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1 egulate cytokine signaling by inhibiting the JAK-STAT pathway.
2 used in leukocytes: the ITAM pathway and the Jak-STAT pathway.
3 r of IFN-alpha-induced signaling through the Jak-STAT pathway.
4 nd negatively regulate signaling through the JAK-STAT pathway.
5 restricts WNV infection by activation of the Jak-STAT pathway.
6 y reduced SOCS5 levels, leading to activated JAK-STAT pathway.
7 addition, LOS-induced IFN-beta activated the JAK-STAT pathway.
8 t, blocking type I IFN signaling through the JAK-STAT pathway.
9 tors of cytokine receptors that activate the JAK-STAT pathway.
10 e originally identified as inhibitors of the JAK-STAT pathway.
11 downregulation of several components in the JAK-STAT pathway.
12 fied as transcriptional co-regulators of the JAK-STAT pathway.
13 d), which encodes the secreted ligand of the JAK-STAT pathway.
14 urrently available mechanistic models of the JAK-STAT pathway.
15 ogical pathways, such as IL-6 signalling via JAK-STAT pathway.
16 was independent of the classical IFN-induced JAK-STAT pathway.
17 nner that was dependent on activation of the JAK/STAT pathway.
18 in genes encoding PAX5 and components of the JAK/STAT pathway.
19 its endocytosis, whereas JAK2 initiates the JAK/STAT pathway.
20 at are well-known negative regulators of the JAK/STAT pathway.
21 es involved in chromatin modification or the JAK/STAT pathway.
22 OCS) proteins are feedback inhibitors of the JAK/STAT pathway.
23 hat IL-6 induces IDO1 expression through the JAK/STAT pathway.
24 demonstrate a new neuronal function for the JAK/STAT pathway.
25 al signaling, but not the interferon-induced JAK/STAT pathway.
26 of multiple signaling pathways including the JAK/STAT pathway.
27 regulating the innate immune response is the JAK/STAT pathway.
28 pinal NMDA receptor and IL-1beta through the JAK/STAT pathway.
29 xpression or number and does not involve the JAK/STAT pathway.
30 o gain-of-function mutants in the Drosophila JAK/STAT pathway.
31 he Stat family of signal transducers via the Jak/Stat pathway.
32 or to the furrow, indicating function of the Jak/STAT pathway.
33 ess of the mutational status of genes in the JAK/STAT pathway.
34 r targeting shared downstream factors of the JAK/STAT pathway.
35 pregulating Claudin-2 expression through the JAK/STAT pathway.
36 nti-STAT3, suggesting the involvement of the JAK/STAT pathway.
37 to primary tumors, and is dependent upon the Jak/Stat pathway.
38 ia into MGPCs in the zebrafish retina is the Jak/Stat-pathway.
39 constitutive activation of the Janus kinase (JAK)/STAT pathway.
40 these genes are linked to the Janus kinase (JAK)/STAT pathway.
41 hogenetic protein (BMP) and the inflammatory JAK-STAT pathways.
42 dent mechanisms and the MAPK, NF-kappaB, and JAK-STAT pathways.
43 nes are distinct from those regulated by the JAK-STAT pathways.
44 transducers and activators of transcription (JAK-STAT) pathway.
45 l transducer and activator of transcription (JAK-STAT) pathway.
46 l transducer and activator of transcription (JAK-STAT) pathway.
47 l transducer and activator of transcription (JAK-STAT) pathway.
48 ediated sequential activation of the Src and JAK/STAT pathways.
49 ctive downregulation mechanism in EOS(A) for JAK/STAT pathways.
50 ansion and expansion/survival cytokines, and JAK/STAT pathways.
51 genes and was able to inhibit NF-kappaB and JAK/STAT pathways.
52 and survival, type I interferon (IFN-I), and JAK/STAT pathways.
53 transducers and activators of transcription (JAK/STAT) pathway.
55 te these critical upstream components of the Jak-Stat pathway, achieving inhibition of Stat phosphory
57 OCS) proteins are negative regulators of the JAK/STAT pathway activated by proinflammatory cytokines,
61 ed (IKK-related) kinase IKBKE expression and JAK/STAT pathway activation compose a cytokine signaling
62 pegIFN-alpha is not the result of prolonged Jak/STAT pathway activation in hepatocytes, but rather i
64 L1 expression in HNC cells in the context of JAK/STAT pathway activation, Th1 inflammation, and HPV s
65 bitor SOCS3 cooperates with IL-6 to maintain JAK/STAT pathway activation, thus contributing to leukem
69 ells (ISCs) by stimulating Wingless (Wg) and JAK/STAT pathway activities, whereas cytokine production
71 nstrate that Et/Lat negatively regulates the JAK/STAT pathway activity and can bind to Dome, thus red
72 lass II receptor families and the downstream JAK-STAT pathway along with its key negative regulators.
76 The G-CSF receptor (G-CSFR) activates the Jak/STAT pathway, although little is understood about ho
77 ified as strong inhibitors of the Drosophila JAK/STAT pathway, an effect conserved to human cells.
79 g new evidence supporting a link between the JAK-STAT pathway and cadherin-based cell-cell interactio
80 s' laboratory has shown how mutations in the JAK-STAT pathway and epigenetic regulators play a role i
81 n vitro, further supporting the roles of the JAK-STAT pathway and herpesviruses in mediating the adve
82 terferon receptors, interferon activates the JAK-STAT pathway and results in the positive feedback of
83 emonstrate a dichotomy between the classical JAK-STAT pathway and the NF-kappaB signaling pathway.
84 IFN receptor (IFNAR), there is activation of Jak-Stat pathways and also engagement of Mnk kinases.
85 lements both the transcriptional activity of Jak-STAT pathways and controls initiation of mRNA transl
86 that is down-regulated by inhibitors of the JAK/STAT pathway and enhanced by inhibitors of the Src k
88 ting form of SOCS3 (CP-SOCS3) to inhibit the JAK/STAT pathway and prevent cytokine-mediated lethal in
89 y of these proteins thus interfering with he JAK/STAT pathway and reducing their ability to inhibit t
90 of lens cell proliferation by inhibitors of JAK/STAT pathways and by the aberrant proliferation of l
93 red independently of the IL-15/IL-2Rbeta and Jak/STAT pathways and instead required IL-15Ralpha signa
95 l transducer and activator of transcription (JAK/STAT) pathway and enhanced the expression of IFN reg
96 ype I, II, and III IFNs, signals through the JAK-STAT pathway, and plays central roles in host defens
97 nd IL-22-induced phosphorylation of MAPK and JAK-STAT pathways, and activation of the NF-kappaB pathw
98 meiotic cohesin complex, via a non-canonical JAK/STAT pathway, and consequently promotes meiotic DSB
99 eins are negative-feedback regulators of the JAK/STAT pathway, and SOCS3 contributes to host immunity
100 okines that are elevated in HLH activate the JAK/STAT pathway, and the JAK1/2 inhibitor ruxolitinib (
101 relationships, such as connection within the JAK/STAT pathway, and was further validated in character
102 ading to apoptotic cell death, NF-kappaB and JAK/STAT pathways, and inflammasome-assembly mediating i
103 iviral responses, components of the Toll and JAK/STAT pathways, and serine protease inhibitors in bot
106 difications mentioned above to the canonical JAK-STAT pathway are necessary to reproduce this behavio
110 ted over the past decade have shown that the JAK/STAT pathways are involved in GH signaling to the nu
112 F produces CXCL13 and that the NF-kappaB and JAK/STAT pathways are required to induce the expression
114 nvasiveness, and migration and implicate the JAK/STAT pathway as a critical mediator of leptin action
115 is suggests the feasibility of targeting the JAK/STAT pathway as a neuroprotective therapy for neurod
116 els of MS, suggesting the feasibility of the JAK/STAT pathway as a target for neuroinflammatory disea
119 eral small-molecule inhibitors targeting the JAK/STAT pathway blocked proliferation elicited by IL-2
120 on of genes involved in RNAi, Toll, Imd, and JAK-STAT pathways, but the majority of differentially ex
121 , SOCS proteins are not only induced via the JAK/STAT pathway, but are also transcribed on triggering
122 eins introduce additional diversity into the JAK-STAT pathway by adjusting the output of activated ST
123 intron, and is induced by the IFN-triggered Jak-STAT pathway by binding of the IFN-stimulated gene f
125 ese changes result from a disturbance of the JAK/STAT pathway by hypoxia, and (3) identify JAK/STAT s
126 Here, we pursue STRA13 involvement in the JAK/STAT pathway by studying its role in STAT1 expressio
128 rs complements the function of IFN-activated JAK-STAT pathways, by allowing mRNA translation of IFN-s
129 o These results indicate that inhibiting the JAK/STAT pathway can prevent neuroinflammation and neuro
130 ization was accompanied by activation of the JAK/STAT pathway, commonly seen in megakaryocytic malign
131 bit enhanced and prolonged activation of the JAK/STAT pathway compared with macrophages from SOCS3(fl
132 ese included components of the Toll, Imd and JAK/STAT pathways, consistent with interactions between
133 e controlled by the evolutionarily conserved JAK-STAT pathway contributes to the antiviral host defen
135 ervations suggest that autoregulation of the Jak-STAT pathway controls the onset of astrogliogenesis.
138 of autocrine interleukin-10, which activates JAK/STAT pathway-dependent tyrosine phosphorylation of S
139 transducers and activators of transcription (JAK/STAT) pathway determines cell fates by regulating ge
140 first documentation that suppression of the JAK/STAT pathway disrupts the circuitry of neuroinflamma
142 s, suggesting that PIV-3 interferes with the JAK/STAT pathway downstream of the IFN-lambdaR1/IL-10R2
144 is the first to characterize a role for the JAK/Stat pathway during cardiogenesis and identifies an
149 ion, focusing on Drosophila and highlighting JAK/STAT pathway functions in proliferation, survival an
150 ly understood, although the cytokine-induced Jak-STAT pathway has been postulated to regulate astrogl
154 2V617F mutation, additional mutations in the JAK-STAT pathway have been discovered including a series
155 s that control their actions, members of the Jak-Stat pathway, ideal targets for pharmacological inte
156 rmine the role of the Janus tyrosine kinase (JAK)-STAT pathway in NF-kappaB activation by IFN, we exa
158 s BCR-ABL, underscores the importance of the JAK-STAT pathway in both normal cellular development and
161 udies identified additional mutations in the JAK-STAT pathway in some patients with JAK2V617F(-) MPD,
162 results implicate the inflammatory IFN-alpha/Jak-Stat pathway in the developmental maturation of embr
163 li cell co-cultures, and direct study of the JAK-STAT pathway in these models and in L cells transfec
167 l Transducer and Activator of Transcription (JAK-STAT) pathway in two adjacent types of stem cells: g
169 okine signaling (SOCS) which can inhibit the JAK/STAT pathway in a classical negative-feedback manner
173 by deregulation of several components of the Jak/STAT pathway in early carcinogenesis, then upregulat
174 re we demonstrate aberrant activation of the JAK/STAT pathway in ETP-ALL blasts relative to non-ETP T
175 potential therapeutic value of targeting the JAK/STAT pathway in lymphoma in the clinical setting.
176 in a male-specific manner, and activates the JAK/STAT pathway in male germ cells at the time of gonad
177 In vitro, alpha-SYN exposure activated the JAK/STAT pathway in microglia and macrophages, and treat
179 y is the first to demonstrate a role for the JAK/STAT pathway in regional specification by acting ant
182 nstrate the ubiquitous activation of Ras and Jak/Stat pathways in HCC and suggest the potential use o
185 l transducer and activator of transcription (JAK/STAT) pathways in MMP induction by B. burgdorferi.
186 transducers and activators of transcription (JAK/STAT) pathway, in adult retinal ganglion cells (RGCs
187 (59%) showed mutations in >=1 member of the JAK/STAT pathway, including STAT3 (38%), JAK1 (18%), and
188 Furthermore, F-actin is regulated by the Jak/STAT pathway-increasing or decreasing pathway activi
190 Our findings document that inhibition of the JAK/STAT pathway influences both innate and adaptive imm
200 Although the discovery of mutations in the JAK-STAT pathway is important from a pathogenetic and di
201 ssential to cytokine receptor signaling, the JAK-STAT pathway is one of the best understood signal tr
204 Previous genetic studies showed that the JAK-STAT pathway is required for full activation of the
207 es in salivary glands and hemolymph when the JAK-STAT pathway is suppressed by RNA interference.
208 to dengue virus infection increases when the JAK-STAT pathway is suppressed through RNAi depletion of
210 tors discovered in cytokine signaling of the JAK-STAT pathway is the suppressor of cytokine signaling
215 established roles in cytokine signaling, the JAK/STAT pathway is involved in synaptic plasticity in t
220 nversely, cytokine signaling through cognate Jak/STAT pathways is reportedly unaffected or even stimu
221 Transducers and Activators of Transcription (JAK/STAT) pathway is aberrantly activated and contribute
222 l transducer and activator of transcription (JAK/STAT) pathway is one of the key signaling cascades i
224 ncomitant genomic alterations activating the JAK-STAT pathway (JAK1, JAK2, IL7R) identified in 63 pat
225 e showed an increased activation of the IL-6-JAK-STAT pathway leading to a systemic lupus erythematos
226 utocrine and paracrine signaling through the JAK-STAT pathway, leading to the transcriptional inducti
227 transducers and activators of transcription (JAK/STAT) pathway, leading to elevated transcription of
228 eling process, demethylation of genes in the JAK-STAT pathway leads to an enhanced activation of STAT
230 leads to ectopic production of the mitogenic JAK-STAT pathway ligand Unpaired, which is secreted from
231 division by repressing the expression of the JAK-STAT pathway ligand Upd3 in differentiating enterobl
232 ell reservoir: through Imd signaling and the Jak/Stat pathway ligand Upd3, hemocytes act as sentinels
233 ions for FSCs depends on gradients of Hh and JAK-STAT pathway ligands, which emanate from opposite, d
235 l transducer and activator of transcription (Jak-STAT) pathway maintains stem cells; germline stem ce
236 ur findings provide direct evidence that the JAK/STAT pathway mediates a key signal from the somatic
239 efficacy were independent of the presence of JAK/STAT pathway mutations, raising the possibility that
241 vestigate the possible role of TNF-alpha and JAK/STAT pathway on de novo lipogenesis and PCSK9 expres
242 ited by blockade of the NF-kappaB, PI3K, and JAK-STAT pathways or the presence of neutralizing anti-I
243 l transducer and activator of transcription (JAK-STAT) pathways, or indirectly via changes in the tum
245 gamma receptor-dependent cytokines and their JAK/STAT pathways play pivotal roles in T cell immunity.
247 f complementary approaches, we show that the JAK/STAT pathway plays an essential role in the inductio
249 ytokine signaling via a restricted number of Jak-Stat pathways positively and negatively regulates al
252 receptor (IL-7R), via its activation of the JAK-STAT pathway, promotes gene programs that change dyn
253 l transducer and activator of transcription (JAK/STAT) pathway provides a sex-specific signal from th
255 identified, and partially characterized, two JAK-STAT pathway-regulated and infection-responsive deng
258 E loss-of-function alleles, we show that the JAK/Stat pathway regulates tin expression prior to heart
259 l transducer and activator of transcription (JAK/STAT) pathway regulates the anterior posterior axis
261 mphoma (DLBCL), we observed higher levels of JAK/STAT pathway-related serum cytokines (ie, IL-6, IL-1
264 , IRF3, Tbk1, extracellular IFNbeta, and the Jak-Stat pathway resulted in reduced activity of GCV and
265 e culture sections through activation of the JAK/STAT pathway, resulting in increased activity of iNO
266 , whereby IFN-alpha/beta signals through the Jak/STAT pathway, resulting in the establishment of the
268 rved molecular mechanism that directly links JAK/STAT pathway signalling to intercellular adhesion an
271 f IFN-alpha therapy are likely to act at the JAK-STAT pathway that controls transcription of downstre
273 ne signaling-3 (SOCS3), 2 key factors of the JAK/STAT pathway that induce and inhibit STAT3 activatio
274 K)1/2, but not induction of apoptosis or the JAK/STAT pathway that is necessary for the antiviral eff
275 f immune responses, and dysregulation of the JAK/STAT pathway, that is, hyperactivation, has patholog
276 presses the activation of the astrogliogenic Jak-Stat pathway, the underlying molecular mechanism was
279 the expression of various components of the Jak-STAT pathway to strengthen STAT signaling and trigge
280 ontribution of the small interfering RNA and JAK-STAT pathways to the control of viral infections, we
281 find that the microRNA miR-279 regulates the JAK/STAT pathway to drive rest:activity rhythms in Droso
285 ediated through the diffusible ligand of the Jak/STAT pathway, Unpaired (Upd), which was recently ide
286 signaling factors for the WNT, TGF-beta, and JAK/STAT pathways use their intrinsically disordered reg
287 the therapeutic potential of inhibiting the JAK/STAT pathway using the JAK1/2 inhibitor, AZD1480.
288 concentrations of pegIFN-alpha in serum, the Jak/STAT pathway was activated in hepatocytes only on th
290 l transducer and activator of transcription (Jak/Stat) pathway was discovered 20 years ago as a media
291 aling 3 (SOCS3), a protein suppressor of the JAK-STAT pathway, was constitutively highly expressed an
292 the dynamical behavior of the HER4 mediated JAK-STAT pathway which could be useful in designing trea
293 acts on interferon-stimulated genes via the JAK-STAT pathway, which has been implicated in developme
294 es 24p3 expression through activation of the JAK/STAT pathway, which culminates in binding of Stat5 t
295 entricles of adult rats did not activate the JAK/STAT pathway, which is potentially due to increased
297 ale soma signals to the germline through the JAK/STAT pathway, while the nature of the signal from th
300 pothesis that using these drugs to block the JAK-STAT pathway would prevent autoimmune diabetes.