ライフサイエンスコーパス: STAT

1 STAT category 1 to 3 (lower risk) operations comprised 7

2 STAT proteins can regulate both pro- and anti-inflammato

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 tivate NF-kappaB, whilst IFN-gamma activated STAT-1.

8 C/EBPbeta and protein inhibitor of activated STAT (PIAS) 1, a small ubiquitin-related modifier E3 lig

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

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

11 A damage- and protein inhibitor of activated STAT 1 (PIAS1)-dependent polySUMOylation upon its associ

12 the SUMO E3, protein inhibitor of activated STAT 4 (PIAS4), which increased wild-type (WT) and F508d

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

14 a, also observed with IL-13, required active STAT signaling, and was dependent on expression of the o

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

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

17 reased STAT-1 (44.6% vs 87.4%; P<0.0001) and STAT-1 phosphorylation (0.7% vs 8.9%; P=0.0005) compared

18 and IFNgamma-response along with STAT-1 and STAT-4 phosphorylation in 29 HCV-infected LTx-recipients

19 STAT 1 to 3 (IDR 3.0 [95% CrI 2.1-4.2]) and STAT 4 or 5 (IDR 3.1 [95% CrI 2.4-3.9]) cases.

20 un N-terminal kinase 1/2/3, Lyn, STAT-3, and STAT-6 phosphokinase signaling.

21 ingle cytokine or by different cytokines and STAT dimerization versus tetramerization are physiologic

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

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

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

25 n the constitutive activity of NF-kappaB and STAT transcription factors, which drive expression of mu

26 PIM) 1, 2, and 3 kinases in a NF-kappaB- and STAT-dependent manner and PIMs enhance survival and expr

27 anslation, and down-regulated NF-kappaB- and STAT-dependent transcription of prosurvival factors BCL2

28 NF-kappaBeta and STAT-1 activation was investigated via immunofluorescenc

29 1 and regulated expression of IL-6, PDPN and STAT-1.

30 ncluding members of Ras/Raf/ERK-, Pi3K-, and STAT-pathways as well as tailless (tll) and foxo whose o

31 The discovery of JAKs and STATs and their roles in cytokine and IFN action represe

32 ranscription factors including NF-kappaB and STATs in epithelial and hemopoietic cells.

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

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

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

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

37 often found altered in patients affected by STAT GOF mutations.

38 , raising the possibility that non-canonical STAT function may contribute to the effects of streptoni

39 t affect CD107a-degranulation, but decreased STAT-1.

40 mor oncogenesis and associated KIT-dependent STAT activation.

41 ggered a positive feedback loop via ATM/E2F1/STAT signaling, amplifying the TRIM37 network in chemore

42 m 0.0% to 8.0% overall and 0.0% to 20.7% for STAT 4 and 5 cases.

43 old mortality variation across hospitals for STAT 1 to 3 (IDR 3.0 [95% CrI 2.1-4.2]) and STAT 4 or 5

44 equences of modulating expression of a given STAT is ultimately critical for determining its potentia

45 A prototype i-STAT cartridge was developed to utilize the monoclonal a

46 The i-STAT assay accurately distinguished Australian blood cul

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

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

49 gh which immune-mediated disease variants in STAT genes contribute to disease pathogenesis.

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

51 LTx-recipients was accompanied by increased STAT-1 (44.6% vs 87.4%; P<0.0001) and STAT-1 phosphoryla

52 atient-derived lymphocytes exhibit increased STAT activation in vitro in response to interferon-gamma

53 e Src family kinase LCK and cytokine-induced STAT-5 signalling, thereby enhancing both CAR T-cell act

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

55 resulting in constitutive Janus kinase (JAK)-STAT activation have been detected and associated with B

56 in other malignancies driven by aberrant JAK-STAT signaling.

57 the adjacent male gonad, which activates JAK-STAT signaling in enterocytes within this intestinal por

58 n which RNA interference, NF-kappaB, and JAK-STAT pathways underlie antiviral immunity.

59 L-22-induced phosphorylation of MAPK and JAK-STAT pathways, and activation of the NF-kappaB pathway w

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

61 mponents in the TGF-beta, GDNF, AKT, and JAK-STAT signaling pathways.

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

63 immune pathways including interferon and JAK-STAT signaling, Fcgamma receptor (FcgammaR)-mediated pha

64 e the receptor tyrosine kinase (RTK) and JAK-STAT-driven proliferation pathways 'parallel' or 'redund

65 Thus, RTK and JAK-STAT-driven proliferation pathways are parallel; those o

66 Adult muscles show basal JAK-STAT signalling activity in the absence of any immune ch

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

68 cations mentioned above to the canonical JAK-STAT pathway are necessary to reproduce this behavior.

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

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

71 eukemia (aCML) resulting in constitutive JAK-STAT signaling.

72 In this region, local endogenous JAK-STAT and JNK signaling creates a tissue microenvironment

73 Together these results clarify how JAK-STAT signaling actively inhibits hair growth.

74 tein, specifically the p22 form, impedes JAK-STAT signaling to help the virus evade the host innate i

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

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

77 gulated BALF ILs and cytokines including Jak-STAT (Janus kinases-signal transducer and activator of t

78 ad-spectrum immunosuppression, including JAK-STAT inhibitors, and sheds light on an additional neurot

79 Type I IFNs induce JAK-STAT signaling and expression of IFN-stimulated genes (I

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

81 Infection-induced JAK-STAT pathway is both required and sufficient for differe

82 regulated genes related to inflammation, JAK-STAT and TNF-alpha signaling after doxorubicin.

83 s with unique modes of action to inhibit JAK-STAT signalling in disease.

84 ude cell cycle inhibitors and interferon-JAK-STAT signaling genes critically involved in tumor suppre

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

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

87 otal signaling pathways, including MAPK, JAK-STAT, and PI3K-Akt.

88 dynamical behavior of the HER4 mediated JAK-STAT pathway which could be useful in designing treatmen

89 lls demonstrate increased IL-15-mediated JAK-STAT signaling activity.

90 Type I IFN-mediated JAK-STAT signaling is severely impaired, and activation of M

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

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

93 kinase inhibition blocked activation of JAK-STAT pathway TFs.

94 function is essential for the control of JAK-STAT signaling and the regulation of IFN responses.

95 Therefore, inhibition of Jak-STAT signaling is insufficient to explain inhibition of

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

97 K (SH2B3) is a key negative regulator of JAK-STAT signaling which has been extensively studied in mal

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

99 indicate that the use of pharmacological JAK-STAT inhibitors may be promising targets for future ther

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

101 PI3K-Akt-mTOR signaling, p53 signaling, Jak-STAT signaling, TGF-beta and notch signaling), rap1-sign

102 We show that JAK-STAT pathway activity, which declines from posterior to

103 ation of JAK inhibitors, suggesting that JAK-STAT signaling is required for maintaining hair follicle

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

105 aboratory has shown how mutations in the JAK-STAT pathway and epigenetic regulators play a role in my

106 tro, further supporting the roles of the JAK-STAT pathway and herpesviruses in mediating the adverse

107 The JAK-STAT pathway critically regulates T-cell differentiation

108 d thereby stimulated the activity of the JAK-STAT pathway in intestinal stem cells.

109 The JAK-STAT pathway is an evolutionarily conserved signal trans

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

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

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

113 ate cytokine signaling by inhibiting the JAK-STAT pathway.

114 ntly available mechanistic models of the JAK-STAT pathway.

115 of cytokine receptors that activate the JAK-STAT pathway.

116 nregulation of several components in the JAK-STAT pathway.

117 Interferons activate the Jak-STAT signaling pathway and induce overlapping patterns o

118 h refractory DiHS/DRESS, identifying the JAK-STAT signaling pathway as a potential target.

119 otensin-regulated airway remodeling, the JAK-STAT signaling pathway, and interferon gamma.

120 so targeted several key factors from the JAK-STAT signaling pathway, but nonimmune conditions were no

121 ses that are essential components of the JAK-STAT signaling pathway.

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

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

124 ick immune defence pathways, such as the JAK-STAT, immune deficiency and cross-species interferon-gam

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

126 ansducer and activator of transcription (JAK-STAT) signalling pathway in cancers, haematological dise

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

128 JAK/STAT inhibition or IFNbeta neutralization during LPS sti

129 JAK/STAT signaling is best known for its roles in immunity.

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

131 y, methotrexate has been identified as a JAK/STAT inhibitor in a functional screen, causing reduced p

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

133 130-like receptor, domeless, to activate JAK/STAT signalling in Drosophila.

134 IFN-activated Jak/STAT signaling induces robust expression of ZBP1, which

135 AT2 is a key player in the IFN-activated JAK/STAT signaling.

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

137 lammation in fibrosis-driving cells, and JAK/STAT activation in both megakaryocytes and stromal cells

138 , we demonstrate that STAT3 deletion and JAK/STAT inhibition in macrophages increases expression of t

139 inases, second-messenger generation, and JAK/STAT or NFAT transcriptional responses.

140 including the Ras/Raf/Erk, PI3K/Akt, and JAK/STAT pathways and immune checkpoint receptors.

141 oduces CXCL13 and that the NF-kappaB and JAK/STAT pathways are required to induce the expression of t

142 aling factors for the WNT, TGF-beta, and JAK/STAT pathways use their intrinsically disordered regions

143 ly in AM by activating the NF-kappaB and JAK/STAT pathways, respectively.

144 on and expansion/survival cytokines, and JAK/STAT pathways.

145 es and was able to inhibit NF-kappaB and JAK/STAT pathways.

146 survival, type I interferon (IFN-I), and JAK/STAT pathways.

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

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

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

150 pendent type I IFN synthesis followed by JAK/STAT-dependent interferon-stimulated gene expression.

151 tic cohesin complex, via a non-canonical JAK/STAT pathway, and consequently promotes meiotic DSB repa

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

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

154 a/beta expression or signaling following JAK/STAT inhibition may control catastrophic hyperinflammati

155 these proteins thus interfering with he JAK/STAT pathway and reducing their ability to inhibit type-

156 focusing on Drosophila and highlighting JAK/STAT pathway functions in proliferation, survival and ce

157 6 GO terms and 6 KEGG pathways including JAK/STAT signaling pathway.

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

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

160 recently reported that cytokine-induced JAK/STAT signaling mediates DEX resistance in T cell acute l

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

162 anti-inflammatory response by inhibiting JAK/STAT-signaling activation.

163 enes were enriched in pathways involving JAK/STAT signaling.

164 on of nuclear factor kappaB (NF-kappaB), JAK/STAT signaling, and programmed cell death protein 1 (PD-

165 , we hypothesized that cytokine-mediated JAK/STAT signaling might similarly contribute to DEX resista

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

167 ing proinflammatory macrophages, but not JAK/STAT signaling, can attenuate granulomatous interstitial

168 echanisms underlying the upregulation of JAK/STAT activity in this disease context is completely unkn

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

170 demonstrate that combined inhibition of JAK/STAT signaling and LSD1 is a promising therapeutic strat

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

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

173 Here, we provide an overview of JAK/STAT signaling in stem cells and regeneration, focusing

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

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

176 demonstrates synergy with inhibitors of JAK/STAT signaling, doubling median survival in vivo.

177 plified via IFN-stimulated activation of JAK/STAT signaling.

178 Combinatorial targeting of JAK/STAT, PI3K, and "BCR-like" signaling with multiple TKIs

179 c landscape is characterized by not only JAK/STAT activating mutations but also loss-of-function alte

180 In the posterior, JAK/STAT works with the epidermal growth factor receptor (EG

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

182 Type I IFNs stimulate JAK/STAT signaling in DRG neurons but this does not apparent

183 ion of IFNK transcription and subsequent JAK/STAT-dependent upregulation of several IFN-stimulated ge

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

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

186 ost antiviral response by activating the JAK/STAT (Janus kinase/signal transducer and activator of tr

187 n and newly identified components of the JAK/STAT and NF-kappaB signaling pathways and frequent B2M a

188 In contrast, inhibiting the JAK/STAT inflammatory pathway with tofacitinib was not renop

189 e to resistance of mammary tumors to the JAK/STAT inhibitor ruxolitinib in vivo and that ruxolitinib-

190 of CNA encompassed genes involved in the JAK/STAT pathway and epigenetic regulators.

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

192 The JAK/STAT pathway is a conserved metazoan signaling system th

193 es that are elevated in HLH activate the JAK/STAT pathway, and the JAK1/2 inhibitor ruxolitinib (RUX)

194 tionships, such as connection within the JAK/STAT pathway, and was further validated in characterizin

195 %) showed mutations in >=1 member of the JAK/STAT pathway, including STAT3 (38%), JAK1 (18%), and STA

196 Inhibition of the JAK/STAT pathway, which was expressed in both malignant cell

197 Furthermore, F-actin is regulated by the Jak/STAT pathway-increasing or decreasing pathway activity c

198 rgeting shared downstream factors of the JAK/STAT pathway.

199 of the mutational status of genes in the JAK/STAT pathway.

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

201 that was dependent on activation of the JAK/STAT pathway.

202 re well-known negative regulators of the JAK/STAT pathway.

203 nvolved in chromatin modification or the JAK/STAT pathway.

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

205 ticulum chaperone protein, activates the JAK/STAT signaling pathway via a pathogenic binding interact

206 s are transcriptionally regulated by the JAK/STAT signaling pathways, which can be disabled by small

207 STAT2 is indispensable in the JAK/STAT signaling since it is also involved in activation o

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

209 ly targetable oncogenic mutations in the JAK/STAT, MAPK, MYC, and chromatin modification pathways.

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

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

212 uces FLT3L expression in UC-MSCs through JAK/STAT signaling pathway.

213 terferon-stimulated genes (ISGs) through JAK/STAT signaling.

214 effects of ruxolitinib on adipose tissue JAK/STAT signaling in a mouse model.

215 sducers and Activators of Transcription (JAK/STAT) pathway is aberrantly activated and contributes to

216 ansducer and activator of transcription (JAK/STAT) pathway regulates the anterior posterior axis of t

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

218 tivation of adaptive immune response via JAK/STAT signaling.

219 es, IL-6 promoted muscle degradation via JAK/STAT, FOXO3a, and atrogin-1 upregulation.

220 I IFN score and IL18 expression, whereas JAK/STAT inhibition strongly reduced IL-18 serum levels in t

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

222 Serum IL-18 expression with or without JAK/STAT inhibition was analyzed in two MAS mouse models and

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

224 nown to act at multiple levels of NF-kappaB, STAT and AP-1 signaling cascades.

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

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

227 ppressed c-Jun N-terminal kinase 1/2/3, Lyn, STAT-3, and STAT-6 phosphokinase signaling.

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

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

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

231 applied structural equation models to the MS-STAT trial in which 140 patients with SPMS were randomiz

232 iates KRAS-driven malignancies through a non-STAT-signaling pathway.

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

234 N) pathogenesis and results in activation of STAT, PI3K/AKT, and MEK/ERK signaling.

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

236 tudied the effects of IFNL and inhibitors of STAT-signaling pathway.

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

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

239 l screen, causing reduced phosphorylation of STAT proteins.

240 particular, the differential utilization of STAT proteins by a single cytokine or by different cytok

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

242 25 416 (5.7%) highest complexity operations (STAT [Society of Thoracic Surgeons-European Association

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

244 trations in cells and fails to degrade other STAT proteins.

245 and demonstrates high selectivity over other STAT members.

246 ysis detects no significant binding to other STATs or additional off-target proteins, confirming thei

247 dy, we demonstrate nuclear localization of p-STAT(Y705), with significant overexpression of several S

248 transducer and activator of transcription (p-STAT) 1 activation.

249 udy of monogenic diseases, and in particular STAT mutations, may not only improve our understanding o

250 For the ATR pathway, STAT-5 increases expression of the topoisomerase IIbeta-

251 d proliferation (MAPK), and proinflammatory (STAT) pathways in the immune cells of MS patients, prima

252 cer and activator of transcription proteins (STAT) family of transcription factors.

253 nsducer activator of transcription proteins (STATs) in myogenic and osteogenic differentiation after

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

255 these pathways through the immune regulator STAT-5.

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

257 s involved the PI3K/AKT, JAK/STAT3, and SMAD/STAT signaling pathways.

258 Activation of the cGAS-STING-STAT pathway detected in these cells further substantiat

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

260 pean Association for Cardiothoracic Surgery [STAT] category) and simulations evaluated the potential

261 emodeling controlled by signal-regulated TFs STATs.

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

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

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

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

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

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

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

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

270 37% to 60% of the improvement related to the STAT 1 to 3 (lower risk) group across outcomes.

271 downstream effectors, more particularly the STATs.

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

273 Even subtle decreases to STAT activity are sufficient to precociously age young G

274 l transducer and activator of transcription (STAT) (ruxolitinib) or mitogen-activated protein kinase

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

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

277 l transducer and activator of transcription (STAT) 3 signaling in female skin; and a larger response

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

279 l transducer and activator of transcription (STAT) 4 and STAT6 signaling in the lungs after OVA sensi

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

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

282 l transducer and activator of transcription (STAT) pathway and nitric oxide production, as well as th

283 l transducer and activator of transcription (STAT) pathways.

284 l transducer and activator of transcription (STAT) protein family, namely gain-of-function (GOF) muta

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

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

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

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

289 l transducer and activator of transcription (STAT) signaling pathways.

290 l transducer and activator of transcription (STAT)-1, IL-6, IFN regulatory factor (IRF) 5, and TLR4 a

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

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

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

294 l transducer and activator of transcription (STAT)5 via the GHR (Ghr-391(-/-)) as for GHR-null (GHR(-

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

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

297 r previous observation that unphosphorylated STAT (uSTAT) promotes heterochromatin formation in both

298 Using these vectors, we vaccinated STAT-1 knock-out mice, an animal model for CCHFV.

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

300 granulation and IFNgamma-response along with STAT-1 and STAT-4 phosphorylation in 29 HCV-infected LTx