ライフサイエンスコーパス: SOCS1

1 ssion of suppressor of cytokine signaling 1 (SOCS1).

2 egulator, suppressor of cytokine sinaling-1 (SOCS1).

3 riant in suppressor of cytokine signaling 1 (SOCS1).

4 ncluding suppressor of cytokine signaling 1 (SOCS1).

5 signaling by negatively regulating Ship1 and Socs1.

6 fibrotic molecules through downregulation of SOCS1.

7 of cytokine signaling (SOCS) genes, CISH and SOCS1.

8 he genes, CACNA1G, IGF2, NEUROG1, RUNX3, and SOCS1.

9 t this is associated with high expression of SOCS1.

10 growth, indicating resistance of FLT3-ITD to SOCS1.

11 IL-12 and IL-10 secretion were inhibited by SOCS1.

12 cell effector molecules, including IL-10 and SOCS1.

13 T1 and overexpression of the STAT1 inhibitor SOCS1.

14 ent of type I IFN secretion and induction of SOCS1.

15 ction with adenoviral vectors overexpressing SOCS1.

16 includes tyrosine (Y)80 in the SH2 domain of SOCS1.

17 Analysis demonstrated that the SOCS1+1125G > C SNP was in complete linkage disequilibri

18 otide polymorphism (SNP) in the SOCS-1 gene (SOCS1+1125G > C; rs33932899) were found to have signific

19 015) disrupt the miR-155 binding site in the SOCS1 3' UTR in the mouse germline and show that this ax

20 n negative regulators, including SOCS3 (6%), SOCS1 (3%), and PTPN1 (3%).

21 te expression of the anti-inflammatory genes Socs1-3 or sirtuin-1 but reduced levels of IL-1beta + IF

22 L-17C, and TNF-alphas), negative regulators (SOCS1-3, TGF-beta1b), antimicrobial peptides (cathelicid

23 ily of proteins consisting of eight members, SOCS1-7 and CIS.

24 nkage disequilibrium with an SNP at position SOCS1-820G > T (rs33977706) of the SOCS-1 promoter.

25 Carriers of the T-allele at the SOCS1-820G > T were also found to be associated with the

26 of human suppressor of cytokine signaling 1 (SOCS1), a feedback inhibitor of the Janus-activated kina

27 s tools, suppressor of cytokine signaling 1 (SOCS1), a negative regulator of IFN-gamma, was identifie

28 g cells subjected to a selective ablation of SOCS1, a key negative regulator of Stat1 phosphorylation

29 The data demonstrate that SOCS1 acts as a conditional oncogene, providing novel mo

30 lysis of suppressor of cytokine signaling 1 (SOCS1), alleviating its repression of NF-kappaB transcri

31 from human lymphomas that often overexpress SOCS1 also displayed SRC family kinase activation, const

32 -1 Tax oncoprotein induced the expression of SOCS1, an inhibitor of interferon signaling.

33 te increases in Stat1 and IL-6, induction of SOCS1 and -3 (suppressor of cytokine signaling 1 and 3)

34 ns may be mediated by Egr1, and silencing of Socs1 and -3 either alone or in combination resulted in

35 report that alveolar macrophages can secrete SOCS1 and -3 in exosomes and microparticles, respectivel

36 These data reveal a role for SOCS1 and -3 in the seemingly paradoxical hyperresponsiv

37 ted expression of several targets, including SOCS1 and A20, signaling inhibitors that limit IL-13 and

38 -II interferon response (for example, Ptpn2, Socs1 and Adar1) in mediating CTL evasion, and show that

39 effects of cold exposure, reducing Ship1 and Socs1 and altering TNF and IL-10 production.

40 w transplantation model, the coexpression of SOCS1 and FLT3-ITD significantly shortened the latency o

41 patients through a novel nuclear function of SOCS1 and identify SOCS1 as an important therapeutic tar

42 ations similar to the adult counterpart (eg, SOCS1 and KMT2D), gains of 2p16/REL, and losses of 19p13

43 Akt and NF-kappaB, to down-regulate PTEN and SOCS1 and promote growth of tumors in mice.

44 , caused a strong and sustained induction of SOCS1 and refractoriness to further stimulation with IFN

45 C and miR-155 antagomirs increased Ship1 and Socs1 and reversed the alterations in cytokine productio

46 Our data suggest that JAK2-SOCS1 and SHP2 reciprocally regulate ASK1 phosphorylatio

47 that L. donovani preferentially upregulates SOCS1 and SOCS3 expression in macrophages and T cells, r

48 negative feedback response occurred included SOCS1 and SOCS3 gene up-regulation and IL-6-induced endo

49 cytokine signals and defective expression of SOCS1 and SOCS3 has been reported in a number of human d

50 Small interfering RNA-mediated silencing of SOCS1 and SOCS3 in macrophage and T cells, respectively,

51 iggering of cGAS-STING induced expression of SOCS1 and SOCS3 in pDCs, indicating a possible autoinhib

52 Vivo morpholino-mediated silencing of SOCS1 and SOCS3 resulted in protective cytokine response

53 ly down-regulated, whereas the expression of SOCS1 and SOCS3 was up-regulated by vorinostat treatment

54 SOCS proteins, especially SOCS1 and SOCS3, are expressed by immune cells and cells

55 gamma and TNF-alpha, and the upregulation of SOCS1 and SOCS3, which are important regulatory molecule

56 ding to an enhanced association of ASK1 with SOCS1 and subsequent ASK1 degradation.

57 ol phosphatase PTEN, the signaling inhibitor SOCS1 and the deubiquitinase A20.

58 Our data show that SOCS1 and type I interferons are critical GC targets for

59 ssion of suppressor of cytokine signaling-1 (SOCS1) and SOCS3, inhibitors of STAT1 and STAT3, and als

60 argeting suppressor of cytokine signaling-1 (SOCS1) and Src homology-2 domain-containing inositol 5-p

61 protein suppressor of cytokine signaling 1 (SOCS1) and upregulated profibrotic proteins in both prox

62 increased miR-155, suppression of Ship1 and Socs1, and alterations in TNF and IL-10.

63 substantial expression of TGF-beta1, reduced SOCS1, and an increase in profibrotic proteins.

64 , which was associated with increased Ship1, Socs1, and IL-10.

65 -beta1 induced miR-150 expression, decreased SOCS1, and increased profibrotic proteins in proximal tu

66 ompared with normal tissues, whereas PPP2CA, SOCS1, and PTEN mRNAs were reduced significantly.

67 rosis factor-alpha (TNF-alpha), IL-6, IL-10, SOCS1, and SOCS3 in the spleen.

68 Expression of IFN-gamma, TNF-alpha, SOCS1, and SOCS3 was also reduced in the hearts of infec

69 RNA interference studies against STAT1, SOCS1, and STAT3 were performed to elucidate a signaling

70 ve fitness of Treg cell subsets by targeting SOCS1, and they provide experimental support for a propo

71 -31, MLH1, NEUROG1, p14 (CDKN2A/arf), RUNX3, SOCS1, and WRN] was quantified by real-time PCR.

72 demonstrated that both Cys147 and Cys179 on SOCS1 are required for its NO-dependent degradation.

73 Here, we identify SOCS1 as a key negative regulator of IL-4-induced IRS-2

74 Further, we identified SOCS1 as a key negative regulator to inhibit MyD88-depen

75 These results identify SOCS1 as a novel target to improve the immune function i

76 novel nuclear function of SOCS1 and identify SOCS1 as an important therapeutic target for asthma exac

77 ese loci implicated BATF3, CCDC88B and CIITA-SOCS1 as new susceptibility genes for leprosy.

78 during PC lung infection type-I IFNs induce SOCS1-associated regulatory mechanisms, which prevent ex

79 However, STAT1 phosphorylation and SOCS1 augmentation waned at 24 h, while STAT3 activity i

80 h strongly induced STAT1 phosphorylation and SOCS1 augmentation, and decreased STAT3 activity.

81 ce studies revealed that activation of STAT1-SOCS1 axis decreased STAT3 activity.

82 ed by STAT1-SOCS1 axis, suggesting the STAT1-SOCS1 axis is important in IFN-gamma-induced activation

83 RPTCs via STAT3 activity modulated by STAT1-SOCS1 axis, suggesting the STAT1-SOCS1 axis is important

84 5 target suppressor of cytokine signaling 1 (Socs1) because Socs1 knockdown in microRNA-155 knockout

85 of ASK1 when phosphorylated is critical for SOCS1 binding and SOCS1-mediated degradation of ASK1.

86 Furthermore, we observed IL-23-induced SOCS1 binding to the IFN-gamma transcription complex.

87 ow that IFN-lambda signaling is regulated by SOCS1 but not by SOCS3 or USP18.

88 Inhibition of SOCS1 by RNA-mediated interference in the HTLV-1-transfo

89 We now show that SOCS1 can also be induced by the non-TLR pattern recogni

90 The present work aimed at analyzing the SOCS1 cell signaling and expression of proteins relevant

91 A [p16], CRABP1, IGF2, MLH1, NEUROG1, RUNX3, SOCS1, CHFR, HIC1, IGFBP3, MGMT, MINT1, MINT31, p14 [ARF

92 KN2A, CRABP1, IGF2, MLH1, NEUROG1, RUNX3 and SOCS1); CIMP-(+) tumors were defined as having >= 5 meth

93 h immune functions (BACH2, CCR4, CD80, CIITA-SOCS1-CLEC16A, ICOSLG and ZMIZ1), with ETS1, RUNX3, THEM

94 In addition, SOCS1 coexpression did not affect FLT3-ITD-mediated sign

95 Importantly, SOCS1 coexpression inhibited interferon-alpha and interf

96 SOCS1 coimmunoprecipitated with TIRAP in wild type hepat

97 By co-immunoprecipitation, we found that SOCS1 complexes with IRS-2 at baseline, and this associa

98 al biopsy staining, overexpression of mutant SOCS1 constructs, and confocal microscopy.

99 ddition, these results strongly suggest that SOCS1 contributes to the stability of the Foxp3(+) Treg

100 itutive phosphorylation of SOCS1 on Y80, and SOCS1 cytoplasmic localization.

101 Down-regulation of SOCS1 decreased the expression of epidermal growth facto

102 SOCS1-deficient mice develop severe skin and eye disease

103 We show that SOCS1-deficient mice have increased numbers of T cells w

104 uman epithelium, mouse lung macrophages, and SOCS1-deficient mice, SOCS1 suppressed rhinovirus induct

105 using overexpression with reporter genes and SOCS1-deficient mice.

106 ng that aberrant recruitment of T cells into SOCS1-deficient mouse skin or eye results from abrogatio

107 CCR6 and CXCR3 are also up-regulated on SOCS1-deficient T cells and in situ analysis of the corn

108 S1(-/-) cells with exogenous NO rescues both SOCS1 degradation and stabilization of p65 protein.

109 irus, vesicular stomatitis virus (VSV), in a SOCS1-dependent manner.

110 SOCS1 did not modulate Dectin-1 signaling but affected T

111 Conversely, knockdown of SOCS1 enhanced induction of ISGs and reduced viral yield

112 NK cells constitutively expressing Noxa and SOCS1 exhibit profound defects in expansion during the r

113 esponses were also decreased in mice lacking SOCS1 expression in CD11c(+) cells but did not explain t

114 Unexpectedly, in mice lacking SOCS1 expression in CD11c(+) cells, we observed a decrea

115 lture of MM cells with healthy PBMCs induced SOCS1 expression in effector cells; conversely, treatmen

116 Although SOCS1 expression in murine bone marrow severely impaired

117 inflammatory diseases (uveitis) and whether SOCS1 expression is defective in patients with ocular in

118 ng (SOCS) 1 in HSCs, and we demonstrate that SOCS1 expression is sufficient to inhibit TPO-induced ST

119 SOCS1 expression was also increased in primary BECs from

120 expression, STAT1 and STAT3 activities, and SOCS1 expression were evaluated.

121 We found that DCs lacking SOCS1 expression were functional in driving Ag-specific

122 -gamma-induced STAT1 signaling by augmenting SOCS1 expression.

123 AT1 phosphorylation as well as a decrease in SOCS1 expression.

124 ely, treatment with IMiDs down-regulated the SOCS1 expression.

125 AHR signaling in BMM s to maintain prolonged SOCS1 expression.

126 ncreased suppressor of cytokine signaling 1 (SOCS1) expression accompanied by impaired activation of

127 -induced suppressor of cytokine signaling-1 (SOCS1) expression, contributing to the proinflammatory p

128 SOCS1 impairs its binding to p65 and targets SOCS1 for proteolysis.

129 CCR7 expression and lymphocyte migration by SOCS1, forced overexpression of SOCS1 in T cells up-regu

130 a catalytically inactive mutant, dissociated SOCS1 from ASK1.

131 ion (KIR), a peptide that partially restores SOCS1 function, mediated a statistically significant but

132 , germline loss-of-function mutations in the SOCS1 gene in ten patients from five unrelated families

133 SOCS1 gene promoter methylation, with its potential effe

134 n in the suppressor of cytokine signaling 1 (SOCS1) gene in smokers and non-smokers with chronic peri

135 Hence, SOCS1 haploinsufficiency causes a dominantly inherited p

136 roretinal cells from apoptosis, suggest that SOCS1 has neuroprotective function in the retina, implyi

137 We find that human SOCS1 (hSOCS1)-silenced DCs have an enhanced stimulatory

138 t were epigenetically modified to re-express SOCS1; IMiDs induced more potent CTL responses against S

139 NOS1-dependent S-nitrosation of SOCS1 impairs its binding to p65 and targets SOCS1 for p

140 ional signalling factors-including PTPN2 and SOCS1-improves the therapeutic efficacy of REGNASE-1-def

141 producing Th cells were clearly increased by SOCS1 in BMMs.

142 Furthermore, Tax interacted with SOCS1 in both transfected cells and in HTLV-1-transforme

143 We report induction of SOCS1 in bronchial epithelial cells (BECs) by asthma exa

144 Thus, loss of SOCS1 in CD11c(+) cells skewed the balance of immune res

145 Overexpression of SOCS1 in chIFN-alpha-stimulated DF-1 led to a relative d

146 We hypothesized that loss of SOCS1 in dendritic cells (DCs) would improve T cell resp

147 unveiled a previously unappreciated role for Socs1 in directly modulating p53 activity and the DNA da

148 of this study was to investigate the role of SOCS1 in intraocular inflammatory diseases (uveitis) and

149 Forced expression of SOCS1 in macrophages depleted of METTL14 or YTHDF1 rescu

150 The present work shows the role of SOCS1 in murine melanoma development and the potential o

151 Defective expression of SOCS1 in patients with scleritis, taken together with SO

152 in children, suggesting the contributions of SOCS1 in regulating the inflammatory response characteri

153 rom patients with scleritis failed to induce SOCS1 in response to IL-2.

154 Constitutive overexpression of SOCS1 in retina inhibited expression of chemokines (CCL1

155 migration by SOCS1, forced overexpression of SOCS1 in T cells up-regulates CCR7 expression and enhanc

156 fector functions were recovered by silencing SOCS1 in T cells.

157 B, but not CREB, to induce the expression of SOCS1 in T cells.

158 ines and suppressor of cytokine signaling 1 (SOCS1) in a human monocytic cell line and in HEK293-TLR4

159 Noxa and suppressor of cytokine signaling 1 (SOCS1) in NK cells at distinct stages of homeostasis and

160 ntiated the SOCS1-p53 pathway and reinforced SOCS1-induced senescence.

161 induces Socs1 m(6)A methylation and sustains SOCS1 induction by promoting Fto mRNA degradation, and f

162 We conclude that m(6)A methylation-mediated SOCS1 induction is required to maintain the negative fee

163 binding to the m(6)A sites, which diminishes SOCS1 induction leading to the overactivation of TLR4/NF

164 Consistent with the lack of SOCS1 induction, STAT1 phosphorylation was prolonged upo

165 tivation of the MAPK ERK, thereby triggering SOCS1 induction.

166 sis factor (TNF)-alpha production and lacked SOCS1-induction at day 7.

167 siRNA knockdown of SOCS1 inhibited ubiquitin accumulation on IRS-2, althoug

168 Y80 by a phosphomimetic residue inhibits p53-SOCS1 interaction and its functional consequences, inclu

169 Paradoxically, SOCS1 is also overexpressed in many human cancers.

170 The cytokine suppressor SOCS1 is also upregulated.

171 Because SOCS1 is an E3 ubiquitin ligase, we examined the effect

172 SOCS1 is an essential negative regulator of type I and t

173 Our results show that SOCS1 is expressed via a new, NF-kappaB-independent path

174 althy and allergic individuals revealed that SOCS1 is induced by IL-4 in healthy monocytes but not al

175 ion or deletion of SOCS1, to examine whether SOCS1 is involved in regulating lymphocyte trafficking t

176 The intracellular protein SOCS1 is known to downregulate cytokine signaling by inh

177 SOCS1 is known to interact with Toll/IL-1 receptor assoc

178 Although SOCS1 is normally a short-lived protein, in the presence

179 m that targets CD11c(+) DCs in mice in which SOCS1 is selectively deleted in all CD11c(+) cells.

180 n of the suppressor of cytokine signaling-1 (SOCS1) is inactivated in hematopoietic and solid cancers

181 , CD4(+) T lymphocytes, or administration of SOCS1 kinase inhibitory region (KIR), a peptide that par

182 rary screen identified the SRC family as Y80-SOCS1 kinases.

183 Both SOCS1-KIR and Tkip inhibited vaccinia virus transcriptio

184 Moreover, the CD4(+)/SOCS1-KIR combined therapy resulted in decreased leukocy

185 These data show that CD4(+)/SOCS1-KIR combined treatment can synergistically promote

186 ction of mice intraperitoneally with Tkip or SOCS1-KIR containing a palmitate for cell penetration, b

187 hocytes, combined with the administration of SOCS1-KIR, resulted in a significant increase in the sur

188 g to the kinase-inhibitory region of SOCS-1, SOCS1-KIR, similarly interacts with the activation loop

189 Furthermore, SOCS1 knockdown in hiPSCs enhances their ability to resp

190 ssor of cytokine signaling 1 (Socs1) because Socs1 knockdown in microRNA-155 knockout macrophages lar

191 ced degradation of ASK1 in normal but not in SOCS1-KO endothelial cells (EC).

192 of SOCS1 protein with shRNAi lentivirus (shR-SOCS1) led to partial reversion of the tumorigenic pheno

193 hages and T cells, respectively, whereas the SOCS1 level remains consistently high in BMM s and SOCS3

194 SOCS1 levels were also correlated with asthma-related cl

195 Nuclear SOCS1 levels were also increased in BECs from asthmatic

196 riants and common variants (at the PTPN2 and SOCS1 loci).

197 METTL14 depletion blunts Socs1 m(6)A methylation and reduces YTHDF1 binding to th

198 We further show that LPS treatment induces Socs1 m(6)A methylation and sustains SOCS1 induction by

199 ata therefore demonstrate that modulation of SOCS1 may enhance immune response and efficacy of IMiDs

200 phorylated is critical for SOCS1 binding and SOCS1-mediated degradation of ASK1.

201 patients with scleritis, taken together with SOCS1-mediated protection of neuroretinal cells from apo

202 SOCS1-mediated protection of retinal cells from apoptosi

203 in a significant increase in the survival of SOCS1(-/-) mice both short and long term, where 100% dea

204 We observed that SOCS1(-/-) mice were deficient in peripheral Tregs despi

205 cally significant but short-term survival of SOCS1(-/-) mice.

206 e the long-term survival of perinatal lethal SOCS1(-/-) mice.

207 uppressor of cytokine signaling 1-deficient (SOCS1(-/-)) mice, which are lymphopenic, die <3 wk after

208 the retina, implying that administration of SOCS1 mimetic peptides may be useful in treating uveitis

209 In conclusion, our study identifies SOCS1 mimicking as a feasible therapeutic strategy to ha

210 , EOS(A) express significantly more CISH and SOCS1 mRNA and CISH protein than EOS(PB) counterparts.

211 SOCS1 mRNA and protein expression increased after LPS st

212 We assessed SOCS1 mRNA and protein levels in vitro, bronchial biopsy

213 mma-induced robust STAT1 phosphorylation and SOCS1 mRNA expression, with modest, transient STAT3 phos

214 TEN) and suppressor of cytokine signaling 1 (SOCS1) mRNA, potential targets of miR-21 and miR-155, re

215 Heterozygous loss-of-function SOCS1 mutations are associated with enhanced IFN signali

216 SOCS1 negatively regulates IL-6 signaling and is silence

217 by GRAIL (CARD11, FCRL2, CHST12, SYK, TCF7, SOCS1, NFKBIZ and NPAS1).

218 s-induced interferon levels was dependent on SOCS1 nuclear translocation but independent of proteasom

219 activation, constitutive phosphorylation of SOCS1 on Y80, and SOCS1 cytoplasmic localization.

220 o studies that have examined the function of SOCS1 or SOCS3 under various neuroinflammatory or neurop

221 lators such as silencer of cell signaling 1 (SOCS1) or protein-tyrosine phosphatase 1B (PTP1B) in thi

222 togenic T cells, and investigated effects of SOCS1 overexpression on EAU.

223 SRC family kinase inhibitors potentiated the SOCS1-p53 pathway and reinforced SOCS1-induced senescenc

224 ults reveal a mechanism that inactivates the SOCS1-p53 senescence pathway and suggest that inhibition

225 ting its initiation (Aicda) and termination (Socs1/p53 response), suggesting a mechanism to explain t

226 Mice treated with the SOCS1 peptidomimetic also exhibited reduced kidney leuko

227 tant inactive peptide, administration of the SOCS1 peptidomimetic at either early or advanced stages

228 These findings show that SOCS1 phosphorylation by the SRC family inhibits its tum

229 ity, indicating that patients with increased SOCS1 phosphorylation may benefit from SRC family kinase

230 We found that siRNA knockdown of SOCS1 prolonged IRS-2 tyrosine phosphorylation and enhan

231 nuclear translocation and binding of Egr2 to SOCS1 promoter for its early induction in infected BMM s

232 d to determine the methylation status of the SOCS1 promoter in 45 saliva samples from smokers and non

233 7.08 times more likely to have a methylated SOCS1 promoter than cells from the saliva of non-smoking

234 tified two T-bet DNA-binding elements in the Socs1 promoter that are functionally used to down-regula

235 The authors also show that SOCS1 protected retinal cells from staurosporine as well

236 ated NOS1(-/-) macrophages contain increased SOCS1 protein and decreased levels of p65 protein compar

237 Silencing of SOCS1 protein with shRNAi lentivirus (shR-SOCS1) led to

238 egulated suppressor of cytokine signaling 1 (SOCS1) protein in T cells, which inhibited IFN-gamma pro

239 Ds induced more potent CTL responses against SOCS1 re-expressing-MM cells than unmodified MM cells.

240 Consequently, SOCS1 reduces induction of the IFN signalling pathway in

241 Collectively, these results suggest that SOCS1 regulates steady-state levels of chemokine recepto

242 reduced suppressor of cytokine signaling-1 (Socs1) regulation by miR-142-5p.

243 egion of suppressor of cytokine signaling-1 (SOCS1) regulatory protein protects against nephropathy b

244 tivation of STAT1 was unaltered, deletion of Socs1 relieved inhibition of GBP1 expression by TDM.

245 f hDCs to prime CTLs is likely controlled by SOCS1-restricted production and signaling of proinflamma

246 ethylation status was evaluated for CACNAG1, SOCS1, RUNX3, NEUROG1, MLH1, and long interspersed nucle

247 The SOCS1/SGK1 subtype showed biological overlap with primar

248 subtypes were resolved, termed MYD88, BCL2, SOCS1/SGK1, TET2/SGK1, and NOTCH2, along with an unclass

249 ional levels (including inhibitory molecules SOCS1, SHIP1, A20 and IkappaBalpha), exerting an overall

250 analysis of B16F10-Nex2 melanoma cells with SOCS1 silenced by shRNAi-SOCS1 was undertaken in compari

251 Human CTLs activated by SOCS1-silenced DCs, but not wild-type DCs, have an activ

252 ne melanoma development and the potential of SOCS1-silenced tumor cells in raising an effective anti-

253 SOCS1 silencing inhibited cell migration and invasion as

254 translational potential of this alternative SOCS1 silencing strategy to develop effective DC vaccine

255 silencing in WT macrophages and restored by Socs1 siRNA in 5-LO-deficient macrophages.

256 , IL-4, IL-13, IL-22, and TSLP secretion and SOCS1/SOCS2/SOCS3 induction.

257 gulators suppressor of cytokine signaling 1 (SOCS1), SOCS3, and ubiquitin-specific peptidase 18 (USP1

258 ding the STAT signalling inhibitory proteins SOCS1, SOCS3 and CISH were marked by m(6)A, exhibited sl

259 In this study, we first identify Socs1, Socs3, and Tcf7 (TCF-1) as gene targets that are

260 y improve glucose metabolism, while elevated SOCS1/SOCS3 expression during uveitis induces insulin re

261 al cells depleted of SOCS6 or overexpressing SOCS1/SOCS3, and 5) oxidative stress and light-induced r

262 -/-) BM-derived DCs expressed high levels of SOCS1/SOCS3, known inhibitors of GM-CSF signaling, provi

263 sgenic rats and retinal cells overexpressing SOCS1/SOCS3.

264 In this study, we have used SOCS1-, STAT1-, or STAT6-deficient mice, as well as, T c

265 However, the adoptive transfer of SOCS1-sufficient CD4(+) T lymphocytes, combined with the

266 The adoptive transfer of SOCS1-sufficient Tregs, CD4(+) T lymphocytes, or adminis

267 lung macrophages, and SOCS1-deficient mice, SOCS1 suppressed rhinovirus induction of interferons.

268 B-mediated inflammation in the lungs through Socs1 suppression and suggest that miR-155 may be an imp

269 Compared with wild-type littermates, SOCS1-Tg rats/mice developed less severe EAU.

270 rs generated SOCS1 transgenic rats and mice (SOCS1-Tg), induced experimental autoimmune uveoretinitis

271 five core genes, Mx1, IRF1, IRF7, STAT1, and SOCS1, that are up-regulated regardless of subline.

272 (-/-) mice displayed increased expression of Socs1, the overexpression of miR-155 led to its suppress

273 ey physiological regulators of inflammation, SOCS1 to -3, associated with the production of cytokines

274 Surprisingly, Tax required SOCS1 to inhibit RIG-I-dependent antiviral signaling, bu

275 We report here that the ability of SOCS1 to interact with p53 and regulate cellular senesce

276 utated the 3' UTR of a major miR-155 target (SOCS1) to specifically disrupt its regulation by miR-155

277 ls with stable overexpression or deletion of SOCS1, to examine whether SOCS1 is involved in regulatin

278 Subcutaneous immunization with shR-SOCS1-transduced viable tumor cells rendered protection

279 The authors generated SOCS1 transgenic rats and mice (SOCS1-Tg), induced exper

280 g in retina, is validated in retina-specific SOCS1 transgenic rats and retinal cells overexpressing S

281 ated in 1) an experimental uveitis model, 2) SOCS1 transgenic rats, 3) insulin-deficient diabetic rat

282 ators of the IFN response, such as USP18 and SOCS1 Transient treatment of PHHs with IFN-lambda4, but

283 LPS-induced SOCS1 upregulation increases degradation of TIRAP and pr

284 Similarly, inhibition of SOCS1 using small interfering (si)RNA-mediated knockdown

285 In our study, SOCS1 was expressed independently of any TLR engagement

286 in, in the presence of Tax, the stability of SOCS1 was greatly increased.

287 We found that SOCS1 was increased in vivo in bronchial epithelium and

288 The role of SOCS1 was inferred by proof-of-concept studies using ove

289 Induction of SOCS1 was mediated by a novel pathway encompassing the t

290 A nuclear role of SOCS1 was shown by using bronchial biopsy staining, over

291 Nonnuclear Socs1 was sufficient for inhibition, suggesting a noncan

292 melanoma cells with SOCS1 silenced by shRNAi-SOCS1 was undertaken in comparison with cells transduced

293 Indeed, Ship1 and Socs1 were suppressed at 32 degrees C and miR-155 antago

294 ers (CACNA1G, IGF2, RUNX3, MGMT, MINT-1, and SOCS1) were differentially clustered with CIMP-high and

295 LR4, IRF3, TRAF-6, TIRAP, TRIF, IKK-1, ST-2, SOCS1) were found to modulate the effect of endotoxin on

296 AT3) and suppressor of cytokine signaling-1 (SOCS1)] were also elevated by exendin-4.

297 or largely attributable to the regulation of SOCS1, whereas others could be accounted only partially

298 ction of suppressor of cytokine signaling 1 (SOCS1), which increases throughout the 6-h period after

299 lated type-I IFN-responsive genes as well as SOCS1, which is a critical negative-regulator of type-I

300 Directly targeting SOCS1 with a small interfering RNA produced similar resu

301 Mass spectrometry confirmed SOCS1 Y80 phosphorylation in cells, and a new mAb was ge