ライフサイエンスコーパス: SOCS1

1 aining Elongins B and C, Cul2 and SOCS1 (ECS(SOCS1)).

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

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

4 ncluding suppressor of cytokine signaling 1 (SOCS1).

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

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

7 t this is associated with high expression of SOCS1.

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

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

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

11 T1 and overexpression of the STAT1 inhibitor SOCS1.

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

13 ction with adenoviral vectors overexpressing SOCS1.

14 hosphorylation and dissociation of ASK1 from SOCS1.

15 signaling by negatively regulating Ship1 and Socs1.

16 fibrotic molecules through downregulation 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 te expression of the anti-inflammatory genes Socs1-3 or sirtuin-1 but reduced levels of IL-1beta + IF

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

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

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

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

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

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

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

28 In the present study, we have shown that SOCS1, a member of suppressor of cytokine signaling, ind

29 In addition, SOCS1, a negative regulator of IFNgamma signaling and wh

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

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

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

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

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

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

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

43 igase by stabilizing the interaction between SOCS1 and RelA.

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

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

46 Additionally, although SOCS1 and SOCS2 are degraded in the presence of JAK2 V61

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

48 oma has led to speculation that silencing of SOCS1 and SOCS3 genes might promote oncogenic transforma

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

50 l inhibitory RNA-mediated down-regulation of SOCS1 and SOCS3 in Jurkat cells and normal T cells enhan

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

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

53 Overexpression of SOCS1 and SOCS3, but not SOCS2, in the Jurkat T cell lin

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

55 e to induce the cytokine and TLR suppressors SOCS1 and SOCS3.

56 P. gingivalis DNA significantly up-regulated SOCS1 and SOCS5 expression and down-regulated interleuki

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

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

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

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

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

62 sed expression of an anti-inflammatory gene, Socs1, and a gene associated with healing, Mmp1a, were e

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

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

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

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

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

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

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

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

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

72 -31, MLH1, NEUROG1, p14 (CDKN2A/arf), RUNX3, SOCS1, and WRN] was quantified by real-time PCR.

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

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

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

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

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

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

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

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

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

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

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

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

85 5 target suppressor of cytokine signaling 1 (Socs1) because Socs1 knockdown in microRNA-155 knockout

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

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

88 phosphotyrosine-718 of ASK1 is critical for SOCS1 binding.

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

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

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

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

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

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

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

96 Importantly, SOCS1 coexpression inhibited interferon-alpha and interf

97 SOCS1 coimmunoprecipitated with TIRAP in wild type hepat

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

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

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

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

102 expression and activity were up-regulated in SOCS1-deficient mice and derived EC, resulting in enhanc

103 SOCS1-deficient mice develop severe skin and eye disease

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

105 presentation of the inflammatory disease of Socs1-deficient mice is complex, we have tested here the

106 itumor effects of IFN-alpha in tumor-bearing SOCS1-deficient mice were markedly inhibited following d

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

108 eatment eliminated melanoma tumors in 70% of SOCS1-deficient mice, whereas IFN-treated SOCS-competent

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

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

111 Socs1-deficient T cell receptor-transgenic mice showed s

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

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

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

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

116 ligase containing Elongins B and C, Cul2 and SOCS1 (ECS(SOCS1)).

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

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

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

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

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

122 Although SOCS1 expression in murine bone marrow severely impaired

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

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

125 SOCS1 expression was also increased in primary BECs from

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

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

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

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

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

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

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

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

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

135 a catalytically inactive mutant, dissociated SOCS1 from ASK1.

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

137 We concluded that SOCS1 functions as a negative regulator in TNF-induced i

138 OCS2, SOCS3, SOCS5, SOCS6, SOCS7, CIS and/or SOCS1 genes in the human cancer cells.

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

140 nd p21(cip1-/-) hepatocytes, but enhanced in SOCS1(-/-) hepatocytes.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

159 a attributable to the targeted expression of SOCS1 in these cells.

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

161 nal (STAT1) and genes (IRF-1, p21(cip1), and SOCS1) in liver regeneration and hepatocyte proliferatio

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

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

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

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

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

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

168 CC1937 breast-cancer cells, transcription of SOCS1 is dramatically up-regulated by IFNgamma and/or io

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

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

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

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

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

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

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

176 Both SOCS1-KIR and Tkip inhibited vaccinia virus transcriptio

177 The fact that SOCS1-KIR binds to pJAK2(1001-1013) suggests that the JA

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

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

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

181 Furthermore, SOCS-1 competed with SOCS1-KIR for pJAK2(1001-1013).

182 Both Tkip and SOCS1-KIR inhibited IFN-gamma activation of Raw 264.7 mu

183 -response competitions suggest that Tkip and SOCS1-KIR similarly recognize the autophosphorylation si

184 KIR of SOCS-1, ((53))DTHFRTFRSHSDYRRI((68)) (SOCS1-KIR), both bound similarly to the autophosphorylat

185 N-gamma-induced STAT1-alpha phosphorylation, SOCS1-KIR, like SOCS-1, did not inhibit JAK2 autophospho

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

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

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

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

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

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

192 SOCS1 levels were also correlated with asthma-related cl

193 Nuclear SOCS1 levels were also increased in BECs from asthmatic

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

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

196 We further show that the kinetics of SOCS1-mediated feedback inhibition of IFNgamma signaling

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

198 SOCS1-mediated protection of retinal cells from apoptosi

199 PLP/SOCS1 mice developed EAE with an accelerated onset assoc

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

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

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

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

204 unity contributes to the disease observed in Socs1(-/-) mice.

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

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

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

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

209 SOCS1 mRNA and protein expression increased after LPS st

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

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

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

213 Thus a SOCS1 mutant defective in phosphotyrosine binding failed

214 SOCS1 negatively regulates IL-6 signaling and is silence

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

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

217 Loss of SOCS1 or SOCS3 in murine immune effectors was associated

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

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

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

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

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

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

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

225 cantly higher frequency of RASSF1A, CIS, and SOCS1 promoter methylation than HCC without cirrhosis (P

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

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

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

229 to normal breast cells, indicating that the SOCS1 protein in breast-cancer cells is functional.

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

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

232 y, we generated a transgenic mouse line [PLP/SOCS1 (proteolipid protein/suppressor of cytokine signal

233 marily in group 1 loci (HIC-1, CASP8, GSTP1, SOCS1, RASSF1A, p16, APC), which was significantly highe

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

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

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

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

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

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

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

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

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

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

244 SOCS1 silencing inhibited cell migration and invasion as

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

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

247 Transcripts for SOCS1, SOCS2, SOCS3, and cytokine-inducible Src homology

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

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

250 expression of p60 was not required to induce socs1, socs3, and il10 expression in infected mouse bone

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

252 6, CD25, Tox, Gadd45a, Gadd45b, Gfi1, Gfi1b, Socs1, Socs3, Id2, Eto2, and Xbp1.

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

254 3)Cys, a synthetic lipopeptide, also induced SOCS1/SOCS3 expression under these conditions, but unlip

255 translation inhibitor cycloheximide blocked SOCS1/SOCS3 induction by B. burgdorferi and its lipoprot

256 r surface protein A (L-OspA) augmented their SOCS1/SOCS3 mRNA and protein expression, with SOCS3 bein

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

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

259 sgenic rats and retinal cells overexpressing SOCS1/SOCS3.

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

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

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

263 utation at Tyr-718 diminished the binding to SOCS1, suggesting that the phosphotyrosine-718 of ASK1 i

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

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

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

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

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

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

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

271 The capacity of SOCS1 to inhibit the effects of IFN-gamma suggests a the

272 nd tumor, which can be achieved by silencing SOCS1 to unleash the unbridled signaling of IL-12 and th

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

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

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

276 demonstrate that oligodendrocytes in the PLP/SOCS1 transgenic mice are protected against the injuriou

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

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

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

280 tein/suppressor of cytokine signaling 1 (PLP/SOCS1)] transgenic mouse line that displays suppressed o

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

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

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

284 SOCS1 was constitutively expressed in EC and formed a la

285 The phosphotyrosine-binding SH2 domain of SOCS1 was critical for its association with ASK1.

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

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

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

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

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

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

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