ライフサイエンスコーパス: JAK

1 JAK (Janus family of cytoplasmic tyrosine kinases) famil

2 JAK inhibitor sensitivity correlated with the STAT3 phos

3 JAK inhibitor suppressed senescent cell activin A produc

4 JAK inhibitors may be a viable therapeutic option for th

5 JAK kinase inhibitors have depressed leukemic T cell lin

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

7 JAK-STAT signaling mediates the actions of numerous cyto

8 JAK-STAT signaling was critical for TA-CA1 LTD as inhibi

9 ta reveal a signaling framework wherein IL-2-JAK-controlled pathways coordinate with IL-2-independent

10 We identified an IL-2-JAK-independent SRC family Tyr-kinase-controlled signali

11 transducer and activator of transcription 3 (JAK/STAT3) signalling plays an important role in atheros

12 d c-myc signaling circuit linked to the IL-6-JAK-STAT3 pathway essential for the tumorigenesis of the

13 f the major downstream effectors in the IL-6-JAK-STAT3 pathway.

14 h contributes to hyperactivation of the IL-6-JAK-STAT3 signaling important for the pathogenesis of MM

15 ur results suggest that LNK suppresses IL-7R/JAK/STAT signaling to restrict pro-/pre-B progenitor exp

16 , hybrid synthekine ligands that dimerized a JAK/STAT cytokine receptor with a receptor tyrosine kina

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

18 ed the efficacy and safety of momelotinib, a JAK 1 and JAK 2 inhibitor, versus best available therapy

19 AK-STAT) signaling pathway by ruxolitinib, a JAK-STAT-specific inhibitor.

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

21 Taken together, aberrant JAK/STAT3 signaling epigenetically silences a potential

22 While aberrant JAK/STAT signaling is crucial to the development of gast

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

24 tions of CRLF2, JAK2, and EPOR that activate JAK/STAT signaling.

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

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

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

28 rs accumulate additional mutations affecting JAK/STAT signaling, protein translation, and epigenetic

29 ed a uniform and specific sensitivity to all JAK inhibitors tested irrespective of their CSF3R mutati

30 n mutations were found in some, but not all, JAK inhibitor-sensitive cells.

31 icacy and safety of momelotinib, a JAK 1 and JAK 2 inhibitor, versus best available therapy (BAT) in

32 signaling pathways AKT, NFkappaB, ERK1/2 and JAK/STAT.

33 or diurnal rhythmicity of insulin action and JAK/STAT signaling in adipose tissue.

34 vestigate the possible role of TNF-alpha and JAK/STAT pathway on de novo lipogenesis and PCSK9 expres

35 din-inducing pathways, including the BMP and JAK/STAT3 pathways.

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

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

38 dependent processes, apical delamination and JAK/STAT activation, are concurrently required for the i

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

40 athway inhibitors to perturb ABL1, FLT3, and JAK TK signaling in four xenografted patient samples.

41 tivator of the Rho family small GTPases, and JAK/STAT is activated ectopically in these coldspot nTSG

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

43 ed with inflammatory bowel disease (IBD) and JAK inhibitors are being evaluated for therapy targeting

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

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

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

47 bers of main immune pathways (Toll, Imd, and JAK/STAT), and immune effectors in P. xylostella in resp

48 itors of cytokine-receptor interactions, and JAK kinase inhibitors that may revolutionize therapy for

49 synergistic administration of PI3K/mTOR and JAK inhibitors further abrogated leukemia development.

50 naling pathways, including PI3K/Akt/mTOR and JAK/STAT.

51 d lateral diffusion in lipid nanodomains and JAK/STAT signaling in patient cells, whereas adding gale

52 signaling and that combined PI3K pathway and JAK inhibition or PI3K pathway and SRC/ABL inhibition wo

53 ctivation of AMPK is independent of PI3K and JAK activity.

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

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

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

57 and suggest targeting pre-BCR signaling and JAK kinases as potential therapeutic strategies.

58 cardiac factors along with canonical Wnt and JAK/STAT signaling reprogrammed adult mouse cardiac, lun

59 60c (MTGNB) along with activation of Wnt and JAK/STAT signaling.

60 Unexpectedly, another JAK inhibitor, ruxolitinib (RUX), was ineffective in 8 o

61 thout suppressing the kinase activity of any JAK.

62 As JAK pathway-mediated cytokine regulation varies across c

63 there is indirect positive feedback between JAK/STAT and insulin signaling in the muscles.

64 d cap-dependent protein translation, blocked JAK-STAT signaling, and markedly attenuated NFkappaB-dep

65 Surprisingly, both JAK/STAT pathway activation and ruxolitinib efficacy wer

66 we find that Et/Lat is able to bind to both JAK and STAT92E but, despite the presence of putative cy

67 create bispecific single molecules with both JAK and HDAC targeted inhibition.

68 y the onset of pupariation, is controlled by JAK/STAT signaling in early regenerating discs.

69 RS cells, and their expression was driven by JAK-STAT and NFkappaB activity.

70 orylation of these GEFs is fully mediated by JAK protein tyrosine kinases.

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

72 ata indicate an essential role for canonical JAK-STAT signaling in activity-dependent LTD at TA-CA1 s

73 correlation analysis links PinT to host cell JAK-STAT signalling, and we identify infection-specific

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

75 However, unlike common JAK-STAT pathway inhibitors, BRD0476 inhibits JAK-STAT s

76 Consistently, JAK/STAT3 pathway inhibition impaired cell growth in vit

77 Constitutive JAK/STAT signaling is crucial for survival and prolifera

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

79 ugh the molecular basis of this constitutive JAK/STAT signaling in cHL has not been completely unders

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

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

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

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

84 In diffuse large B-cell lymphomas (DLBCLs), JAK signaling is a feature of the activated B-cell (ABC)

85 ds and docking sites for required downstream JAK/STAT proteins.

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

87 her, these data suggest that cytokine-driven JAK-mediated signals, provided by CML cells and/or the m

88 stitutively activated form of the Drosophila JAK kinase (hop(Tum-l)) promotes Madm nuclear translocat

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

90 ol compounds for further exploration of dual JAK-HDAC pathway inhibiton achieved with a single molecu

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

92 survival and fate, specifically PDGFR, ERK, JAK STAT, MAPK, and TCR/NF-kappaB signaling; epigenetic

93 K3/STAT6 and we propose a potential role for JAK inhibitors in combination with BCR kinase inhibitors

94 y those patients most likely to benefit from JAK/STAT targeted chemotherapies.

95 However, the presence of a functional JAK-binding box within IL-31Ralpha is an essential prere

96 o erythropoietin stimulation, and heightened JAK-STAT activation.

97 and stimulation conditions, we examined how JAK signaling and IBD-associated JAK2 variants regulate

98 dose of leptin, the duration of hypothalamic JAK/STAT3 signalling is increased, resulting in enhanced

99 s were sensitive to CHZ868, including type I JAK inhibitor persistent cells.

100 d that MPN cells become persistent to type I JAK inhibitors that bind the active conformation of JAK2

101 0(-8)) and used pathway analysis to identify JAK-STAT/IL12/IL27 signalling and cytokine-cytokine path

102 These data demonstrate that type II JAK inhibition is a viable therapeutic approach for MPN

103 Importantly, JAK inhibitors increased proinflammatory cytokines secre

104 rgeting of specific cell types might improve JAK-targeted therapy in immune-mediated diseases.

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

106 itinib in other clinical contexts, including JAK-mutated acute lymphoblastic leukemia (ALL).

107 tations in key signaling pathways, including JAK-STAT, NOTCH and NF-kappaB, have also been defined, t

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

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

110 inactivation of Mac-1 promotes IL-13-induced JAK/STAT activation in macrophages, resulting in enhance

111 interferon-gamma- and interleukin-4-induced JAK/STAT activity in HEK293 or HEK293-STAT6 cells, and o

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

113 as by an application to data for Epo-induced JAK/STAT signaling.

114 on through inhibiting the interferon-induced JAK-STAT signaling pathway, a key antiviral pathway invo

115 s phenotype is mediated by Nol3(-/-)-induced JAK-STAT activation and downstream activation of cyclin-

116 xpression in CML LTHSCs reduced THPO-induced JAK/STAT signaling and leukemogenic potential.

117 AK-STAT pathway inhibitors, BRD0476 inhibits JAK-STAT signaling without suppressing the kinase activi

118 uscle contraction, focal adhesion, integrin, JAK/STAT, MAPK, growth factor, and p53 signaling pathway

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

120 e fat body through the cytokine Upd3 and its JAK/STAT-coupled receptor, Domeless.

121 rphogenetic protein (BMP), Jun kinase (JNK), JAK/STAT, Notch, Insulin, and Wnt, revealed that many li

122 Janus kinase (JAK) 1/JAK2 inhibitors are in development or clinical us

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

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

125 aling inhibitor tofacitinib, a Janus kinase (JAK) inhibitor targeting JAK3 and JAK1.

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

127 fication of structurally novel Janus kinase (JAK) inhibitors predicted to bind beyond the ATP binding

128 itions enhanced sensitivity to Janus kinase (JAK) inhibitors.

129 -RBP can activate STRA6-driven Janus kinase (JAK) signaling and downstream induction of signal transd

130 The Janus kinase (JAK) system is involved in numerous cell signaling proce

131 The Janus kinase (JAK)-signal transducer and activator of transcription (S

132 tions in cytokine receptor and Janus kinase (JAK)/signal transducer and activator of transcription (S

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

134 RESPONSE study, ruxolitinib, a Janus kinase (JAK)1 and JAK2 inhibitor, was superior to best available

135 ric cell surface receptors via Janus Kinase (JAK/TYK), or Receptor Tyrosine Kinase (RTK)-mediated tra

136 Janus kinases (JAKs) classically signal by activating STAT transcriptio

137 The data revealed that Janus kinases (JAKs) couple IL-2 receptors to the coordinated phosphory

138 l functions of their upstream Janus kinases (JAKs) during postnatal development are less well defined

139 The Janus kinases (JAKs) transduce signals initiated following engagement o

140 3K-AKT, the leukemia inhibitory factor (LIF)-JAK-STAT3 axis, Wnt-GSK3 signalling, and the transformin

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

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

143 Moreover, JAK inhibitors were effective in prolonging survival of

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

145 activation or reduced expression of negative JAK/STAT regulators such as silencer of cell signaling 1

146 pression along with suppression of NFkappaB, JAK/STAT and PI3K pathways.

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

148 vation is mediated by the combined action of JAK, SRC, c-ABL, and JNK kinases.

149 uired for mutant CALR-mediated activation of JAK-STAT signaling.

150 We find that chronic activation of JAK/Stat signaling in the aging gut induces a metaplasia

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

152 ch is facilitated by HER2/HER3 activation of JAK/STAT signaling.

153 d -13, leading to constitutive activation of JAK/STAT signaling.

154 g to reduced phosphorylation (activation) of JAK and STAT1.

155 s study provides new leads for assessment of JAK and HDAC pathway dual inhibiton achieved with a sing

156 Methotrexate might bring the benefits of JAK/STAT pathway inhibition at a lower cost.

157 L1 expression in HNC cells in the context of JAK/STAT pathway activation, Th1 inflammation, and HPV s

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

159 ive potency is supported by demonstration of JAK-STAT and HDAC pathway blockade in several hematologi

160 work has been dedicated to the discovery of JAK kinase inhibitors resulting in several compounds ent

161 Toward this end, we examined the effects of JAK inhibition using a model of primary (inherited) HLH

162 servations also support the incorporation of JAK inhibitors such as ruxolitinib into future clinical

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

164 As small molecule inhibition of JAK activity disrupted CEBPbeta induction and reduced G-

165 sought to examine whether the inhibition of JAK function might lessen inflammation in murine models

166 was critical for TA-CA1 LTD as inhibition of JAK or STAT blocked LTD induction and prevented NMDA-ind

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

168 Accordingly, inhibition of JAK/Stat signaling in the CCR specifically prevents age-

169 ry of 2000 small molecules for modulators of JAK/STAT pathway activation.

170 We propose that overactivation of JAK-STAT signaling is part of the mechanism underlying d

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

172 efficacy were independent of the presence of JAK/STAT pathway mutations, raising the possibility that

173 es responded to JAK inhibition regardless of JAK mutation status.

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

175 AT3 (PIAS3) is the key negative regulator of JAK/STAT3 signalling.

176 encourages further discussion on the role of JAK-STAT signaling in the various stem cell niches of th

177 ional studies underscore the central role of JAK/STAT signaling in myeloproliferative neoplasms (MPNs

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

179 tatus, indicating a general sensitization of JAK-STAT signaling in this leukemia subset.

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

181 TEER can be suppressed with the treatment of JAK inhibitors.

182 ndence from MEK/ERK signaling, dependence on JAK/STAT3 and BMP4 signaling, and naive-specific transcr

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

184 y phosphorylation-defective STAT3 mutants or JAK inhibitor blocked STAT3 binding to myoferlin and nuc

185 e 3 Controlled Myelofibrosis Study with Oral JAK Inhibitor Treatment-I trial, patients with MF, post-

186 , JAK2 or EPOR rearrangements (12.4%), other JAK-STAT sequence mutations (7.2%), other kinase alterat

187 usions in 8.8%, alterations activating other JAK-STAT signaling genes (IL7R, SH2B3, JAK1) in 6.3% or

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

189 of indazoles was identified as selective pan-JAK inhibitors with a type 1.5 binding mode.

190 d in cutaneous T-cell lymphoma pathogenesis, JAK/STAT signaling, we used conditional gene targeting t

191 of abrogating JH2 ATP binding in pathogenic JAK mutants may warrant novel therapeutic approaches.

192 Among the immune/inflammation pathways, JAK/Stat and IL-17A signaling were the most significantl

193 n, which results in cell cycle perturbation, JAK/STAT signal activation, and differential regulation

194 nd this defect is rescued by pharmacological JAK inhibition.

195 matched Q-HB, with increased phosphorylated JAK-2 largely confined to the stromal cells in clusters

196 I interferon (IFN-I) response by preventing JAK-STAT signaling, suggesting that suppression of this

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

198 1 and TAZ in acinar cells, which up-regulate JAK-STAT3 signaling to promote development of PDAC in mi

199 ghboring ISCs non-autonomously by regulating JAK/STAT signaling.

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

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

202 or homeostasis by attenuating IL-7-stimuated JAK/STAT5 signaling via a direct interaction with phosph

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

204 ibiting its enzymatic activity and targeting JAK for proteasomal degradation.

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

206 ine phosphatases and show that, by targeting JAKs, PTPRG downmodulates the rapid activation of integr

207 on in ageing muscle, including Wnt, TGFbeta, JAK/STAT and senescence signalling.

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

209 The insight that JAK/STAT system activation is pervasive in T cell malign

210 Legrand et al show that JAK/STAT5 signaling in the dermal papilla is required fo

211 Built on these findings, we showed that JAK inhibitor (JAKi) significantly reduced aberrant HSPC

212 Interestingly, others have shown that JAK-inhibition is able to induce telogen-to-anagen trans

213 Together, our data suggest that JAK and Aurora kinase inhibitors should be further explo

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

215 The JAK inhibitor tofacitinib effectively suppresses tissue-

216 The JAK-STAT3 pathway was a downstream effector of KRAS sign

217 The JAK/STAT pathway is a highly conserved regulatory module

218 The JAK/STAT pathway is critical for development, regulation

219 In vitro, alpha-SYN exposure activated the JAK/STAT pathway in microglia and macrophages, and treat

220 ncomitant genomic alterations activating the JAK-STAT pathway (JAK1, JAK2, IL7R) identified in 63 pat

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

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

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

224 e CRLF2(+) group identified mutations in the JAK-STAT and Ras pathway in 85% of patients, and 20% had

225 riptional activation of several genes in the JAK-STAT3 signaling pathway; this could be a mechanism b

226 n insertions could be mapped to genes in the JAK/STAT and MAPK pathways, confirming the ability of th

227 e replication of CSFV through inhibiting the JAK-STAT signaling pathway.

228 o These results indicate that inhibiting the JAK/STAT pathway can prevent neuroinflammation and neuro

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

230 oss-talk among enriched pathways, mainly the JAK/STAT signalling pathway and the EGF receptor signall

231 rts, illuminating the molecular basis of the JAK-cytokine receptor association.

232 receptor (IL-7R), via its activation of the JAK-STAT pathway, promotes gene programs that change dyn

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

234 racterised by pathological activation of the JAK/STAT (Janus kinase and signal transducer and activat

235 OCS) proteins are negative regulators of the JAK/STAT pathway activated by proinflammatory cytokines,

236 that is down-regulated by inhibitors of the JAK/STAT pathway and enhanced by inhibitors of the Src k

237 first documentation that suppression of the JAK/STAT pathway disrupts the circuitry of neuroinflamma

238 Given the importance of the JAK/STAT pathway in activating microglia and inducing cy

239 Our findings document that inhibition of the JAK/STAT pathway influences both innate and adaptive imm

240 Importantly, inhibition of the JAK/STAT pathway prevented the degeneration of dopaminer

241 f immune responses, and dysregulation of the JAK/STAT pathway, that is, hyperactivation, has patholog

242 nti-STAT3, suggesting the involvement of the JAK/STAT pathway.

243 inhibited monkeys revealed engagement of the JAK/STAT signaling pathway, suggesting alternative gamma

244 overexpress the endogenous inhibitor of the JAK/STAT3 pathway [suppressor of cytokine signaling 3 (S

245 uding IL-11 production and activation of the JAK/STAT3 pathway in tumor epithelia concomitant with pr

246 s lead to the constitutive activation of the JAK/STAT3 pathway, which was proved oncogenic.

247 th either the PI3K inhibitor LY294002 or the JAK inhibitor CP-690550, suggesting that IL-10-mediated

248 nstrate that Et/Lat negatively regulates the JAK/STAT pathway activity and can bind to Dome, thus red

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

250 Targeting the JAK pathway holds promise for treating age-related dysfu

251 is suggests the feasibility of targeting the JAK/STAT pathway as a neuroprotective therapy for neurod

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

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

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

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

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

257 vival, but were not previously linked to the JAK/STAT or MAPK pathways nor shown to functionally cont

258 Taken together, the JAK signaling threshold determines whether PRR-induced p

259 ng reporters, demonstrating that it uses the JAK-STAT signaling pathway.

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

261 (-) cystine and glutamate antiporter via the JAK/STAT1 pathway.

262 In this study, we examined whether the JAK/STAT3 pathway promotes astrocyte reactivity in sever

263 ow that treating CADM1 null tumours with the JAK/STAT inhibitor ruxolitinib mimics CADM1 gene restora

264 s, suggesting that PIV-3 interferes with the JAK/STAT pathway downstream of the IFN-lambdaR1/IL-10R2

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

266 Collectively, these findings highlight the JAKs as novel, druggable targets for mitigating the cyto

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

268 diagnosis and the development of therapeutic JAK inhibitors.

269 Therefore, JAK inhibitor therapy might benefit patients with ALK- A

270 thymic stromal lymphopoietin regulated these JAK-dependent outcomes in myeloid cells.

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

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

273 r receptor gene CSF3R, which signals through JAK-STAT proteins.

274 sitivity of JAK1-mutated primary SS cells to JAK inhibitor treatment.

275 ests a greater role of MAPK/PI3K compared to JAK/STAT with the orphan nuclear receptor RXRalpha playi

276 cytokine-independent cell lines responded to JAK inhibition regardless of JAK mutation status.

277 ined AML subset, which uniformly responds to JAK inhibitors and paves the way to personalized clinica

278 T cells, which were exquisitely sensitive to JAK and Aurora kinase inhibitors.

279 s with EPOR rearrangements were sensitive to JAK-STAT inhibition, suggesting a therapeutic option in

280 bitor treatment but increased sensitivity to JAK inhibitors.

281 41C and W341C/W791X exhibited sensitivity to JAK inhibitors.

282 l transducer and activator of transcription (JAK-STAT) pathways, or indirectly via changes in the tum

283 l transducer and activator of transcription (JAK-STAT) signaling pathway by ruxolitinib, a JAK-STAT-s

284 l transducer and activator of transcription (JAK/STAT) activation by IFN-gamma could not occur.

285 l transducer and activator of transcription (JAK/STAT) signaling activity.

286 transducers and activators of transcription (JAK/STAT) signaling via the IL-22 receptor, resulting in

287 tory cytokines at lower therapeutically used JAK inhibitor doses.

288 ot fully delineated, and clinically utilized JAK inhibitors have limited ability to reduce disease bu

289 Whereas the vertebrate JAK/STAT signaling cascade is transduced via multiple re

290 drate metabolism in the infected animal, via JAK/STAT and insulin signaling in the muscles, and that

291 mutants, blocked IFNG-induced signaling via JAK and STAT.

292 ogical pathways, such as IL-6 signalling via JAK-STAT pathway.

293 However, it is unclear whether JAK-STAT signaling also regulates excitatory synaptic fu

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

295 persphosphorylation and signaling along with JAK-dependent upregulation of antiapoptotic proteins Bcl

296 b in ETP-ALL extends beyond those cases with JAK mutations.

297 ras/Irs-1(+/+) and Kras/Irs-1(-/-) mice with JAK inhibitors significantly reduced tumor burden, most

298 l lines of various histological origins with JAK inhibitors.

299 m which CM was derived had been treated with JAK inhibitors, the resulting CM was much less proinflam

300 therapies markedly improve when treated with JAK inhibitors.

301 precise mechanism of action is unclear, with JAKs being signaling hubs for several cytokines.