ライフサイエンスコーパス: SOCS

1 SOCS knocked down cells also displayed decreased parasit

2 SOCS performs its mapping within the context of 'color s

3 SOCS proteins can define host susceptibility to infectio

4 SOCS proteins regulate cytokine signals that control the

5 SOCS proteins, especially SOCS1 and SOCS3, are expressed

6 SOCS secretion into lung lining fluid was diminished by

7 SOCS, therefore, are essential controllers of macrophage

8 SOCS-1 and SOCS-3 transcriptional activity is induced by

9 SOCS-1 inhibits both type I and type II IFN activities b

10 SOCS-1 is a critical regulator of multiple signaling pat

11 SOCS-3 and SOCS-4 appear to play regulatory roles in a n

12 SOCS-3 deficiency in myeloid cells also promotes a highe

13 SOCS-3 expression was assessed in human cholangiocarcino

14 SOCS-3 gene induction by cAMP-elevating agents or the pr

15 SOCS-3 over-expression and SOCS-4 knockdown mutant lines

16 SOCS-3/IL-4 receptor complexes, however, were increased

17 SOCS-4 knockdown significantly reduced HaCaT migration a

18 SOCS-mediated insulin resistance and neuroprotection in

19 SOCS-mediated insulin resistance, as indicated by its in

20 The suppressor of cytokine signaling 1 (SOCS-1) protein modulates cytokine signaling by binding

21 target, suppressor of cytokine signaling 1 (SOCS-1).

22 role of suppressor of cytokine signaling-1 (SOCS-1) in this refractiveness.

23 creasing suppressor of cytokine signaling-1 (SOCS-1) mRNA stability.

24 D-1) and suppressor of cytokine signaling-1 (SOCS-1), the aim of this study was to examine their role

25 f Stat3, suppressor of cytokine signaling-1 (SOCS-1), was reduced in the brain metastatic melanoma ce

26 hy subjects or the THP-1 cell line for PD-1, SOCS-1, and IL-12 expression following HCV core treatmen

27 s beta-catenin-mediated expression of COX-2, SOCS-3, and MMP-9.

28 ssion of suppressor of cytokine signaling 3 (SOCS-3), a downstream target, are inhibited by CK2 small

29 IRAK-M), suppressor of cytokine signaling 3 (SOCS-3), and activating transcription factor 3 (ATF-3),

30 -3), and suppressor of cytokine signaling 3 (SOCS-3).

31 entified Suppressor of Cytokine Signaling-3 (SOCS-3) as a gene that exhibits greatly increased transc

32 ction of suppressor of cytokine signaling-3 (SOCS-3), a negative regulator of IL-6 receptor signaling

33 recruitment and activation of STAT1; and 3) SOCS-1, which normally terminates IFN-gamma-signaling, w

34 ing the formation of the Elongin BC/Cullin 5/SOCS (EC5S(mLANA)) complex and mLANA's E3 ligase activit

35 usion between a GFP-targeting nanobody and a SOCS-box containing ubiquitin ligase adaptor to target G

36 a PLCbeta regulator, STOPS, which encodes a SOCS box protein.

37 teins leads to VHL protein degradation, in a SOCS domain-containing manner.

38 ne kinase inhibitor peptide (Tkip) that is a SOCS-1 mimetic.

39 Moreover, a SOCS-3-specific lean phenotype was revealed on the stand

40 Our biochemical analysis of a SOCS-family regulator from a lower organism highlights t

41 )-associated osteoclastogenesis, we analyzed SOCS expression profiles in CD4(+) T cells and the effec

42 CV core protein displayed increased PD-1 and SOCS-1 expression and decreased IL-12 expression, an eff

43 6 h) attenuated IL-13-induced eotaxin-1 and SOCS-1 gene expression.

44 PD-1 and SOCS-1 were found to associate by coimmunoprecipitation

45 /M(Phi)s triggers the expression of PD-1 and SOCS-1, which can associate to deliver negative signalin

46 kinase inhibitory region of both SOCS-1 and SOCS-3 and blocks their inhibitory effects on the IFN-ga

47 ulatory cytokine IFN-beta induces SOCS-1 and SOCS-3 expression in primary astrocytes at the transcrip

48 inhibition of IFN-beta-inducible SOCS-1 and SOCS-3 in astrocytes enhances their proinflammatory resp

49 ts indicate that IFN-beta induces SOCS-1 and SOCS-3 in primary astrocytes to attenuate its own chemok

50 SOCS-1 and SOCS-3 transcriptional activity is induced by IFN-beta t

51 uppressor of cytokine signaling (SOCS)-1 and SOCS-3.

52 cs of 4 TSGs (p15(INK4B), CDH-1, DAPK-1, and SOCS-1) were studied in sequential bone marrow samples f

53 significantly with IL-6 (groups 1 and 2) and SOCS-3 (group 2) gene expression.

54 tion was observed between phospho-STAT-3 and SOCS-3 protein expression in cholangiocarcinoma.

55 SOCS-3 and SOCS-4 appear to play regulatory roles in a number of ke

56 aims to explore the importance of SOCS-3 and SOCS-4 in regulating cellular traits associated with wou

57 n-induced expression of TNF-alpha, IL-6, and SOCS-3 in the liver.

58 The ankyrin and SOCS (suppressor of cytokine signaling) box (ASB) family

59 in "3-box" motif, analogous to the F-box and SOCS box motifs of other Cullin-based E3s.

60 ole in the coordinated regulation of CIS and SOCS expression in epithelial cells in response to C. pa

61 The results implicate Cul5 and SOCS proteins in down-regulation of Dab1 in vivo and sho

62 The mammalian SPRY domain- and SOCS box-containing proteins, SPSB1 to SPSB4, belong to

63 SOCS-3 over-expression and SOCS-4 knockdown mutant lines were generated and verifie

64 itin ligases, members of the Cbl, Hakai, and SOCS-Cul5-RING ligase families, stimulate the ubiquitina

65 equence variations in the ankyrin repeat and SOCS box containing gene 10 (ASB10) were recently associ

66 t identified the gene for ankyrin repeat and SOCS box protein 4 (ASB4) as the most highly differentia

67 Here we show that WD repeat and SOCS box-containing protein 1 (WSB1) is a negative regul

68 t and find that gustavus, the B30.2/SPRY and SOCS box domain gene, contributes to this phenomenon.

69 anced suboptimal IFN-gamma activity, blocked SOCS-1-induced inhibition of STAT3 phosphorylation in IL

70 C/EBPbeta and -delta isoforms abolished both SOCS-3 induction and inhibition of IL-6 signaling in res

71 inds to the kinase inhibitory region of both SOCS-1 and SOCS-3 and blocks their inhibitory effects on

72 cells to exogenous IFN-alpha is regulated by SOCS proteins.

73 The chSOCS1 "SOCS box" domain (which in mammals, interacts with an E3

74 Under physiologic circumstances, SOCS proteins negatively regulate inflammatory signaling

75 Consistently, SOCS-1 expression was also lower in the human brain meta

76 nition subunit in a subset of Elongin-Cullin-SOCS (ECS) E3 ubiquitin ligases.

77 To date, SOCS proteins have been shown to inhibit protective anti

78 n with miR-155 and miR-146b mimics decreased SOCS-1 levels, increased MyD88 expression, and restored

79 tic melanoma cells might be due to decreased SOCS-1 expression.

80 300, and RNA polymerase II to the endogenous SOCS-3 promoter in a time-dependent manner.

81 Either DAC treatment or enforced SOCS-3 expression sensitized the cells to TRAIL-mediated

82 results suggest that L. donovani may exploit SOCS for subverting macrophage apoptotic machinery towar

83 to bind, and be regulated by, over-expressed SOCS proteins.

84 ating Cul3 binding and its resemblance to F-/SOCS-boxes in other cullin-based E3s.

85 or healthy human volunteers was analyzed for SOCS expression by RNase protection assay and RT-PCR.

86 ombined inactivation of the genes coding for SOCS-3 and PTP-1B in brain cells, examined their sensiti

87 Transcripts for SOCS proteins were rapidly but variably induced in PBMCs

88 inical trial data from the U.S. NHLBI-funded SOCS trial and validated using data from the NHLBI SLIC

89 y mediated by the direct miR-155 target gene SOCS-1.

90 ased circulating IL-6 with increased hepatic SOCS-3 following LPS, suggesting SOCS-3 inhibited insuli

91 Despite high SOCS-3 expression, STAT3 remained constitutively active,

92 following infection, essentially "hijacking" SOCS function to promote virus survival.

93 e developed mechanisms to induce robust host SOCS protein expression following infection, essentially

94 Understanding how SOCS family members regulate T cell maturation, differen

95 However, SOCS proteins are not only induced via the JAK/STAT path

96 Although some human SOCS proteins contain N-terminal kinase-inhibitory domai

97 Our data implicate SOCS-3 as a critical negative regulator of alveolar bone

98 prevented both the LTB4-mediated decrease in SOCS-1 and increase in MyD88.

99 This increase in SOCS-3 transcription is associated with a four- to fivef

100 and STAT-3 activation play critical roles in SOCS-3 expression, which provides for feedback attenuati

101 results in BIC/miR-155 inhibition, increased SOCS-1 expression, and severely impaired tTreg cell deve

102 leptin and insulin action and that increased SOCS may mediate insulin and leptin resistance in obesit

103 This increased SOCS family activity consequently inhibited IL-7-mediate

104 al labile zinc pools which lead to increased SOCS-3 production through G-coupled receptor activation

105 STAT-1alpha is required for IFN-beta-induced SOCS-1 expression, while STAT-3 small interfering RNA st

106 NA studies demonstrate that IFN-beta-induced SOCS-3 expression relies on STAT-3 activation.

107 LPS-induced SOCS-3 expression was diminished in IL-10-deficient macr

108 to STAT-3, were also involved in LPS-induced SOCS-3 expression.

109 e immunomodulatory cytokine IFN-beta induces SOCS-1 and SOCS-3 expression in primary astrocytes at th

110 These results indicate that IFN-beta induces SOCS-1 and SOCS-3 in primary astrocytes to attenuate its

111 rfering RNA inhibition of IFN-beta-inducible SOCS-1 and SOCS-3 in astrocytes enhances their proinflam

112 s was demonstrated in P. gingivalis-infected SOCS-3-knockout mice as compared with P. gingivalis-infe

113 STAT1-alpha phosphorylation, SOCS1-KIR, like SOCS-1, did not inhibit JAK2 autophosphorylation but inh

114 ce macrophages as was db/db mouse macrophage SOCS-3 expression.

115 Mechanistically, SOCS proteins shield FLT3-ITD from external cytokine con

116 asal transcriptional activity of the minimal SOCS-3 promoter.

117 We show that specific mutations in the mLANA SOCS box (V199A, V199A/L202A, or P203A/P206A) disrupted

118 HV-4 recombinant viruses bearing these mLANA SOCS box mutations exhibited a deficit in latency amplif

119 CS3 specifically deleted in skeletal muscle (SOCS MKO).

120 gest that the JAK2 V617F has overcome normal SOCS regulation by hyperphosphorylating SOCS3, rendering

121 ta potentiated EPAC-mediated accumulation of SOCS-3.

122 pletely blocks transcriptional activation of SOCS-3 by PMA.

123 Administration of SOCS-1 mimetics by the oral route also protected mice ag

124 Additionally, alterations of SOCS-1 expression profoundly affected the expression of

125 RT-PCR analysis of SOCS-1 mRNA expression in HSV-1-infected cells showed a

126 have developed a small peptide antagonist of SOCS-1 that corresponds to the activation loop of JAK2.

127 have developed a small peptide antagonist of SOCS-1, pJAK2(1001-1013), that had both an antiviral eff

128 2 peptide could function as an antagonist of SOCS-1.

129 Deletion of SOCS-3 from brain cells is known to protect mice from di

130 on of Stat3 activation, whereas depletion of SOCS-1 up-regulated Stat3 activation.

131 Here, we report the development of SOCS (short oligonucleotide color space), a program desi

132 and examine whether persistent elevation of SOCS levels in retina by chronic inflammation or cellula

133 insight into how dysregulated expression of SOCS increases IL-4 responses in allergic monocytes, and

134 2 production and decreased the expression of SOCS-1 induced by HCV core.

135 r, were shown to down regulate expression of SOCS-1, a gene frequently silenced in MM that plays a cr

136 s directly correlated with low expression of SOCS-1.

137 Enforced expression of SOCS-3 also reduced IL-6 induction of phospho-STAT-3 and

138 mouse model of T2D, macrophage expression of SOCS-3 is increased, and impaired IL-4-dependent IRS-2/P

139 Over-expression of SOCS-3 resulted in a significantly reduced proliferative

140 s, and its endogenous brake is the family of SOCS proteins.

141 rent study aims to explore the importance of SOCS-3 and SOCS-4 in regulating cellular traits associat

142 Nonetheless, combined inactivation of SOCS-3 and PTP-1B in brain revealed additive effects on

143 Induction of SOCS proteins may be mediated by Egr1, and silencing of

144 fective than wild-type virus in induction of SOCS-1 promoter.

145 We also observed the induction of SOCS-3 mRNA in 3T3-L1 adipocytes following NP treatment.

146 Thus, induction of SOCS-encoding genes is the main mechanism by which ThPOK

147 ip and a peptide corresponding to the KIR of SOCS-1, ((53))DTHFRTFRSHSDYRRI((68)) (SOCS1-KIR), both b

148 y with the kinase inhibitory region (KIR) of SOCS-1 for JAK2 recognition, inhibition of kinase activi

149 similar pattern was observed at the level of SOCS-1 protein induction.

150 om sleep-deprived mice have higher levels of SOCS genes expression, lower migration capacity in vitro

151 s tubulogenesis by controlling the levels of SOCS-3 expression.

152 trated that IgE levels increase with loss of SOCS-1 alleles.

153 ctively, these data suggest that the loss of SOCS-1 expression is a critical event, leading to elevat

154 Loss of SOCS-3 function resulted in an increased number of alveo

155 Importantly, manipulation of SOCS proteins not only facilitates progression of the vi

156 istent with these observations, the mRNAs of SOCS family genes encoding the STAT signalling inhibitor

157 esponding to the kinase-inhibitory region of SOCS-1, SOCS1-KIR, similarly interacts with the activati

158 this study to investigate the regulation of SOCS proteins involved in intracellular signaling pathwa

159 dicating a novel role for TLR8 regulation of SOCS-1 function, whereas selective small interfering RNA

160 ich is identified as a negative regulator of SOCS-1 transcriptional activity.

161 of epithelial cells to direct AM release of SOCS-containing vesicles in response to inflammatory ins

162 Furthermore, restoration of SOCS-1 expression in brain metastatic A375Br cells signi

163 Moreover, restoration of SOCS-1 expression resulted in the inhibition of Stat3 ac

164 r that a better understanding of the role of SOCS proteins in viral diseases will be essential in our

165 Our data suggest two-sided roles of SOCS proteins in retina.

166 se results show that the biological roles of SOCS-3 and PTP-1B do not fully overlap and that targetin

167 Suppression of SOCS-4 influenced the responsiveness of HaCaT and HECV c

168 nscription 3 (Stat3), a downstream target of SOCS, was diminished following miR-203 silencing.

169 The use of SOCS-1 antagonist to abrogate this refractiveness could

170 The use of SOCS-1 mimetics in the treatment of poxvirus infections

171 utations in the highly conserved HCCH and/or SOCS box motifs, which are required for assembly of a fu

172 This suggested that overall SOCS-1 acts as an inhibitor of IgE expression in vivo.

173 Here, we present SOCS-B, a reference-based, un-gapped alignment algorithm

174 vate the genes encoding ASB2 (ankyrin-repeat SOCS box containing protein 2) and SKP2 (S-phase kinase-

175 tivity of E proteins, whereas ankyrin-repeat SOCS box-containing protein 2 facilitates E protein ubiq

176 ed that expression of Id2 and ankyrin-repeat SOCS box-containing protein 2 was elevated in MZ B cells

177 been integrated with the previously reported SOCS alignment tool, and was used to align CpG methylati

178 Consistent with their intracellular roles, SOCS proteins have never been identified in the extracel

179 creases in suppressor of cytokine secretion (SOCS) 3 and suppressor of cytokine secretion 7, which ne

180 expression of Suppressor of Cytokine Signal (SOCS)-1 and enhanced the expression of iNOS.

181 /cytokines/suppressor of cytokine signaling (SOCS) (spleen/heart), and production of nitric oxide (NO

182 Suppressors of cytokine signaling (SOCS) 1 and 3 proteins and reactive oxygen species scave

183 ression of suppressor of cytokine signaling (SOCS) 1 in HSCs, and we demonstrate that SOCS1 expressio

184 ression of suppressor of cytokine signaling (SOCS) 1 in tissues from asthmatic patients and its possi

185 y inducing suppressor of cytokine signaling (SOCS) 2-dependent ubiquitinylation and proteasome-mediat

186 ulated the suppressor of cytokine signaling (SOCS) 3 expression in HSCs.

187 t role for suppressor of cytokine signaling (SOCS) 3 in IL-17 enhancement of IL-6 signaling in astroc

188 on of A20, suppressor of cytokine signaling (SOCS) 3, B-cell CLL/lymphoma (BCL) 3, TNF receptor-assoc

189 Suppressors of cytokine signaling (SOCS) are implicated in the etiology of diabetes, obesit

190 Suppressors of cytokine signaling (SOCS) are important regulators of lipopolysaccharide (LP

191 ression of Suppressor of Cytokine Signaling (SOCS) domain-containing viral proteins and cellular BC-b

192 ng to the suppressors of cytokine signaling (SOCS) family have been shown to regulate cytokine signal

193 ng several suppressor of cytokine signaling (SOCS) family members as well as MAPK pathway-regulating

194 from the suppressors of cytokine signaling (SOCS) family of genes.

195 ber of the suppressor of cytokine signaling (SOCS) family, is induced by TCR stimulation in CD8(+) T

196 rs of the suppressors of cytokine signaling (SOCS) genes, CISH and SOCS1.

197 known as suppressors of cytokine signaling (SOCS) have emerged as frequent targets of viral exploita

198 he role of suppressor of cytokine signaling (SOCS) molecules in periodontal immunity and RANKL-mediat

199 Suppressor of cytokine signaling (SOCS) proteins are feedback inhibitors of the JAK/STAT p

200 Suppressor of cytokine signaling (SOCS) proteins are inhibitors of cytokine signaling path

201 Suppressor of cytokine signaling (SOCS) proteins are key regulators of CD4(+) T cell diffe

202 The suppressor of cytokine signaling (SOCS) proteins are negative regulators of the JAK/STAT p

203 Suppressors of cytokine signaling (SOCS) proteins are negative-feedback regulators of the J

204 Suppressors of cytokine signaling (SOCS) proteins control many aspects of lymphocyte functi

205 Suppressors of cytokine signaling (SOCS) proteins function as feedback inhibitors of the JA

206 overy, the suppressor of cytokine signaling (SOCS) proteins have been studied for their potential use

207 Suppressors of cytokine signaling (SOCS) proteins inhibit signaling by serving as substrate

208 Suppressor of cytokine signaling (SOCS) proteins play a crucial role in inhibiting cytokin

209 The suppressors of cytokine signaling (SOCS) proteins play important roles in inflammatory proc

210 Suppressors of cytokine signaling (SOCS) proteins regulate the intensity and duration of cy

211 er how the suppressor of cytokine signaling (SOCS) proteins regulate the quality and quantity of STAT

212 otein and suppressors of cytokine signaling (SOCS) proteins represents an important element of host c

213 Suppressor of cytokine signaling (SOCS) proteins serve as negative regulators of cytokine

214 an secrete suppressor of cytokine signaling (SOCS) proteins within microparticles.

215 led by the suppressor of cytokine signaling (SOCS) proteins, a family of proteins that negatively reg

216 s, namely, suppressor of cytokine signaling (SOCS) proteins, phosphatases, and protein inhibitor of a

217 ibition by suppressor of cytokine signaling (SOCS) proteins.

218 nuated by suppressors of cytokine signaling (SOCS), a family of proteins consisting of eight members,

219 eptor, and suppressor of cytokine signaling (SOCS)-1 and SOCS-3.

220 restingly, suppressor of cytokine signaling (SOCS)-1 directly associated with TLR8, but not with TLR7

221 Suppressor of cytokine signaling (SOCS)-1 protein modulates signaling by IFN-gamma by bind

222 Suppressor of cytokine signaling (SOCS)-3 and protein-tyrosine phosphatase 1B (PTP-1B) are

223 Suppressor of cytokine signaling (SOCS)-3 expression is increased in skeletal muscle of ob

224 e (COX)-2, suppressor of cytokine signaling (SOCS)-3, and matrix metalloproteinase (MMP)-9, no change

225 ot for the suppressor of cytokine signaling (SOCS)-box-containing ankyrin repeat proteins (ASB1-18),

226 regulator suppressor of cytokine signaling (SOCS)1 expression in immune (CD4T, CD8T, natural-killer

227 Suppressor of cytokine signaling (SOCS)1 is a cross-functional negative regulator of TLR a

228 exposure, suppressor of cytokine signaling (SOCS)1 is highly induced in human monocytes.

229 y STAT5 is suppressor of cytokine signaling (SOCS)1-a surprising finding for a known tumor suppressor

230 Suppressor of cytokine signaling (SOCS)3 belongs to a family of proteins that are known to

231 ression of suppressor of cytokine signaling (SOCS)3, a major negative feedback regulator of STAT3-act

232 show that Suppressor of Cytokine Signaling (SOCS)3, a molecular inhibitor of IFN signaling, may allo

233 leting the suppressor of cytokine signaling (SOCS)3, a negative regulator of gp130-mediated STAT3 act

234 ulation of suppressor of cytokine signaling (SOCS-3) proteins that are associated with hypothalamic l

235 Suppressors of cytokine signaling (SOCSs) are negative regulators of both innate and adapti

236 , IRF1 and suppressor of cytokine signaling [SOCS] 1) was strongly impaired.

237 rs of the suppressor of cytokine signalling (SOCS) family have been implicated in the regulation of a

238 or of the suppressor of cytokine signalling (SOCS) genes, which inhibit HSC migration and homing.

239 im-2, and Suppressor of Cytokine Signalling (SOCS)-1 resulted in partial restoration of v-Abl transfo

240 Conversely, silencing SOCS-1 expression using small interfering RNAs increased

241 tion studies, and blocking PD-1 or silencing SOCS-1 in M/M(Phi) led to activation of STAT-1 during TL

242 Here, we show that some SOCS members are induced, while others are constitutivel

243 ss was induced in 16-wk-old myeloid-specific SOCS-3-knockout and wild-type (WT) C57Bl6-B.129 mice by

244 e required for ERK-dependent, PMA-stimulated SOCS-3 gene activation.

245 sed hepatic SOCS-3 following LPS, suggesting SOCS-3 inhibited insulin signaling which produced the hy

246 treptococci, potentially through suppressive SOCS components triggered by innate mechanisms.

247 f viral E3 ligase activity through targeting SOCS box motifs is a putative strategy to control gammah

248 egradation, and this requires the C-terminal SOCS box domain.

249 via a mechanism that requires the C-terminal SOCS box.

250 We conclude that SOCS-1 plays an important role in the inhibition of the

251 Our previous studies demonstrated that SOCS-3 attenuates macrophage/microglial activation in vi

252 We hypothesized that SOCS proteins would inhibit the antitumor activity of IF

253 We hypothesized that SOCS-3 regulates alveolar bone loss in experimental peri

254 We have determined previously that SOCS-3 induction by cAMP occurs independently of cAMP-de

255 Our data suggest that SOCS protein over-expression may regulate receptor tyros

256 roglial activation in vitro, suggesting that SOCS-3 may exert beneficial effects for immune-mediated

257 New data suggests that SOCS proteins introduce additional diversity into the JA

258 The SOCS antagonist thus presents a novel and effective appr

259 The SOCS proteins, among their other functions, serve as sub

260 The SOCS-3 protein induced by Nod2 activation further facili

261 antiviral effect and synergism with IFN, the SOCS antagonist also exhibits adjuvant effects on humora

262 single nucleotide polymorphism (SNP) in the SOCS-1 gene (SOCS1+1125G > C; rs33932899) were found to

263 Analysis of mice with mutations in the SOCS-1 gene demonstrated that IgE levels increase with l

264 udy to determine if genetic variation in the SOCS-1 locus correlates with altered levels of IgE.

265 e data suggest that genetic variation in the SOCS-1 promoter may affect IgE production.

266 g elements located between -99 to -60 in the SOCS-3 promoter.

267 families of endogenous STAT inhibitors, the SOCS and PIAS families, to potentially inform the develo

268 hepatocytes activates HSC by modulating the SOCS-STAT3 axis.

269 ow report that genes encoding members of the SOCS (suppressor of cytokine signaling) family are criti

270 reduce the transcriptional activation of the SOCS 3 gene in RACT-treated F9 Rex1 null cells.

271 Deletion of the SOCS box in CP-SOCS3 renders it more resistant to protea

272 We found that tyrosine 204 of the SOCS box, the SH2 domain, and the N-terminal kinase inhi

273 In addition, tyrosine 204 of the SOCS box, the SH2 domain, and the N-terminal kinase inhi

274 Signaling inhibitors of the SOCS family negatively regulate the activation of STAT p

275 of cytokine signaling 6) is a member of the SOCS family of E3 ubiquitin ligases that can regulate re

276 the cell-specific activity of members of the SOCS family, which negatively regulate STAT function.

277 C57BL/6 mice to determine the ability of the SOCS-1 mimetics to protect mice against lethal vaccinia

278 NP increased transcriptional activity of the SOCS-1 promoter in reporter assays and human B cells.

279 position SOCS1-820G > T (rs33977706) of the SOCS-1 promoter.

280 iption factors within the same region of the SOCS-3 gene promoter.

281 The minimal, ERK-responsive element of the SOCS-3 promoter was localized to a region spanning nucle

282 loop via the kinase inhibitory region of the SOCS.

283 A direct effect of HSV-1 on the SOCS-1 promoter was shown in a luciferase reporter gene

284 the acetylation of histones H3 and H4 on the SOCS-3 promoter and the recruitment of STAT-3, c-Jun, c-

285 Here we found that the SOCS protein CIS, which was substantially induced by int

286 ning proteins, SPSB1 to SPSB4, belong to the SOCS box family of E3 ubiquitin ligases.

287 positions the ankyrin domain coaxial to the SOCS box-Elongin B/C complex and perpendicular to other

288 activity and recruitment of C/EBPbeta to the SOCS-3 promoter.

289 sophila Elongin B/C and Cullin-5 act via the SOCS-box of SOCS36E to reduce pathway activity specifica

290 Uptake of these SOCS-containing vesicles by epithelial cells inhibits cy

291 protein-tyrosine phosphatases, thioredoxin, SOCS, and Egr1 in L. donovani-infected macrophages was f

292 Consequently, this SOCS box-deleted form of CP-SOCS3 displays persistent in

293 ant-negative mutants greatly diminishes this SOCS-3 transcriptional increase in F9 Rex1(-/-) cells.

294 anscription factors link EPAC1 activation to SOCS-3 induction.

295 tion and transcellular delivery of vesicular SOCS proteins thus represent a new model for the control

296 iR-155 and consequently the STAT pathway via SOCS-1.

297 Whereas SOCS proteins may improve glucose metabolism, mitigate d

298 However, mechanisms by which SOCS genes could be up-regulated are poorly understood.

299 tion, simulated outcomes agreed closely with SOCS trial outcomes, with treatment failure hazard ratio

300 lectively, we report that TLR8 coupling with SOCS-1 inhibits TLR7-mediated antiviral immunity during