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

5 back to WT levels by exogenously expressing SOCS3.

6 pression of the LIF/STAT3 negative regulator SOCS3.

7 L-6-induced STAT3-regulated genes, including 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 ary hepatocytes via deregulation of TNFalpha/SOCS3.

14 sed in part by the leptin signaling molecule SOCS3.

15 ignaling and shows its counter-regulation by SOCS3.

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

17 (3%), and in negative regulators, including SOCS3 (6%), SOCS1 (3%), and PTPN1 (3%).

18 ch as c-Fos (a marker of amylin activation); Socs3 (a leptin inhibitor); and Cart, Pomc and Npy (neur

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

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

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

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

23 ssion of suppressor of cytokine signaling 3 (SOCS3)-a key negative regulator of IL-6 signaling.

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

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

26 Inhibition of SOCS3 abolished the antiinflammatory and vasoprotective

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

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

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

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

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

32 and induced expression of the STAT3 targets SOCS3 and Bcl3, which inhibit IFN-I and NF-kappaB signal

33 es in the inflammatory response by enhancing SOCS3 and CASP1 expression in schizophrenia patients and

34 regulation, thereby ameliorating CIC-induced SOCS3 and CASP1 repression.

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

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

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

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

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

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

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

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

43 mpared the effects of adoptively transferred SOCS3(-/-) and SOCS3(+/+) bone marrow-derived DCs (BMDCs

44 ported sites, cg1963031 (TXNIP), cg18181703 (SOCS3), and cg09152259 (PROC), was significantly associa

45 idase 4, suppressor of cytokine signaling 3 (SOCS3), and insulin receptor substrate 1 phosphorylation

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

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

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

49 MMP12 and SPARCL1), immune regulators (IDO1, SOCS3, and IL10), and a proinflammatory antimicrobial pe

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

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

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

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

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

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

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

57 Thus, an LIF-driven STAT3 pathway induces SOCS3, Bcl3, and Id2, which render pDCs and late DC prog

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

59 cts of adoptively transferred SOCS3(-/-) and SOCS3(+/+) bone marrow-derived DCs (BMDCs) on airway inf

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

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

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

63 Synthetic liposomes encapsulating SOCS3 can rescue this defect and may serve as a framewor

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

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

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

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

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

69 SOCS3(-/-) DCs slightly attenuated BMDC-induced immunoge

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

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

72 SOCS3-deficient M1 macrophages also have a stronger capa

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

91 Socs3 downregulation may also contribute to Stat3 activa

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

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

94 Derepression of SOCS3 enhances the anti-inflammatory response by inhibit

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

96 of T cells and macrophages, but the roles of SOCS3-expressing DCs in the pathogeneses of allergic inf

97 7 cells induced in vitro displayed increased SOCS3 expression and diminished capacity to produce inte

98 SOCS3 expression in AgRP neurons increases after 2 d of

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

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

101 onovani preferentially upregulates SOCS1 and SOCS3 expression in macrophages and T cells, respectivel

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

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

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

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

106 level remains consistently high in BMM s and SOCS3 expression is pronounced and long lasting in T cel

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

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

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

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

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

112 Consistent with findings from SKGNur mice, SOCS3 expression was similarly down-regulated in RA syno

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

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

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

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

117 imately leading to the early upregulation of socs3 expression.

118 signaling through Smad3-mediated blockade of Socs3 expression.

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

120 ading to SP1, CREB, and GATA1 activation and SOCS3 expression.

121 ongly correlated with a dramatic increase of SOCS3 expression.

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

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

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

125 ) and/or suppressor of cytokine signaling 3 (SOCS3), factors that inhibit STAT3 activation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

140 e in OVA-sensitized mice might not be due to SOCS3 gene depletion.

141 de [LPS]-induced DCs, DClps) with or without SOCS3 gene expression significantly ameliorated allergic

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

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

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

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

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

147 DClps with or without SOCS3 greatly improved lung pathology scores and allevia

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

149 SOCS3 has a crucial role in inhibiting STAT3 activation,

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

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

152 SOCS3 has only a modest effect on promoting Brk degradat

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

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

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

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

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

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

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

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

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

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

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

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

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

166 erfering RNA-mediated silencing of SOCS1 and SOCS3 in macrophage and T cells, respectively, restored

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

168 f cGAS-STING induced expression of SOCS1 and SOCS3 in pDCs, indicating a possible autoinhibitory loop

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

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

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

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

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

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

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

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

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 3, IL-22, and TSLP secretion and SOCS1/SOCS2/SOCS3 induction.

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

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

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

183 SOCS3 inhibits leptin signaling in the hypothalamus and

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

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

193 Suppressor of cytokine signaling 3 (SOCS3) is involved in regulating the functions of T cell

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

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

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

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

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

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

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

201 In vitro, SOCS3 knockdown increases proliferation and sprouting of

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

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

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

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

206 f tumor suppressors (e.g. ARHGEF4, EPHB2 and SOCS3), leading to increased oncogenic potency.

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

208 n of adiponectin and GLUT 4 and increases in SOCS3 levels in a TNF-alpha-induced insulin-resistant 3T

209 3 protein quantification and detected higher SOCS3 levels induced by M tuberculosis specific T-cell a

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

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

212 Both AM-derived EVs and synthetic SOCS3 liposomes inhibited the activation of STAT3 and ST

213 tenuated by intrapulmonary pretreatment with SOCS3 liposomes.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

236 SOCS3 promoter binding and gene transactivation by PPARg

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

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

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

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

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

242 We also examined Socs3 protein expression and phosphorylated Stat3 to det

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

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

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

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

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

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

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

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

251 Host SOCS3 regulates the innate immune response by controllin

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

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

254 ch gene, Suppressor of Cytokine Signaling 3 (Socs3), rescued the self-renewal defect of Sox2-ablated

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

256 o morpholino-mediated silencing of SOCS1 and SOCS3 resulted in protective cytokine responses, thereby

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

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

259 Here we examined the role of vesicular SOCS3 secretion as a mechanism by which AMs restrain all

260 Ex vivo SOCS3 secretion was reduced in AMs from challenged mice

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

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

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

264 SOCS3 significantly inhibited this pathway in astrocytes

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

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

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

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

269 Overexpression of SOCS3 strongly inhibited phosphorylation of STAT1 and PD

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

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

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

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

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

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

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

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

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

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

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

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

282 Socs3 was identified as a novel HIF1alpha target gene ba

283 SOCS3 was required for CXCR4-mediated growth inhibition.

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

285 Hypermethylation of cg18181703 (SOCS3) was associated with higher scores of both Mediter

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

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

288 ronchoalveolar lavage fluid (BALF) levels of SOCS3 were reduced in asthmatics and in allergen-challen

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

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

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

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

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

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

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

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

297 r727 and fail to upregulate the STAT3 target Socs3, which is required to turn off IFNAR signaling.

298 Overall, AM secretion of SOCS3 within EVs serves as a brake on airway EC response

299 ivery of suppressor of cytokine signaling 3 (SOCS3) within extracellular vesicles (EVs).

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