ライフサイエンスコーパス: JAK

1 JAK inhibition is not curative and fails to induce a per

2 JAK inhibitor sensitivity correlated with the STAT3 phos

3 JAK inhibitors (ruxolitinib and tofacitinib) inhibited t

4 JAK inhibitors are selective for acute megakaryoblastic

5 JAK inhibitors are valuable therapeutic agents in myelof

6 JAK-dependent activation of the rho module of integrin a

7 JAK-STAT3 gain-of-function mutations within this pathway

8 JAK/STAT inhibition or IFNbeta neutralization during LPS

9 JAK/STAT signaling is best known for its roles in immuni

10 eparanase expression via the Janus kinase 2 (JAK-2) pathway.

11 Interruption of IL-6/JAK/STAT3 pathway by a JAK inhibitor AZD1480 reverses th

12 ) and proinflammatory gene sets such as IL-6/JAK/STAT5 (Janus kinase/signal transducer and activator

13 rsible with targeted inhibition of the IL-7R/JAK/STAT5/BCL-2 axis.

14 s to determine if A77 1726 can function as a JAK inhibitor to control IAV infection.

15 ingly, methotrexate has been identified as a JAK/STAT inhibitor in a functional screen, causing reduc

16 Interruption of IL-6/JAK/STAT3 pathway by a JAK inhibitor AZD1480 reverses the pro-metastatic effect

17 On the other hand, a JAK inhibitor and an IL-7-blocking antibody decreased th

18 ed what we believe to be a new function of a JAK inhibitor, filgotinib, that suppresses HIV-1 splicin

19 rvations were made with Ruxolitinib (Rux), a JAK-specific inhibitor.

20 Ruxolitinib, a JAK 1 and JAK 2 inhibitor, showed superiority over best

21 ne the activity and safety of ruxolitinib, a JAK inhibitor, in adults with secondary haemophagocytic

22 mune-mediated diseases who were exposed to a JAK inhibitor.

23 the patient was treated with tofacitinib, a JAK inhibitor, leading to the rapid resolution of clinic

24 mmatory secretome of senescent cells using a JAK inhibitor (JAKi).

25 and in other malignancies driven by aberrant JAK-STAT signaling.

26 tive JAK3 specific inhibitor, which achieves JAK isoform specificity through covalent interaction wit

27 a GP130-like receptor, domeless, to activate JAK/STAT signalling in Drosophila.

28 STAT2 is a key player in the IFN-activated JAK/STAT signaling.

29 a (Ph-like ALL) is associated with activated JAK/STAT, Abelson kinase (ABL), and/or phosphatidylinosi

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

31 Activating JAK and STAT mutations were not sufficient to initiate l

32 ls and induced their migration by activating JAK/STAT3/AKT signaling.

33 nwhile, these changes involved the PI3K/AKT, JAK/STAT3, and SMAD/STAT signaling pathways.

34 Ruxolitinib, a JAK 1 and JAK 2 inhibitor, showed superiority over best available

35 okine receptor CXCR4 to recruit BCR-ABL1 and JAK kinases in close proximity.

36 c inhibitors, we show that both PI3K/AKT and JAK/STAT5 pathways are activated and functionally import

37 y components in the TGF-beta, GDNF, AKT, and JAK-STAT signaling pathways.

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

39 signaling factors for the WNT, TGF-beta, and JAK/STAT pathways use their intrinsically disordered reg

40 inflammation in fibrosis-driving cells, and JAK/STAT activation in both megakaryocytes and stromal c

41 Thus CRYs link the circadian clock and JAK-STAT signaling through control of STAT5B phosphoryla

42 ansion and expansion/survival cytokines, and JAK/STAT pathways.

43 ally, we demonstrate that STAT3 deletion and JAK/STAT inhibition in macrophages increases expression

44 in the time scales of the JAK-dependent and JAK-independent pathways was found to be the main contri

45 as blunted with decreased MX1 expression and JAK activation.

46 CR kinases, second-messenger generation, and JAK/STAT or NFAT transcriptional responses.

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

48 on of genes involved in RNAi, Toll, Imd, and JAK-STAT pathways, but the majority of differentially ex

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

50 F produces CXCL13 and that the NF-kappaB and JAK/STAT pathways are required to induce the expression

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

52 genes and was able to inhibit NF-kappaB and JAK/STAT pathways.

53 a, in which RNA interference, NF-kappaB, and JAK-STAT pathways underlie antiviral immunity.

54 nd IL-22-induced phosphorylation of MAPK and JAK-STAT pathways, and activation of the NF-kappaB pathw

55 a role in myeloproliferative neoplasms, and JAK inhibitors are now successfully used to treat myelop

56 ntifies calcium, actin, Ras, Raf1, PI3K, and JAK as key regulators of cardiac mechano-signaling and c

57 Thus, RTK and JAK-STAT-driven proliferation pathways are parallel; tho

58 Are the receptor tyrosine kinase (RTK) and JAK-STAT-driven proliferation pathways 'parallel' or 're

59 JAK1/2 inhibitors (such as ruxolitinib and JAK inhibitor I) strongly stimulate VSV replication and

60 60c (MTGNB) along with activation of Wnt and JAK/STAT signaling.

61 nical profile compared to currently approved JAK inhibitors.

62 dysregulation of signaling pathways such as JAK-STAT3 that could be targeted to improve treatment of

63 Adult muscles show basal JAK-STAT signalling activity in the absence of any immun

64 r-dependent type I IFN synthesis followed by JAK/STAT-dependent interferon-stimulated gene expression

65 inhibition of VZV replication is mediated by JAK/STAT1 signaling.

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

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

68 difications mentioned above to the canonical JAK-STAT pathway are necessary to reproduce this behavio

69 Current clinical JAK inhibitors target the tyrosine kinase domain and lac

70 Combined JAK/MEK inhibition suppressed MEK/ERK activation in Jak2

71 Most importantly, combined JAK/BET inhibition resulted in a marked reduction in the

72 administration fully rescued the compromised JAK-STAT3 pathway and reactive astrogliosis, and reverse

73 id leukemia (aCML) resulting in constitutive JAK-STAT signaling.

74 nic driver mutations leading to constitutive JAK-STAT activation, the cellular and molecular biology

75 L in cytokine receptor-like factor 2 (CRLF2)/JAK-mutant models with mean 92.2% (range, 86.0%-99.4%) r

76 datolisib and ruxolitinib treatment of CRLF2/JAK-mutant models more effectively inhibited ALL prolife

77 orders, giving rise to a new class of drugs, JAK inhibitors (or Jakinibs).

78 its the efficacy of JAK2 inhibition and dual JAK/MEK inhibition provides an opportunity for improved

79 In this region, local endogenous JAK-STAT and JNK signaling creates a tissue microenviron

80 e inhibitors with high potency and excellent JAK family subtype selectivity.

81 alpha/beta expression or signaling following JAK/STAT inhibition may control catastrophic hyperinflam

82 es, including iNOS, by suppressing IFN-gamma-JAK-STAT1 transcription-factor signaling while supportin

83 at ZDHHC5 and ZDHHC8 were required for Gp130/JAK/STAT3, but not DLK/JNK, axon-to-soma signaling.

84 Signals via the Gp130/JAK/STAT3 and DLK/JNK pathways are important for axonal

85 y of these proteins thus interfering with he JAK/STAT pathway and reducing their ability to inhibit t

86 ion, focusing on Drosophila and highlighting JAK/STAT pathway functions in proliferation, survival an

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

88 However, JAK inhibition is associated with an increased infection

89 Paracrine IL6/JAK/STAT3-mediated HT resistance was confirmed in patien

90 protein, specifically the p22 form, impedes JAK-STAT signaling to help the virus evade the host inna

91 re linked to differential gene expression in JAK-STAT signaling, NADPH oxidation, and other cancer-re

92 broad-spectrum immunosuppression, including JAK-STAT inhibitors, and sheds light on an additional ne

93 in 36 GO terms and 6 KEGG pathways including JAK/STAT signaling pathway.

94 identified correlates of severity, including JAK/STAT, prolactin, and interleukin 9 signaling.

95 Type I IFNs induce JAK-STAT signaling and expression of IFN-stimulated gene

96 We recently reported that cytokine-induced JAK/STAT signaling mediates DEX resistance in T cell acu

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

98 Infection-induced JAK-STAT pathway is both required and sufficient for dif

99 nds on peroxisomes and their action inducing JAK/Stat signaling and Sox21a.

100 g upregulated genes related to inflammation, JAK-STAT and TNF-alpha signaling after doxorubicin.

101 drugs with unique modes of action to inhibit JAK-STAT signalling in disease.

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

103 include cell cycle inhibitors and interferon-JAK-STAT signaling genes critically involved in tumor su

104 e that LTD at adult TA-CA1 synapses involves JAK-STAT signaling, but unlike SC-CA1 synapses, requires

105 se genes were enriched in pathways involving JAK/STAT signaling.

106 canonical gp130 signaling, SarA function is JAK-independent but requires GSK-3, a key regulator of m

107 As a member of the Janus (JAK) family of nonreceptor tyrosine kinases, TYK2 plays

108 vation of nuclear factor kappaB (NF-kappaB), JAK/STAT signaling, and programmed cell death protein 1

109 AT3 by inhibiting the upstream Janus kinase (JAK) 1 or JAK2 or by STAT3 knockdown was found to increa

110 PKR-like ER kinase (PERK) and Janus kinase (JAK) 1.

111 Janus kinase (JAK) 2 plays pivotal roles in signaling by several cytok

112 Activating Janus kinase (JAK) and signal transducer and activator of transcriptio

113 7 as a clinical target using a Janus kinase (JAK) inhibitor and an IL-7-blocking antibody.

114 The Janus kinase (JAK) inhibitor ruxolitinib is the only approved therapy

115 RNAs could be prevented by the Janus kinase (JAK) inhibitor ruxolitinib.

116 recently, clinical trials with Janus kinase (JAK) inhibitors have shown that cytokine receptors that

117 To identify Janus kinase (JAK) inhibitors that selectively target gastrointestinal

118 In organoids, inhibitors of Janus kinase (JAK) signaling via STAT1 (glucocorticoids, tofacitinib,

119 on activation of the canonical Janus kinase (JAK)-signal transducer and activator of transcription (S

120 he nucleus, signalling via the Janus kinase (JAK)-signal transducer and activator of transcription (S

121 receptor that signals via the Janus kinase (JAK)-signal transducer and activator of transcription an

122 a inhibition of the downstream Janus kinase (JAK)-signal transducer and activator of transcription pa

123 ions resulting in constitutive Janus kinase (JAK)-STAT activation have been detected and associated w

124 Chronic activation of the Janus kinase (JAK)/signal transducer and activator of transcription (S

125 ctors induce activation of the Janus kinase (JAK)/signal transducer and activator of transcription 3

126 Upadacitinib, an oral Janus kinase (JAK)1-selective inhibitor, showed efficacy in combinatio

127 Ruxolitinib is an FDA approved janus kinase (JAK)1/2 inhibitor used to treat myeloproliferative neopl

128 ecent studies have shown that Janus kinases (JAK), JAK1, and JAK2, play an important role in IAV repl

129 Inhibitors of Janus kinases (JAKs) are being developed for treatment of inflammatory

130 Janus kinases (JAKs) are non-receptor tyrosine kinases that are essenti

131 Janus kinases (JAKs) have a key role in regulating the expression and f

132 Janus kinases (JAKs) mediate responses to cytokines, hormones and growt

133 RKs), protein kinase B (Akt), Janus kinases (JAKs), and signal transducer activator of transcription

134 Janus kinases (JAKs; JAK1 to JAK3 and tyrosine kinase 2) mediate cytoki

135 However, the signaling events linking JAKs to rho small GTPase activation by chemokines is sti

136 pivotal signaling pathways, including MAPK, JAK-STAT, and PI3K-Akt.

137 K cells demonstrate increased IL-15-mediated JAK-STAT signaling activity.

138 ings, we hypothesized that cytokine-mediated JAK/STAT signaling might similarly contribute to DEX res

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

140 Type I IFN-mediated JAK-STAT signaling is severely impaired, and activation

141 Small molecule JAK inhibitors have emerged as a major therapeutic advan

142 tibody or administration of a small-molecule JAK inhibitor, abolishes FGF19-induced tumorigenesis, wh

143 rgeting proinflammatory macrophages, but not JAK/STAT signaling, can attenuate granulomatous intersti

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

145 CDK8 kinase inhibition blocked activation of JAK-STAT pathway TFs.

146 like cytokine Upd3, leading to activation of JAK/STAT signaling, differentiation of cells that form t

147 e amplified via IFN-stimulated activation of JAK/STAT signaling.

148 use hair follicles by topical application of JAK inhibitors, suggesting that JAK-STAT signaling is re

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

150 tency of 24 is supported by demonstration of JAK-STAT and HDAC pathway blockade in hematological cell

151 ta indicate that IL-11-mediated induction of JAK/STAT3 is critical in gastrointestinal tumorigenesis

152 AK2 activity and suggests that inhibition of JAK activity contributes to its antiviral activity.

153 hors went on to show that dual inhibition of JAK and the MAP kinase pathway provided enhanced therape

154 ults demonstrate that combined inhibition of JAK/STAT signaling and LSD1 is a promising therapeutic s

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

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

157 These findings highlight the potential of JAK inhibitors to counteract stroma-induced resistance t

158 LNK (SH2B3) is a key negative regulator of JAK-STAT signaling which has been extensively studied in

159 that PTP1BDelta6 is a positive regulator of JAK/STAT signaling in cHL.

160 GF-BB production persisted in the setting of JAK inhibition.

161 aling in MPN cell survival in the setting of JAK inhibition.

162 Specifically, stimulation of JAK/STAT signaling in the muscles can rescue the deficie

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

164 he mechanisms underlying the upregulation of JAK/STAT activity in this disease context is completely

165 ator of transcription pathway and the use of JAK inhibitors to treat autoimmune and inflammatory dise

166 We thus demonstrate the utility of JAK inhibitors with low intrinsic permeability as a feas

167 iochemical assays to measure the activity of JAKs in reconstituted cells.

168 The discovery of JAKs and STATs and their roles in cytokine and IFN actio

169 Finally, pharmacologic inhibitors of JAKs and STAT5 significantly curtailed B-CLL cycling whe

170 ies into the clinic, including inhibitors of JAKs, IRAK4, RIPKs, BTK, SYK and TPL2.

171 6 expression in macrophages was dependent on JAK signaling.

172 ur findings reveal a critical perspective on JAK-STAT1 signaling that might apply to multiple inflamm

173 nomic landscape is characterized by not only JAK/STAT activating mutations but also loss-of-function

174 , which was reversed by inhibition of IL6 or JAK signaling.

175 ibition of RAS or PTPN11, but not of PI3K or JAK-signaling, prevented TSLP-induced RAS-GTP boost.

176 tream of IFN-gamma, as well as several other JAK-dependent cytokines.

177 d or topical delivery resulted in potent pan-JAK inhibitor 2 (PF-06263276), which was advanced into c

178 o the discovery of pyridone 34, a potent pan-JAK inhibitor with good selectivity, long lung retention

179 JAK1 activity and transactivates partnering JAKs, independent of its catalytic domain.

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

181 In combination with pharmacological JAK inhibition, YBX1 inactivation induces apoptosis in J

182 -inhibitor or PTPN11-inhibitor, but not PI3K/JAK-inhibitors, suggesting a unified treatment target fo

183 In the posterior, JAK/STAT works with the epidermal growth factor receptor

184 The antiapoptotic, prometastatic JAK-STAT3 pathway was activated in chemoresistant tumors

185 cal evaluation of a series of novel purinone JAK inhibitors with profiles suitable for inhaled admini

186 zoster infection among patients who received JAK inhibitors (relative risk 1.57; 95% confidence inter

187 pears differentiated from all other reported JAK inhibitors and has been advanced as the first pseudo

188 1 were sensitive to TP-0903 and ruxolitinib (JAK inhibitor) treatments, supporting the CyTOF findings

189 or IL-2Rgamma induced cell death in selected JAK inhibitor-sensitive cells.

190 The discovery of isoform selective JAK inhibitors that traditionally target the catalytical

191 tivation to enable design of novel selective JAK inhibitors.

192 as a potential target for pathway-selective JAK inhibitors in patients with diseases with unmutated

193 or Tofacitinib, a clinically used selective JAK small molecule inhibitor.

194 kine itself and related downstream signaling JAK pathway genes and the interleukin-17 (IL-17) pathway

195 Type I IFNs stimulate JAK/STAT signaling in DRG neurons but this does not appa

196 ression of IFNK transcription and subsequent JAK/STAT-dependent upregulation of several IFN-stimulate

197 o new molecules that are bispecific targeted JAK/HDAC inhibitors.

198 tigate the clinical application of targeting JAK for ALK- ALCL, we treated ALK- cell lines of various

199 t research suggests that therapies targeting JAK proteins warrant investigation in BIA-ALCL.

200 edicted the use of therapeutically targeting JAKs as a new strategy for treating immune and inflammat

201 all-molecule inhibitors, collectively termed JAK inhibitors, are US Food and Drug Administration-appr

202 ate with NP23 to induce pro-B1 ALL, and that JAK inhibitors are potential therapies for pro-B1 ALL.

203 ala et al. explored the key observation that JAK inhibition successfully suppresses MAPK activation i

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

205 However, preclinical studies have shown that JAK or PI3K pathway inhibition is insufficient to eradic

206 plication of JAK inhibitors, suggesting that JAK-STAT signaling is required for maintaining hair foll

207 The JAK gene JAK2 is frequently mutated in the ageing haemat

208 The JAK inhibitor baricitinib, used to treat rheumatoid arth

209 The JAK pathway is a potential therapeutic target in ankylos

210 The JAK-STAT pathway critically regulates T-cell differentia

211 The JAK-STAT pathway is an evolutionarily conserved signal t

212 The JAK/STAT pathway is a conserved metazoan signaling syste

213 tors of cytokine receptors that activate the JAK-STAT pathway.

214 okines that are elevated in HLH activate the JAK/STAT pathway, and the JAK1/2 inhibitor ruxolitinib (

215 was impaired as sIL6R failed to activate the JAK/STAT3 signaling pathway.

216 pha and IFN-gamma co-treatment activated the JAK/STAT1/IRF1 axis, inducing nitric oxide production an

217 c reticulum chaperone protein, activates the JAK/STAT signaling pathway via a pathogenic binding inte

218 in host antiviral response by activating the JAK/STAT (Janus kinase/signal transducer and activator o

219 In addition, the JAK-STAT3 pathway, which is critical for the induction o

220 re, we discovered that PRRSV antagonizes the JAK/STAT3 signaling by inducing degradation of STAT3, a

221 of tick immune defence pathways, such as the JAK-STAT, immune deficiency and cross-species interferon

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

223 ators are transcriptionally regulated by the JAK/STAT signaling pathways, which can be disabled by sm

224 st JAK2 and HDAC11, and is selective for the JAK family against a panel of 97 kinases.

225 d also targeted several key factors from the JAK-STAT signaling pathway, but nonimmune conditions wer

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

227 s' laboratory has shown how mutations in the JAK-STAT pathway and epigenetic regulators play a role i

228 downregulation of several components in the JAK-STAT pathway.

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

230 ess of the mutational status of genes in the JAK/STAT pathway.

231 STAT2 is indispensable in the JAK/STAT signaling since it is also involved in activati

232 tially targetable oncogenic mutations in the JAK/STAT, MAPK, MYC, and chromatin modification pathways

233 egulate cytokine signaling by inhibiting the JAK-STAT pathway.

234 In contrast, inhibiting the JAK/STAT inflammatory pathway with tofacitinib was not r

235 Tyrosine kinase 2 (TYK2) is a member of the JAK kinase family that regulates signal transduction dow

236 The difference in the time scales of the JAK-dependent and JAK-independent pathways was found to

237 Here, we review the biology of the JAK-signal transducer and activator of transcription pat

238 n vitro, further supporting the roles of the JAK-STAT pathway and herpesviruses in mediating the adve

239 s and thereby stimulated the activity of the JAK-STAT pathway in intestinal stem cells.

240 urrently available mechanistic models of the JAK-STAT pathway.

241 kinases that are essential components of the JAK-STAT signaling pathway.

242 ignificant increase in the expression of the JAK-STAT target gene Pim1 and muscles from 2-day and 3-w

243 ved E2 was critical for the induction of the JAK-STAT3 signaling pathway, as well as the A2 reactive

244 known and newly identified components of the JAK/STAT and NF-kappaB signaling pathways and frequent B

245 (59%) showed mutations in >=1 member of the JAK/STAT pathway, including STAT3 (38%), JAK1 (18%), and

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

247 r targeting shared downstream factors of the JAK/STAT pathway.

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

249 at are well-known negative regulators of the JAK/STAT pathway.

250 ion of NOS2 using the inhibitor 1400W or the JAK inhibitor tofacitinib dramatically improved the in v

251 Inhibition of heparanase or the JAK-2 pathway may reduce thrombotic risk in thalassemia.

252 es involved in chromatin modification or the JAK/STAT pathway.

253 angiotensin-regulated airway remodeling, the JAK-STAT signaling pathway, and interferon gamma.

254 he soluble receptor (sIL6R), stimulating the JAK/STAT3 signaling pathway by IL-6 trans-signaling mech

255 Previously, we reported that the JAK inhibitor ruxolitinib dampens T-cell activation and

256 utocrine and paracrine signaling through the JAK-STAT pathway, leading to the transcriptional inducti

257 pregulating Claudin-2 expression through the JAK/STAT pathway.

258 cytokines, many of which signal through the JAK/STAT signaling pathway to exert their biological eff

259 t cytokine receptors that signal through the JAK/STAT signalling pathway are important for disease, i

260 ibute to resistance of mammary tumors to the JAK/STAT inhibitor ruxolitinib in vivo and that ruxoliti

261 tead, inhibition of STAT3 activity using the JAK inhibitor ruxolitinib decreases breast cancer invasi

262 t UVB exposure, melanocytes treated with the JAK inhibitor ruxolitinib reduced expression of HMGB1 an

263 ntly reduced when mice were treated with the JAK-2 inhibitor ruxolitinib (P < 0.0001).

264 insight into the PRRSV interference with the JAK/STAT3 signaling, leading to perturbation of the host

265 relationships, such as connection within the JAK/STAT pathway, and was further validated in character

266 A knockdown, we have demonstrated that these JAK inhibitor-sensitive cells are dependent on both JAK1

267 ntrast to ruxolitinib, indicating that these JAK inhibitors in fact have a distinct target spectrum.

268 f interferon-stimulated genes (ISGs) through JAK/STAT signaling.

269 induces FLT3L expression in UC-MSCs through JAK/STAT signaling pathway.

270 y regulates hair growth by signaling through JAK-STAT5 to maintain HFSC quiescence.

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

272 rs that promote resistance of tumor cells to JAK inhibition in vitro.

273 41C and W341C/W791X exhibited sensitivity to JAK inhibitors.

274 l transducer and activator of transcription (JAK-STAT) signalling pathway in cancers, haematological

275 Transducers and Activators of Transcription (JAK/STAT) pathway is aberrantly activated and contribute

276 l transducer and activator of transcription (JAK/STAT) pathway regulates the anterior posterior axis

277 Of the regenerative treatments, JAK inhibitors and bimatoprost stimulate repopulation of

278 Pase in M2 influenced neither IL-4-triggered JAK/STAT6 nor the mTOR complex 1 signaling but strongly

279 Here, we identify a requirement for unpaired-JAK signalling as a metabolic regulator in healthy adult

280 In addition to unprecedented JAK isoform and kinome selectivity, 11 shows excellent p

281 In clinical use, JAK inhibitors have mixed effects on the overall disease

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

283 n turn upregulated expression of endocan via JAK/STAT3 and ERK/ELK cascades, thus forming a positive

284 m the microenvironment is often mediated via JAK signaling.

285 e activation of adaptive immune response via JAK/STAT signaling.

286 ype I IFN score and IL18 expression, whereas JAK/STAT inhibition strongly reduced IL-18 serum levels

287 However, whether JAK inhibitors are useful in CLL therapy has not been st

288 While JAK inhibition therapy does not seem to create a clear e

289 nalling inhibits the growth of losers, while JAK/STAT signalling promotes competition-induced winner

290 Treatment of both patients' cells with JAK inhibitors in vitro reduced phosphorylated STAT1 to

291 STAT1 phosphorylation in their NK cells with JAK inhibitors suggests a novel approach to therapy.

292 l lines of various histological origins with JAK inhibitors.

293 ersal of fibrosis to an extent not seen with JAK inhibitors.

294 y was not increased in patients treated with JAK inhibitors compared with patients given placebo or a

295 therapies markedly improve when treated with JAK inhibitors.

296 s with immune-mediated diseases treated with JAK inhibitors.

297 re not increased among patients treated with JAK inhibitors.

298 (MF) patients while receiving treatment with JAK inhibitors (mean follow-up 3.9 years).

299 es cells that persist despite treatment with JAK inhibitors to apoptosis and results in RNA mis-splic

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