerative response o

60 Our data indicate that loss of the inhibitor SOCS3 cooperates with IL-6 to maintain JAK/STAT pathway

61 In the present study, we show that SOCS3 curbs pathologic angiogenesis.

62 ned under standard diet, we demonstrate that Socs3 deficiency in the mediobasal hypothalamus (MBH) re

63 Consequently, in SOCS3-deficient cells glucocorticoids do not affect IL-6

64 SOCS3-deficient M1 macrophages also have a stronger capa

65 In vitro, SOCS3-deficient macrophages exhibit heightened STAT3 act

66 Furthermore, SOCS3-deficient macrophages have higher levels of the M1

67 The myeloid-specific SOCS3-deficient mice are vulnerable to myelin oligodendr

68 Mechanistically, MBH Socs3-deficient mice display increased hindbrain sensiti

69 tive transfer of M2 macrophages into myeloid SOCS3-deficient mice leads to delayed onset and reduced

70 minent in the cerebellum of myeloid-specific SOCS3-deficient mice, as is enhanced STAT3 signaling and

71 Importantly, infiltrating SOCS3-deficient neutrophils produce high levels of CXCL2

72 These data show that deletion of SOCS3 delays the onset of leptin resistance and infertil

73 immune encephalomyelitis in myeloid-specific SOCS3-deleted mice, CD4-SOCS3KO mice were protected from

74 We have shown here that myeloid-restricted Socs3 deletion (Socs3(Lyz2cre)) resulted in resistance t

75 in neuroinflammation, mice with conditional SOCS3 deletion in myeloid cells (LysMCre-SOCS3(fl/fl)) w

76 Mice with Socs3 deletion in myeloid cells exhibit enhanced STAT3 s

77 In this study, we generated mice with Socs3 deletion in the CD4 T cell compartment (CD4-SOCS3

78 ressing expression of the negative regulator SOCS3 dependent on the transcription factor NF-kappaB, I

79 Here we show that SOCS3-dependent cytokine expression regulates bone corti

80 mammalian optic axons is partly mediated by Socs3-dependent inhibition of Jak/Stat signaling.

81 -CSF-driven neutrophil differentiation via a SOCS3-dependent inhibition of STAT3 phosphorylation.

82 d by proinflammatory cytokine TNF-alpha in a SOCS3-dependent manner.

83 ion of these cytokines by T cells, through a SOCS3-dependent pathway.

84 differentiation, although siRNA knockdown of SOCS3 did not affect either.

85 Thus, neutrophils lacking SOCS3 display elevated STAT3 activation and expression o

86 These data indicate that skeletal muscle SOCS3 does not play a critical role in regulating muscle

87 Socs3 downregulation may also contribute to Stat3 activa

88 r the expansion of regulatory T cells in CD4-SOCS3 during EAU.

89 tory cytokines, and that expression of human SOCS3 enhances budding of Ebola VLPs and infectious viru

90 In addition, HepG2(SOCS3) express higher mRNA levels of key enzymes involve

91 In addition, SOCS3 expression and beta-cell fate are dependent on STA

92 7 cells induced in vitro displayed increased SOCS3 expression and diminished capacity to produce inte

93 Recombinant IL-7 inhibited SOCS3 expression and reduced IL-17-expressing T-cell pro

94 STAT3 phosphorylation, OSM and IL-6/R induce SOCS3 expression at the mRNA and protein level.

95 SOCS3 expression in AgRP neurons increases after 2 d of

96 Furthermore, modulation of SOCS3 expression in AgRP neurons may play a dynamic and

97 Therefore, increased SOCS3 expression in human tuberculosis may reflect polar

98 n the current study, we created mice lacking SOCS3 expression in macrophages and neutrophils (LysM-cr

99 Ectopic SOCS3 expression in primary CD4(+) T cells by lentiviral

100 man tuberculosis is accompanied by increased SOCS3 expression in T cells, and this may influence susc

101 -cell activation and a transient decrease of SOCS3 expression in the presence of mycobacteria-infecte

102 iferation of human T cells with differential SOCS3 expression in the present study.

103 Lastly, we show that SOCS3 expression is induced by EBOV glycoprotein (GP) ex

104 se data suggest that AhR-mediated control of SOCS3 expression is probably involved in the phenotype s

105 ivation of the IL6 inflammatory loop induced SOCS3 expression leading to pathway inactivation.

106 Thus, IL-6/R and OSM-induced SOCS3 expression may be an important factor limiting the

107 L1 up-regulation, suggesting that diminished SOCS3 expression may lead to the observed effects.

108 molecular pathway by which PPARgamma-induced SOCS3 expression prevents IL-17-mediated cancer growth.

109 Notably increased SOCS3 expression was detected in IL-17-expressing T-cell

110 Ls with a demethylating agent, IL-6-mediated SOCS3 expression was restored with consequent P-STAT3 an

111 -deficient macrophages resulted in increased SOCS3 expression with decreased STAT3 activation.

112 shown to depend on epigenetic suppression of SOCS3 expression, further suggesting involvement of SOCS

113 partial loss of A20 in hepatocytes increased SOCS3 expression, hampering IL-6-induced STAT3 phosphory

114 P6 treatment inhibits SOCS3 expression, indicating that STAT3 is required for

115 s MAPK and NF-kappaB activation and enhances SOCS3 expression, which could explain its negative effec

116 signaling through Smad3-mediated blockade of Socs3 expression.

117 ongly correlated with a dramatic increase of SOCS3 expression.

118 hway, which are also negatively regulated by SOCS3 expression.

119 STAT3 is required for OSM and IL-6/R-induced SOCS3 expression.

120 imately leading to the early upregulation of socs3 expression.

121 ncreased suppressor of cytokine signaling 3 (SOCS3) expression.

122 e treatment of gonadectomized female Dmp1Cre.Socs3 (f/f) mice restores normal cortical morphology, wh

123 Young male and female Dmp1Cre.Socs3 (f/f) mice, in which SOCS3 has been ablated in ost

124 Our studies demonstrate that impaired SOCS3 feedback leads to permissive IL10/STAT3 signalling

125 LPS-induced sepsis is exacerbated in LysMCre-SOCS3(fl/fl) mice and is associated with enhanced STAT1/

126 nflammatory response to LPS in both LysM-cre SOCS3(fl/fl) mice and the wild-type (WT) mice (SOCS3(fl/

127 into the cerebellum and brainstem of LysMCre-SOCS3(fl/fl) mice closely correlates with atypical EAE c

128 LysM-cre SOCS3(fl/fl) mice displayed significant increase of the

129 ng that the atypical EAE observed in LysMCre-SOCS3(fl/fl) mice is characterized by extensive neutroph

130 Macrophages obtained from LysMCre-SOCS3(fl/fl) mice, which lack SOCS3 in myeloid lineage c

131 ell differentiation than M1 macrophages from SOCS3(fl/fl) mice.

132 /STAT pathway compared with macrophages from SOCS3(fl/fl) mice.

133 nal SOCS3 deletion in myeloid cells (LysMCre-SOCS3(fl/fl)) were tested for experimental autoimmune en

134 ion in macrophages and neutrophils (LysM-cre SOCS3(fl/fl)).

135 CS3(fl/fl) mice and the wild-type (WT) mice (SOCS3(fl/fl)).

136 of proinflammatory cytokines, which induced SOCS3 for negative-feedback regulation.

137 n which AECs use PGE2 as a signal to request SOCS3 from AMs to dampen their endogenous inflammatory r

138 Deletion of SOCS3 from brain neurons delays the onset of diet-induce

139 These inhibitory effects were abrogated when SOCS3 gene expression was silenced, indicating that SEA-

140 e significantly attenuated Serpina3n but not SOCS3 gene expression, whereas vascular changes includin

141 binding of STAT3 to the SOCS3 promoter, and SOCS3 gene expression.

142 RIB1 and suppressor of cytokine signaling 3 (SOCS3) genes, which have opposing roles in the regulatio

143 ation of suppressor of cytokine signaling 3 (SOCS3), glycoprotein A repetitions predominant (GARP), t

144 lation on IRS-2, although siRNA knockdown of SOCS3 had no effect on ubiquitination of IRS-2.

145 SOCS3 has a crucial role in inhibiting STAT3 activation,

146 These results indicate that SOCS3 has a protective role in LPS-induced ALI by suppre

147 nd female Dmp1Cre.Socs3 (f/f) mice, in which SOCS3 has been ablated in osteocytes, have high trabecul

148 SOCS3 has only a modest effect on promoting Brk degradat

149 Genes that dampen inflammation (Socs3, Il10, Crem, Stat3, Thbd, Thbs1, Abca1) and genes

150 Aberrant activation of Socs3 impairs Tpo signaling and leads to impaired HSC ho

151 Consistently, transgenic overexpression of SOCS3 in AgRP neurons produces metabolic phenotypes rese

152 xpression, further suggesting involvement of SOCS3 in autoimmunity and tumor immunity.

153 infection resulted in enhanced expression of SOCS3 in brain, which was absent in infected AhR-KO mice

154 f negative regulatory genes PIAS3, SHP2, and SOCS3 in CD4 T cells.

155 of adiponectin and reduced the expression of SOCS3 in cultured 3T3-L1 adipocytes.

156 vel property of gemfibrozil in up-regulating SOCS3 in glial cells via PI 3-kinase-AKT-mediated activa

157 ing drug, in up-regulating the expression of SOCS3 in glial cells.

158 Retroviral overexpression of SOCS3 in HepG2 cells (HepG2(SOCS3)) strongly inhibited S

159 gested that HCV-exo carry miR-19a and target SOCS3 in HSC, which in turn activates the STAT3-mediated

160 Because the role of SOCS3 in human T-cell function is not well defined, we c

161 Overexpression of SOCS3 in keratinocytes significantly diminished this enh

162 studies have confirmed the important role of Socs3 in leptin resistance and obesity.

163 BP) delta as a critical downstream target of SOCS3 in LPS-induced ALI.

164 To determine the role of SOCS3 in myeloid cells in neuroinflammation, mice with c

165 d from LysMCre-SOCS3(fl/fl) mice, which lack SOCS3 in myeloid lineage cells, exhibit enhanced and pro

166 Therapies aimed at inhibiting SOCS3 in skeletal muscle may be effective in reversing o

167 AhR modulated the basal expression of SOCS3 in spleen and brain, and P. berghei Anka infection

168 ytokines and reduced expression of SOCS2 and SOCS3 in the heart.

169 n and insulin signaling, thereby implicating SOCS3 in the pathogenesis of obesity and associated meta

170 r-alpha (TNF-alpha), IL-6, IL-10, SOCS1, and SOCS3 in the spleen.

171 to determine in vivo effects of the loss of Socs3 in the T cell-mediated autoimmune disease, experim

172 ty; however, the physiological importance of SOCS3 in this tissue has not been examined.

173 tive to suppress IL-27(p28) with deletion of SOCS3 in Tie2-Cre/SOCS3flox macrophages.

174 Using a Cre/Lox system, we deleted SOCS3 in vessels and studied developmental and pathologi

175 egulated lipoprotein lipase and up-regulated Socs3 in visceral adipose tissue.

176 role of Suppressor Of Cytokine Signaling-3 (SOCS3) in regulating excitotoxic neuronal death in vitro

177 sion of suppressors of cytokine signaling 3 (SOCS3) in the presence of erlotinib and enhanced express

178 Further, we showed that SOCS3 induction is essential to the effects of Ba, given

179 ransient suppressor of cytokine signaling-3 (SOCS3) inhibition of the STAT5b transcription factor sig

180 ppressor of cytokine signaling-1 (SOCS1) and SOCS3, inhibitors of STAT1 and STAT3, and also blocked t

181 Investigation of the mechanism by which SOCS3 inhibits Brk reveals the SOCS3 protein binds to Br

182 SOCS3 inhibits leptin signaling in the hypothalamus and

183 We further show that SOCS3 interacts with CTLA-4 and negatively regulates CTL

184 Expression of IL10, SOCS3, IP10, and ICAM1 mRNA in DS patients was significa

185 n of the suppressor of cytokine signaling 3 (SOCS3) irrespective of viral load.

186 Thus, SOCS3 is a potential therapeutic target in uveitis and o

187 SOCS3 is also implicated in hypertriglyceridemia associa

188 SOCS3 is an important negative regulator of IL-6-type cy

189 Here, we demonstrate that SOCS3 is critically involved in regulating the cell-spec

190 hy monocytes but not allergic cells, whereas SOCS3 is highly induced in allergic monocytes.

191 SOCS3 is induced in lung during LPS-induced lung injury,

192 These findings collectively indicate that SOCS3 is involved in repressing the M1 proinflammatory p

193 gain, and limits adiposity, suggesting that Socs3 is necessary for normal body weight maintenance.

194 Suppressor of cytokine signaling 3 (SOCS3) is a major negative regulator of both leptin and

195 Suppressor of cytokine signaling-3 (SOCS3) is an inducible negative feedback regulator of in

196 ack regulator of leptin receptor signalling, Socs3, is inhibited in the hypothalamus of RIIbeta KO mi

197 ts main inhibitory effect is mediated by the SOCS3 kinase inhibitory region (KIR).

198 uld be induced in almost all neuron-specific SOCS3 knock-out mice on this diet.

199 We used neuron-specific SOCS3 knock-out mice to elucidate this and the effects o

200 As expected, male and female neuron-specific SOCS3 knock-out mice were protected from HCD-induced obe

201 RH/LH surge were overcome by neuron-specific SOCS3 knock-out.

202 WT and SOCS3 knockdown C57BL6 mice were treated for 5 days with

203 In vitro, SOCS3 knockdown increases proliferation and sprouting of

204 Wild-type (WT) and SOCS3 knockdown MIN6 cells were cultured with CNTF, IL1b

205 deletion in the CD4 T cell compartment (CD4-SOCS3 knockout [KO]) to determine in vivo effects of the

206 deed, titers of infectious EBOV derived from SOCS3 knockout mouse embryonic fibroblasts (MEFs) were s

207 M-derived DCs expressed high levels of SOCS1/SOCS3, known inhibitors of GM-CSF signaling, providing a

208 ssion of Suppressor of Cytokine Signaling 3 (SOCS3), leading to increases in STAT3 phosphorylation an

209 Conditional loss of SOCS3 leads to increased pathologic neovascularization,

210 3 protein quantification and detected higher SOCS3 levels induced by M tuberculosis specific T-cell a

211 Upstream of SOCS3, levels of its microRNA regulator miR203 were sign

212 ve signals in hepatocytes by down-regulating SOCS3, likely through a miR203-dependent manner.

213 nced regulatory T (Treg) cell recruitment by Socs3(Lyz2cre) cells, whereas Treg cell recruitment was

214 plus IL-13-induced STAT6 phosphorylation in Socs3(Lyz2cre) macrophages.

215 striking bias toward M2-like macrophages in Socs3(Lyz2cre) mice, whereas the M1-like population was

216 here that myeloid-restricted Socs3 deletion (Socs3(Lyz2cre)) resulted in resistance to LPS-induced en

217 ata indicate that host innate immune protein SOCS3 may play an important role in budding and pathogen

218 d lung injury, suggesting that generation of SOCS3 may represent a regulatory product during ALI.

219 mice with muscle-specific overexpression of SOCS3 (MCK/SOCS3 mice).

220 Despite similar body weight, MCK/SOCS3 mice develop impaired systemic and muscle-specific

221 With regards to leptin action, MCK/SOCS3 mice exhibit suppressed basal and leptin-stimulate

222 muscle-specific overexpression of SOCS3 (MCK/SOCS3 mice).

223 The SOCS3 MKO mice had normal muscle development, body mass,

224 degrees of obesity when fed a high-fat diet, SOCS3 MKO mice were protected against the development of

225 Gemfibrozil increased the expression of Socs3 mRNA and protein in mouse astroglia and microglia

226 Here, we demonstrate that SOCS3 mRNA expression is increased in murine skeletal mu

227 tivation (increase of STAT3 and reduction of SOCS3 mRNA) indicates an important modulation of the imm

228 the increase in bronchoalveolar lavage fluid SOCS3 noted in lungs of mice challenged with LPS in vivo

229 ation of suppressor of cytokine signaling-3 (SOCS3) occurs in AgRP neurons before proopiomelanocortin

230 is study, we have evaluated the influence of SOCS3 on macrophage polarization and function.

231 In transformed cells, enforced expression of SOCS3 or interfering with IL6 pathway via IL6R blockade

232 a signaling is regulated by SOCS1 but not by SOCS3 or USP18.

233 Muscle SOCS3 overexpression also suppresses leptin-regulated ge

234 stimulation produced an additive effect with SOCS3 overexpression, further inducing PCSK9, SREBP-1, f

235 However, the degree to which Socs3 participates in the regulation of energy homeostas

236 Rb that mediates signaling through the STAT3/SOCS3 pathway also resulted in decreased mucosal chemoki

237 sets into account, we propose that the stat3/socs3 pathway is a key response in all tissue regenerati

238 ered pro-inflammatory response via the STAT3-Socs3 pathway.

239 S3, which correlated with methylation of the SOCS3 promoter and increased expression and activation o

240 SOCS3 promoter binding and gene transactivation by PPARg

241 Methylation in the SOCS3 promoter was not detectable, suggesting that an ep

242 horylation of STAT3, binding of STAT3 to the SOCS3 promoter, and SOCS3 gene expression.

243 ed STAT3 and enhances its recruitment to the SOCS3 promoter, concomitant with histone hyperacetylatio

244 , but not proximal, KLF4-binding site of the Socs3 promoter.

245 edly reduced in CD4-SOCS3KO, suggesting that SOCS3 promotes expansion of the Th17/IFN-gamma subset as

246 nism by which SOCS3 inhibits Brk reveals the SOCS3 protein binds to Brk primarily via its SH2 domain,

247 ion in vitro, with a correlating increase in SOCS3 protein expression.

248 stablished a flow cytometry-based method for SOCS3 protein quantification and detected higher SOCS3 l

249 In this study, we report that SOCS3 protein was elevated in bronchoalveolar lavage flu

250 K2), and suppressor of cytokine signaling 3 (SOCS3) protein abundance was increased in skeletal muscl

251 teriole suppressor of cytokine signalling 3 (SOCS3) protein, and (9) coronary arteriole gp91(phox) pr

252 lipopolysaccharide plasma levels, TLR4, and SOCS3 proteins (p<0.001, p=0.041 and p=0.008, respective

253 These findings indicate that myeloid cell SOCS3 provides protection from EAE through deactivation

254 Moreover, in hepatocytes lacking the SOCS3 recruiting motif within gp130, IL-6-dependent gamm

255 Consistently, siRNA anti-SOCS3 reduced PCSK9 mRNA levels, whereas an opposite eff

256 Host SOCS3 regulates the innate immune response by controllin

257 Suppressor of cytokine signaling 3 (SOCS3) regulates STAT3 activation in response to cytokin

258 and treatment with RNA interference against SOCS3 relieved virus-induced inhibition of IFN-gamma-ind

259 ed that myeloid lineage-specific deletion of SOCS3 resulted in a severe, nonresolving atypical form o

260 ation of suppressor of cytokine signaling 3 (SOCS3) resulting in low levels of this protein in basal/

261 AEC-conditioned medium (AEC-CM) enhanced AM SOCS3 secretion above basal levels.

262 jor AEC-derived factor mediating enhanced AM SOCS3 secretion.

263 HepG2(SOCS3) show lower phosphorylation levels of insulin rece

264 ic Th17 responses was largely abolished when SOCS3 signaling was knocked down.

265 of IL-2 suppression, IL-10 upregulation, or SOCS3 signaling, we observed that IL-27-driven suppressi

266 SOCS3 significantly inhibited this pathway in astrocytes

267 Therefore, we generated mice that had SOCS3 specifically deleted in skeletal muscle (SOCS MKO)

268 ssed the expression of adiponectin through a SOCS3-STAT3 pathway.

269 tissue was essential for ACF to improve the SOCS3-STAT3-adiponectin pathway to counteract insulin re

270 In vivo, ACF also regulated the SOCS3-STAT3-adiponectin pathway, and inhibition of HIF1a

271 Overexpression of SOCS3 strongly inhibited phosphorylation of STAT1 and PD

272 verexpression of SOCS3 in HepG2 cells (HepG2(SOCS3)) strongly inhibited STAT3 phosphorylation and ind

273 d, we observed an overexpression of IL-6 and SOCS3, suggesting an overactivation of JAK/STAT3, a shar

274 the brain, as well as reduced expression of SOCS3, suggesting involvement of the STAT signaling path

275 ro and synergized with IL-22 in upregulating SOCS3 (suppressor of cytokine signaling 3), a key regula

276 -mediated STAT3 silencing, overexpression of SOCS3 (suppressor of cytokine signaling 3), and antioxid

277 ay directly, and elevated TNFAIP3 suppressed SOCS3 (suppressor of cytokine signaling 3)-activated STA

278 KSHV-inoculated EC via a mechanism involving SOCS3 (suppressor of cytokine signaling 3).

279 induced expression of the feedback inhibitor SOCS3, thereby leading to enhanced expression of acute-p

280 cts with suppressor of cytokine signaling 3 (SOCS3); therefore, absence of CD37 drives tumor developm

281 We demonstrate a higher ratio of SOCS3 to IL-6 receptor in adult monocytes than in fetal

282 further evaluate the contribution of muscle SOCS3 to leptin and insulin resistance in obesity, we ge

283 Lack of SOCS3 up-regulation in skin epithelial cells was accompa

284 thors show that this process is regulated by SOCS3 via a mechanism dependent on IL-6 and expression o

285 In addition, we found that SOCS3 was down-modulated in LGL and unresponsive to IL-6

286 SOCS3 was found to be significantly up-regulated by IL-2

287 Socs3 was identified as a novel HIF1alpha target gene ba

288 SOCS3 was required for CXCR4-mediated growth inhibition.

289 gulated, whereas the expression of SOCS1 and SOCS3 was up-regulated by vorinostat treatment.

290 The endogenous STAT3 target gene, SOCS3, was upregulated in HSFs and showed increased STAT

291 the inflammatory pathway genes MAPK8IP1 and SOCS3 were associated with increased overall survival in

292 In human psoriatic skin, both CXCR4 and SOCS3 were upregulated in the junctional region at the b

293 or either rs3824872 (MAPK8IP1) or rs8064821 (SOCS3) were associated with a 10- and 6-month survival a

294 anges in suppressor of cytokine signaling 3 (SOCS3) were determined by using methylation-specific PCR

295 periphery through a modulated expression of SOCS3, whereas cholinergic innervation-mediated suppress

296 pe-specific impaired capacity to up-regulate SOCS3 which may crucially determine the course of chroni

297 TNF-alpha, and the upregulation of SOCS1 and SOCS3, which are important regulatory molecules in the I

298 IL-6 reduced expression of SOCS3, which correlated with methylation of the SOCS3 pr

299 atory response, possibly mediated in part by SOCS3, which could serve as a target in the treatment or

300 Elucidating the function of SOCS3 would represent prospective targets for a new gene