ライフサイエンスコーパス: STAT

1 STAT (Sarcoidosis Treated with Anti-TNF) is a French ret

2 STAT proteins are a family of transcription factors that

3 n (12% decrease in DTN time, 95% CI 3%-20%), STAT stroke protocol (11% decrease in DTN time, 95% CI 1

4 n as PTPN2, as a negative regulator of IL-7R-STAT signaling in T cell progenitors, contributing to bo

5 24, 2015), 3 changes were implemented: (1) a STAT stroke protocol to prenotify the stroke team about

6 kines and growth hormones typically activate STATs and could therefore act as humoral transfer factor

7 Oylation, the protein inhibitor of activated STAT (PIAS) E3-ligases were initially described as trans

8 The protein inhibitor of activated STAT (PIAS) family of SUMO ligases is predominantly asso

9 phatases, and protein inhibitor of activated STAT (PIAS) proteins.

10 er of the Siz/protein inhibitor of activated STAT (PIAS) RING family of SUMO E3 ligases, as essential

11 rotein ligase protein inhibitor of activated STAT 4 (PIAS4) is a pivotal protein in regulating the TG

12 e SUMO ligase protein inhibitor of activated STAT 4 (PIAS4) is upregulated during HSV-1 infection and

13 The PIAS (protein inhibitor of activated STAT) family of SUMO (small ubiquitin-like modifier) lig

14 ases (JAKs) classically signal by activating STAT transcription factors but can also regulate gene ex

15 with other studies of constitutively active STAT mutants, provides insight into the pathogenesis and

16 Although STAT activation has been widely implicated in cancer, th

17 y or advanced stages of diabetes ameliorated STAT activity and resulted in reduced serum creatinine l

18 (CTLA-4), CD154 (CD40L), T-bet, GATA-3, and STAT-1.

19 Activating JAK and STAT mutations were not sufficient to initiate leukemic

20 , blocked IFNG-induced signaling via JAK and STAT.

21 s from this patient exhibit reduced JAK1 and STAT phosphorylation following cytokine stimulations, re

22 ing-related loss in binding of NF-kappaB and STAT factors.

23 e factor 1alpha (HIF-1alpha), NF-kappaB, and STAT proteins, and are the targets for the interactions

24 esion through integrin alpha5beta1, MAPK and STAT activity, and initiation of pluripotency signalling

25 thways including Elk1/SRF, AP1, NFkappaB and STAT, and reduces EGFR expression in ovarian cancer cell

26 1 and regulated expression of IL-6, PDPN and STAT-1.

27 Smad and STAT proteins are critical signal transducers and transc

28 ate transcriptional activity of NFkappaB and STATs, we hypothesized that these kinases support RS cel

29 transcription factors, such as NFkappaB and STATs.

30 es as privileged structures for antagonizing STAT SH2 domains, and demonstrates that apoptosis can be

31 tional NF-kappaB, activator protein 1 (AP1), STAT, and Smad DBS in the TSLP promoter region.

32 These effects seem to be regulated by AP1, STAT-3 and NF-kappaB signaling pathways.

33 K293 or HEK293-STAT6 cells, and on the basal STAT activity in stably transfected L-428 and U-HO1 cHL

34 own the association and coordination between STATs and SMADs in mediating TGF-beta functions in hepat

35 on with AP-1 components (c-Fos or Jun), bind STAT-1 in a homodimer like complex (HDLC).

36 Of interest, RvD1 blocked STAT-1 and its target inflammatory genes (i.e., CXCL9),

37 during the viral life cycle is controlled by STAT-5 and the kinase GSK3beta.

38 Under physiologic conditions, STAT signaling is stimulus dependent and tightly regulat

39 Here we show that cytokine-STAT signalling promotes mycobacterial survival within m

40 isms of action of two families of endogenous STAT inhibitors, the SOCS and PIAS families, to potentia

41 ally, ticks lacking the transcription factor STAT, which signals downstream of IFNgamma, did not indu

42 evels found in the C26 CM was sufficient for STAT reporter activation and atrophy in myotubes.

43 The heightened STAT signaling is critical to maintain the expression of

44 ns in hepatic cells, but it is not clear how STATs are activated under these circumstances.

45 ymal/CSCs have a significantly repressed IFN/STAT gene expression signature and an enhanced ability t

46 ansducer and activator of transcription (IFN/STAT) gene signature and are often enriched for cancer s

47 hages through TLR2, associated with impaired STATs signaling pathway.

48 tivation of transcription factors, including STATs, is known to promote tumor initiation and progress

49 Moreover, mTOR-independent STAT-5 signaling contributed to improved NK-cell functio

50 JAK2 inhibitors also blocked C26 CM-induced STAT reporter activation, STAT3 phosphorylation, and atr

51 y epithelial cells inhibits cytokine-induced STAT activation.

52 Mycobacterium marinum, mycobacterium-induced STAT activity triggered by unpaired-family cytokines red

53 Additionally, NBQX treatment inhibited STAT-3 phosphorylation, but not astrogliosis or transcri

54 Whether this signaling involves STAT activation, epigenetic modification of chromatin, o

55 vival and fate, specifically PDGFR, ERK, JAK STAT, MAPK, and TCR/NF-kappaB signaling; epigenetic regu

56 JAK-STAT signaling mediates the actions of numerous cytokine

57 JAK-STAT signaling was critical for TA-CA1 LTD as inhibition

58 TAT) signaling pathway by ruxolitinib, a JAK-STAT-specific inhibitor.

59 f genes involved in RNAi, Toll, Imd, and JAK-STAT pathways, but the majority of differentially expres

60 Complete and conserved Toll, IMD and JAK-STAT signaling pathways were found in P. xylostella.

61 Thus CRYs link the circadian clock and JAK-STAT signaling through control of STAT5B phosphorylation

62 p-dependent protein translation, blocked JAK-STAT signaling, and markedly attenuated NFkappaB-depende

63 IFN-stimulated genes (ISGs) by blocking Jak-STAT signaling; however, this occurs by different mechan

64 ells, and their expression was driven by JAK-STAT and NFkappaB activity.

65 indicate an essential role for canonical JAK-STAT signaling in activity-dependent LTD at TA-CA1 synap

66 Canonical JAK-STAT signaling is pivotal for long-term depression at ad

67 elation analysis links PinT to host cell JAK-STAT signalling, and we identify infection-specific alte

68 However, unlike common JAK-STAT pathway inhibitors, BRD0476 inhibits JAK-STAT signa

69 driver mutations leading to constitutive JAK-STAT activation, the cellular and molecular biology of m

70 II receptor families and the downstream JAK-STAT pathway along with its key negative regulators.

71 ythropoietin stimulation, and heightened JAK-STAT activation.

72 )) and used pathway analysis to identify JAK-STAT/IL12/IL27 signalling and cytokine-cytokine pathways

73 Here we review recent advances in Jak-STAT biology, focusing on immune cell function, disease

74 inked to differential gene expression in JAK-STAT signaling, NADPH oxidation, and other cancer-relate

75 ons in key signaling pathways, including JAK-STAT, NOTCH and NF-kappaB, have also been defined, the s

76 This was associated with increased JAK-STAT signaling in NK cells in which Cish was deleted.

77 enotype is mediated by Nol3(-/-)-induced JAK-STAT activation and downstream activation of cyclin-depe

78 hrough inhibiting the interferon-induced JAK-STAT signaling pathway, a key antiviral pathway involved

79 TAT pathway inhibitors, BRD0476 inhibits JAK-STAT signaling without suppressing the kinase activity o

80 at LTD at adult TA-CA1 synapses involves JAK-STAT signaling, but unlike SC-CA1 synapses, requires rap

81 (TLR), mitogen-activated protein kinase, Jak-STAT, and the nucleotide oligomerization domain-like rec

82 nt, and these mutations all activate MPL-JAK-STAT signaling in MPN stem cells.

83 /HPCs were associated with inhibition of JAK-STAT activity, leading to the induction of apoptosis.

84 y of 24 is supported by demonstration of JAK-STAT and HDAC pathway blockade in hematological cell lin

85 potency is supported by demonstration of JAK-STAT and HDAC pathway blockade in several hematological

86 urages further discussion on the role of JAK-STAT signaling in the various stem cell niches of the ha

87 s, indicating a general sensitization of JAK-STAT signaling in this leukemia subset.

88 We propose that overactivation of JAK-STAT signaling is part of the mechanism underlying disea

89 d for mutant CALR-mediated activation of JAK-STAT signaling.

90 K2 or EPOR rearrangements (12.4%), other JAK-STAT sequence mutations (7.2%), other kinase alterations

91 ns in 8.8%, alterations activating other JAK-STAT signaling genes (IL7R, SH2B3, JAK1) in 6.3% or othe

92 nterferon (IFN-I) response by preventing JAK-STAT signaling, suggesting that suppression of this path

93 alysis of the 17-gene signature revealed Jak-STAT signaling pathway as the most significantly represe

94 Our findings suggest that JAK-STAT pathway inhibition may represent a therapeutic stra

95 LF2(+) group identified mutations in the JAK-STAT and Ras pathway in 85% of patients, and 20% had a C

96 itant genomic alterations activating the JAK-STAT pathway (JAK1, JAK2, IL7R) identified in 63 patient

97 esis that using these drugs to block the JAK-STAT pathway would prevent autoimmune diabetes.

98 rine and paracrine signaling through the JAK-STAT pathway, leading to the transcriptional induction o

99 eptor (IL-7R), via its activation of the JAK-STAT pathway, promotes gene programs that change dynamic

100 tural proteins 1 and/or 2 perturbing the Jak-STAT signaling pathway, with concomitant reduced express

101 plication of CSFV through inhibiting the JAK-STAT signaling pathway.

102 eporters, demonstrating that it uses the JAK-STAT signaling pathway.

103 ficant increase in the expression of the JAK-STAT target gene Pim1 and muscles from 2-day and 3-week

104 ceptor gene CSF3R, which signals through JAK-STAT proteins.

105 cell antigens to CD4(+) T cells through Jak-STAT signal transduction.

106 th EPOR rearrangements were sensitive to JAK-STAT inhibition, suggesting a therapeutic option in high

107 ansducer and activator of transcription (JAK-STAT) pathways, or indirectly via changes in the tumor m

108 ansducer and activator of transcription (JAK-STAT) signaling pathway by ruxolitinib, a JAK-STAT-speci

109 al pathways, such as IL-6 signalling via JAK-STAT pathway.

110 However, it is unclear whether JAK-STAT signaling also regulates excitatory synaptic functi

111 Jak/STAT research has not only impacted basic science, parti

112 esults suggest that LNK suppresses IL-7R/JAK/STAT signaling to restrict pro-/pre-B progenitor expansi

113 brid synthekine ligands that dimerized a JAK/STAT cytokine receptor with a receptor tyrosine kinase (

114 IL-2 induced IL-36R gene expression in a JAK/STAT-dependent manner.

115 While aberrant JAK/STAT signaling is crucial to the development of gastric

116 s of CRLF2, JAK2, and EPOR that activate JAK/STAT signaling.

117 h-like ALL) is associated with activated JAK/STAT, Abelson kinase (ABL), and/or phosphatidylinositol

118 ccumulate additional mutations affecting JAK/STAT signaling, protein translation, and epigenetic cont

119 ndent processes, apical delamination and JAK/STAT activation, are concurrently required for the initi

120 tor of the Rho family small GTPases, and JAK/STAT is activated ectopically in these coldspot nTSG-def

121 igate the possible role of TNF-alpha and JAK/STAT pathway on de novo lipogenesis and PCSK9 expression

122 cross-coupling between the CREB/CRTC and JAK/STAT pathways contributes to BM homeostasis.

123 Pharmacologic inhibition of ERK and JAK/STAT pathways reversed miR-194-driven phenotypes.

124 included components of the Toll, Imd and JAK/STAT pathways, consistent with interactions between the

125 iurnal rhythmicity of insulin action and JAK/STAT signaling in adipose tissue.

126 teral diffusion in lipid nanodomains and JAK/STAT signaling in patient cells, whereas adding galectin

127 iac factors along with canonical Wnt and JAK/STAT signaling reprogrammed adult mouse cardiac, lung, a

128 factors involved in B-cell receptor and JAK/STAT signaling, the nonclassical NF-kappaB pathway, cell

129 (MTGNB) along with activation of Wnt and JAK/STAT signaling.

130 of main immune pathways (Toll, Imd, and JAK/STAT), and immune effectors in P. xylostella in response

131 ing with Glide/Gcm: Notch, Hedgehog, and JAK/STAT, which all involve feedback loops.

132 ng pathways, including PI3K/Akt/mTOR and JAK/STAT.

133 aling pathways AKT, NFkappaB, ERK1/2 and JAK/STAT.

134 re is indirect positive feedback between JAK/STAT and insulin signaling in the muscles.

135 Surprisingly, both JAK/STAT pathway activation and ruxolitinib efficacy were in

136 e onset of pupariation, is controlled by JAK/STAT signaling in early regenerating discs.

137 The HEL cell line, in which constitutive JAK/STAT pathway activation is caused by JAK2V617F, was used

138 JAK3 mutants induce constitutive JAK/STAT signaling and cause leukemia when expressed in the

139 the molecular basis of this constitutive JAK/STAT signaling in cHL has not been completely understood

140 Constitutive JAK/STAT signaling is crucial for survival and proliferation

141 nd docking sites for required downstream JAK/STAT proteins.

142 d as strong inhibitors of the Drosophila JAK/STAT pathway, an effect conserved to human cells.

143 with high MPL expression showed enhanced JAK/STAT signaling and proliferation in response to THPO in

144 ose patients most likely to benefit from JAK/STAT targeted chemotherapies.

145 tified correlates of severity, including JAK/STAT, prolactin, and interleukin 9 signaling.

146 erferon-gamma- and interleukin-4-induced JAK/STAT activity in HEK293 or HEK293-STAT6 cells, and on th

147 ssion in CML LTHSCs reduced THPO-induced JAK/STAT signaling and leukemogenic potential.

148 y an application to data for Epo-induced JAK/STAT signaling.

149 l for the inhibition of cytokine-induced JAK/STAT signalling activation in DF-1.

150 e contraction, focal adhesion, integrin, JAK/STAT, MAPK, growth factor, and p53 signaling pathways we

151 t body through the cytokine Upd3 and its JAK/STAT-coupled receptor, Domeless.

152 genetic protein (BMP), Jun kinase (JNK), JAK/STAT, Notch, Insulin, and Wnt, revealed that many ligand

153 vation or reduced expression of negative JAK/STAT regulators such as silencer of cell signaling 1 (SO

154 sion along with suppression of NFkappaB, JAK/STAT and PI3K pathways.

155 ncreatic cancer to examine the effect of Jak/STAT and MAPK pathway inhibition in vitro.

156 xpression in HNC cells in the context of JAK/STAT pathway activation, Th1 inflammation, and HPV statu

157 cacy were independent of the presence of JAK/STAT pathway mutations, raising the possibility that the

158 t PTP1BDelta6 is a positive regulator of JAK/STAT signaling in cHL.

159 l studies underscore the central role of JAK/STAT signaling in myeloproliferative neoplasms (MPNs).

160 Specifically, stimulation of JAK/STAT signaling in the muscles can rescue the deficient i

161 cytokine Upd3, leading to activation of JAK/STAT signaling, differentiation of cells that form the p

162 s facilitated by HER2/HER3 activation of JAK/STAT signaling.

163 3, leading to constitutive activation of JAK/STAT signaling.

164 rs were used to disentangle the roles of JAK/STAT, MAPK, and PI3K signaling pathways.

165 hypothesize that ETP-ALL is dependent on JAK/STAT signaling.

166 cutaneous T-cell lymphoma pathogenesis, JAK/STAT signaling, we used conditional gene targeting to de

167 hich results in cell cycle perturbation, JAK/STAT signal activation, and differential regulation of N

168 These include B-cell receptor, JAK/STAT, NF-kappaB, NOTCH, and Toll-like receptor signaling

169 ring ISCs non-autonomously by regulating JAK/STAT signaling.

170 cancer pathways such as Ras/ERK1/2, Src, JAK/STAT, JNK, NF-kappaB, and PTEN/PI3K/AKT.

171 perimental CP, suggesting that targeting Jak/STAT signaling may represent a promising therapeutic str

172 n ageing muscle, including Wnt, TGFbeta, JAK/STAT and senescence signalling.

173 We recently found that JAK/STAT signaling in skeletal muscles is important for the

174 The insight that JAK/STAT system activation is pervasive in T cell malignanci

175 sertions could be mapped to genes in the JAK/STAT and MAPK pathways, confirming the ability of this s

176 hat treating CADM1 null tumours with the JAK/STAT inhibitor ruxolitinib mimics CADM1 gene restoration

177 l, but were not previously linked to the JAK/STAT or MAPK pathways nor shown to functionally contribu

178 proteins are negative regulators of the JAK/STAT pathway activated by proinflammatory cytokines, inc

179 ate that Et/Lat negatively regulates the JAK/STAT pathway activity and can bind to Dome, thus reducin

180 t is down-regulated by inhibitors of the JAK/STAT pathway and enhanced by inhibitors of the Src kinas

181 uggests the feasibility of targeting the JAK/STAT pathway as a neuroprotective therapy for neurodegen

182 small-molecule inhibitors targeting the JAK/STAT pathway blocked proliferation elicited by IL-2 and

183 ese results indicate that inhibiting the JAK/STAT pathway can prevent neuroinflammation and neurodege

184 st documentation that suppression of the JAK/STAT pathway disrupts the circuitry of neuroinflammation

185 uggesting that PIV-3 interferes with the JAK/STAT pathway downstream of the IFN-lambdaR1/IL-10R2 rece

186 GPR45 regulates POMC expression via the JAK/STAT pathway in a cell-autonomous manner.

187 Given the importance of the JAK/STAT pathway in activating microglia and inducing cytoki

188 vitro, alpha-SYN exposure activated the JAK/STAT pathway in microglia and macrophages, and treatment

189 findings document that inhibition of the JAK/STAT pathway influences both innate and adaptive immune

190 The JAK/STAT pathway is a highly conserved regulatory module, ac

191 These data suggest that the Jak/STAT pathway plays a prominent role in PSC proliferation

192 Importantly, inhibition of the JAK/STAT pathway prevented the degeneration of dopaminergic

193 therapeutic potential of inhibiting the JAK/STAT pathway using the JAK1/2 inhibitor, AZD1480.

194 STAT3, suggesting the involvement of the JAK/STAT pathway.

195 ulating Claudin-2 expression through the JAK/STAT pathway.

196 okines, many of which signal through the JAK/STAT signaling pathway to exert their biological effects

197 bited monkeys revealed engagement of the JAK/STAT signaling pathway, suggesting alternative gammac cy

198 talk among enriched pathways, mainly the JAK/STAT signalling pathway and the EGF receptor signalling

199 tokine receptors that signal through the JAK/STAT signalling pathway are important for disease, infor

200 Mo-DC differentiation by regulating the JAK/STAT/MAPK and NFkappaB pathways.

201 a receptor-dependent cytokines and their JAK/STAT pathways play pivotal roles in T cell immunity.

202 s of IL-21R arose from signaling through JAK/STAT pathways and upregulation of caspase 3.

203 a greater role of MAPK/PI3K compared to JAK/STAT with the orphan nuclear receptor RXRalpha playing a

204 ansducer and activator of transcription (JAK/STAT) activation by IFN-gamma could not occur.

205 ansducer and activator of transcription (JAK/STAT) signaling activity.

206 sducers and activators of transcription (JAK/STAT) signaling via the IL-22 receptor, resulting in enh

207 Whereas the vertebrate JAK/STAT signaling cascade is transduced via multiple recept

208 e metabolism in the infected animal, via JAK/STAT and insulin signaling in the muscles, and that ther

209 ing inhibits the growth of losers, while JAK/STAT signalling promotes competition-induced winner cell

210 n profiling indicates that the non-SMAD JAK1/STAT pathway is essential for the expression of a subset

211 induce ligand-independent activation of JAK2/STAT/phosphatydylinositol-3'-kinase (PI3-K) and mitogen-

212 ssical ISG expression independent of the JAT-STAT signaling pathway.

213 e MEK inhibitor trametinib, the Janus kinase-STAT inhibitor tofacitinib, and the STAT5 inhibitor pimo

214 pid attenuation of keratinocyte Janus kinase/STAT signaling; (2) removal of keratinocyte-induced cyto

215 naling axis and the composition of the c-Kit/STAT signalosome.

216 C-188-9, a small molecule STAT-3 inhibitor, decreased pulmonary fibrosis in the in

217 In the 24-month MS-STAT phase 2 trial, we showed that high-dose simvastatin

218 We did a secondary analysis of MS-STAT, a 24-month, double-blind, controlled trial of pati

219 We now describe the results of the MS-STAT cognitive substudy, in which we investigated the tr

220 ma), and that IL-6 regulation of MMPs is not STAT-3 dependent.

221 n quantitative immunoblotting experiments of STAT proteins, STAT1alpha, phosphorylated-STAT1alpha (pS

222 ving cells, THZ1 decreases the expression of STAT-regulated anti-apoptotic BH3 family members MCL1 an

223 onse characterised by selective induction of STAT target genes in the fat body through the cytokine U

224 In vitro studies show that inhibition of STAT-3 decreased IL-6- and TGF-beta-induced expression o

225 STAT3 is a member of STAT (signal transducer and activator of transcription)

226 h the quantitative and qualitative nature of STAT-gene targeting.

227 ADs, TGF-beta also induces a second phase of STAT phosphorylation that requires SMADs, de novo protei

228 expression heightens the phosphorylation of STAT family members, causing aberrant expression of an i

229 d Janus kinases (Jak) and phosphorylation of STAT proteins in target cells.

230 IL-10 pathway by reducing phosphorylation of STAT proteins.

231 in SMAD2/SMAD3-dependent phosphorylation of STAT-3.

232 s absolutely required for phosphorylation of STATs in a SMAD-independent manner within minutes of TGF

233 tical for TA-CA1 LTD as inhibition of JAK or STAT blocked LTD induction and prevented NMDA-induced AM

234 of these T cell lines whether or not JAKs or STATs were mutated.

235 ion observed in STAT3 likely occurs in other STATs.

236 undant roles in the activation of particular STAT proteins and this tyrosine kinase is essential for

237 dless of the agents used, induces persistent STAT-1 and NF-kappaB activity in carcinoma-associated fi

238 anges in chromatin accessibility and phospho-STAT responsiveness to IFN.

239 Phosphorylated STAT-3 was elevated in lung biopsies from patients with

240 hropoietin (EPO) receptor and phosphorylated STAT-5 relative to matched Q-HB, with increased phosphor

241 cytokines, in which tyrosine-phosphorylated STATs (pSTATs) function as transcription factors.

242 omprised of IRF9 and tyrosine-phosphorylated STATs 1 and 2, transmits the signal from the type I inte

243 However, the recent discovery of rare STAT mutations in hematopoietic malignancies suggests th

244 finity of IFN to the cell surface receptors, STAT phosphorylation, or gene induction.

245 Furthermore, the innate immune regulator STAT-5 and the kinase GSK3beta mediate the activation of

246 otocin diabetic, apoE-deficient mice), renal STAT activation status correlated with the severity of n

247 Resistance to IR-induced apoptosis requires STAT and Wg and is mediated by transcriptional repressio

248 alized with transcription factors RORgammat, STAT-3, and p300 at the Il23r, Il17a/f, and Csf2 cytokin

249 idence that in human cells, SFTSV sequesters STAT proteins in replication complexes, thereby inhibiti

250 Although IL-21 can activate several STAT family transcription factors, previous studies focu

251 In vitro, internalized peptide suppressed STAT activation and target gene expression induced by in

252 protects against nephropathy by suppressing STAT-mediated cell responses to diabetic conditions.

253 These findings demonstrate that STAT-3 contributes to the development of lung fibrosis a

254 evelopment of lung fibrosis and suggest that STAT-3 may be a therapeutic target in pulmonary fibrosis

255 in hematopoietic malignancies suggests that STAT mutants may be oncogenic.

256 The STAT-signalling pathway is highly vulnerable to THZ1 eve

257 myocardial response, and neprilysin and the STAT family as key regulators of intrinsic remote condit

258 ineages, and strengthen the link between the STAT family of transcription factors and autoimmunity.

259 the mRNAs of SOCS family genes encoding the STAT signalling inhibitory proteins SOCS1, SOCS3 and CIS

260 Among 140 patients in the STAT database, 46 had skin involvement.

261 amily and transcription factors (TFs) of the STAT ('signal transducer and activator of transcription'

262 nd due to the structural conservation of the STAT family of proteins, the inter-domain allosteric com

263 c DNA activates STAT3, another member of the STAT family, via an autocrine mechanism involving interf

264 related to inflammation or activation of the STAT signal transduction pathway.

265 t the therapeutic potential of targeting the STAT/TET1 axis by selective inhibitors in AML treatment.

266 downstream effectors, more particularly the STATs.

267 een widely implicated in cancer, therapeutic STAT inhibitors are still largely absent from the clinic

268 -6 family of cytokines, which signal through STAT-3, may also contribute to lung fibrosis.

269 STAT5 triggers its genome-wide relocation to STAT consensus sites with two distinct transcriptional c

270 l transducer and activator of transcription (STAT) 1 and STAT3, which is significantly enhanced by an

271 l transducer and activator of transcription (STAT) 1 pathway in human type 1 diabetes and in mouse mo

272 l transducer and activator of transcription (STAT) 3 signaling pathway, and osteogenic differentiatio

273 l transducer and activator of transcription (STAT) 5 activation by IM allowed the specific enhancemen

274 l transducer and activator of transcription (STAT) 5 signaling by TSLP.

275 l transducer and activator of transcription (STAT) binding elements (SBEs) within the proximal promot

276 l transducer and activator of transcription (STAT) family of transcription factors orchestrate hemato

277 l transducer and activator of transcription (STAT) mutations have been discovered in many T-cell mali

278 l transducer and activator of transcription (STAT) pathway.

279 l transducer and activator of transcription (STAT) protein to promote cell division only in OB-ISCs.

280 l transducer and activator of transcription (STAT) proteins, leads to inappropriate gene expression p

281 l transducer and activator of transcription (STAT) signaling contributes to diabetic nephropathy by i

282 l transducer and activator of transcription (STAT) signaling pathway is involved in numerous cellular

283 l transducer and activator of transcription (STAT) signaling pathways is a hallmark of a variety of B

284 l transducer and activator of transcription (STAT) signaling pathways led us to hypothesize that ETP-

285 l transducer and activator of transcription (STAT) target genes.

286 l transducer and activator of transcription (STAT)-1 knockout mouse showed that IFN-gamma signaling i

287 l transducer and activator of transcription (STAT)-3 signaling to decrease angiogenesis in human and

288 l transducer and activator of transcription (STAT)-6 phosphorylation level in murine heart fibroblast

289 l transducer and activator of transcription (STAT)5 activation in left ventricular myocardium is asso

290 Transducers and Activators of Transcription (STATs) are principal transcription factors downstream of

291 transducers and activators of transcription (STATs), essential functions of their upstream Janus kina

292 l transducer and activator of transcription [STAT] homolog) activity and would normally form the hing

293 However, in tumorigenesis, STAT proteins become constitutively active and promote t

294 retcher, registering the patient as unknown, STAT stroke protocol, and administering alteplase in CT

295 vented Th1 and Th17 cell differentiation via STAT/NFkappaB signaling pathways.

296 ng cytokine regulation of MMP expression via STAT-1, and increases our understanding of the links bet

297 However, the mechanisms by which STAT activation modulates lineage-affiliated transcripti

298 udy was to determine the mechanisms by which STAT-3 activation might result in intestinal fibrosis.

299 the current manuscript, the extent to which STAT-3 inhibition decreases lung fibrosis is investigate

300 lation lead to constitutive activation of WT STATs.