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1 plex stabilization related to the associated Janus kinases.
2 we discovered that miR-373 directly targets Janus kinase 1 (JAK1) and IFN-regulating factor 9 (IRF9)
3 f the FERM and SH2-like domains of the human Janus kinase 1 (JAK1) bound to a fragment of the intrace
4 is required for H(2)O(2) responsiveness, and Janus kinase 1 (JAK1) is required for adequate basal sig
5 enes encoding interferon-receptor-associated Janus kinase 1 (JAK1) or Janus kinase 2 (JAK2), concurre
6 mutations, including activating mutations of Janus kinase 1 (JAK1), in 9.1% of patients and provides
11 validation of one of these candidates, Jak1 (Janus kinase 1), a tyrosine kinase of the nonreceptor ty
12 Finally, we determined that inhibition of Janus kinase 1, inhibition of Glycogen synthase kinase 3
13 10 (IP-10), and the signaling intermediates Janus kinase 1, signal transducer and activator of trans
14 ase 2 study for the treatment of MF with the Janus kinase 1/2 (JAK1/2) inhibitor momelotinib (MMB) de
17 agues report their results on the use of the Janus kinase 1/2 (JAK1/2) inhibitor ruxolitinib in murin
20 ) transcription factor and the JAK1/2-STAT3 (Janus Kinase 1/2 - Signal Transducer and Activator of Tr
21 n of STAT1 signaling with the small-molecule Janus kinase 1/2 inhibitor ruxolitinib in vitro and in v
27 treatment with tofacitinib citrate, an oral Janus kinase 1/3 inhibitor, resulted in significant repi
28 facitinib (CP-690,550), an oral inhibitor of Janus kinases 1, 2, and 3 with in vitro functional speci
29 dogenously processed K(d)-restricted peptide Janus kinase-1(3)(5)(5)(-)(3)(6)(3) (~15,000 copies/cell
31 notypic consequence of the V617F mutation in Janus kinase 2 (encoded by JAK2), but the extent to whic
32 uired gain-of-function V617F mutation in the Janus Kinase 2 (JAK2(V617F)) is the main mutation involv
33 etic deletion in the hematopoietic system of Janus kinase 2 (JAK2) abrogates initiation of myeloproli
34 prevented the decrease of phosphorylation of Janus kinase 2 (JAK2) and phosphorylation of signal tran
35 nhibits interferon-gamma (IFN-gamma)-induced Janus kinase 2 (JAK2) and signal transducer and activati
36 sulting in a loss of downstream signaling by Janus kinase 2 (JAK2) and signal transducer and activato
37 ndocytic AMR controls TPO expression through Janus kinase 2 (JAK2) and the acute phase response signa
38 he prolactin receptor (PRLR), its associated Janus kinase 2 (Jak2) and the signal transducer and acti
40 dermal growth factor receptor (EGFR) utilize Janus kinase 2 (JAK2) as a common signaling node to tran
43 s) is the acquisition of a V617F mutation in Janus kinase 2 (JAK2) in hematopoietic stem cells (HSCs)
45 ETE also induced tyrosine phosphorylation of Janus kinase 2 (Jak2) in VSMCs, and its inhibition subst
47 ncreatic tumors were given gemcitabine and a Janus kinase 2 (JAK2) inhibitor; tumor growth was monito
50 quired for adequate basal signaling, whereas Janus kinase 2 (JAK2) is dispensable upstream of STAT3.
51 "TET2-first patients"), patients in whom the Janus kinase 2 (JAK2) mutation was acquired first ("JAK2
53 eedforward loop in which p27pT157pT198 binds Janus kinase 2 (JAK2) promoting STAT3 (signal transducer
56 on of the phosphoinositol 3-kinase (PI3K) or Janus kinase 2 (Jak2) tyrosine kinase inhibitors abolish
58 combined targeting of the BCR-ABL kinase and Janus kinase 2 (JAK2) with dasatinib and ruxolitinib, re
61 and are characterized by mutually exclusive Janus kinase 2 (JAK2), calreticulin (CALR), and myelopro
62 receptor-associated Janus kinase 1 (JAK1) or Janus kinase 2 (JAK2), concurrent with deletion of the w
64 tracytoplasmic tyrosine kinases, essentially janus kinase 2 (JAK2), which regulates MPL stability and
65 culin (CALR) mutations have been reported in Janus kinase 2 (JAK2)- and myeloproliferative leukemia (
66 red the human PRL-prolactin receptor (hPRLR)-Janus kinase 2 (JAK2)-signal transducer and activator of
67 we demonstrated that inhibition of the IL-6-Janus kinase 2 (JAK2)-STAT3-calprotectin axis with FDA-a
68 uences of Stat1 deficiency on the effects of Janus kinase 2 (JAK2)-V617F in vivo by crossing mice exp
73 ulated by retinoic acid 6" (STRA6), enhanced Janus kinase 2 (JAK2)/STAT5 cascade, up-regulated adenyl
75 patients have a gain of function mutation in Janus kinase 2 (JAK2V617F), but little is known how JAK2
76 Mice with hepatocyte-specific deletion of Janus kinase 2 (L-JAK2 KO mice) develop spontaneous stea
77 r (MPL) to induce constitutive activation of Janus kinase 2 and signal transducer and activator of tr
78 ompounds are designed to bind selectively to Janus kinase 2 and the STAT3 Src homology-2 domain, whic
80 rimary myelofibrosis carry a mutation in the Janus kinase 2 gene (JAK2), and an additional 5 to 10% h
83 x O1, extracellular signal-regulated kinase, Janus kinase 2, or signal transducers and activators of
85 he phosphorylation of Lyn, the Epo receptor, Janus kinase 2, Signal Transducer and Action of Transcri
86 d PD-L2, and their further induction through Janus kinase 2-signal transducers and activators of tran
88 s could be reversed by administration of the Janus kinase 2/3 inhibitor tofacitinib, which blocks IL-
89 d this required intact signaling through the Janus Kinase 2/phosphatidylinositol-4,5-bisphosphate 3-k
90 oid progenitors EPOR engagement of canonical Janus kinase 2/signal transducer and activator of transc
96 ing is well known to regulate lymphopoiesis, Janus kinase 3 (JAK3) also plays a critical role in prom
99 SGs was prevented through the activation of Janus kinase 3 (JAK3) by the vitamin K3 analog menadione
100 NK cells on SIV infection, use was made of a Janus kinase 3 (JAK3) inhibitor that has previously been
105 microarray-based analyses and showed reduced Janus kinase 3 (JAK3) phosphorylation upon activation.
106 mitogen-activated protein kinase (MAPK), and Janus kinase 3 (JAK3) signaling are necessary for F. tul
109 lso report that PLD2 is under the control of Janus kinase 3 (JAK3), with the kinase phosphorylating P
110 receptor common gamma chain cytokines and a Janus kinase 3 (JAK3)-dependent pathway in malignant T c
112 ations are usually absent in the SCID-X1 and Janus kinase 3 forms of SCID and greatly reduced in aden
113 vide adequate immunosuppression, whereas the Janus kinase 3 inhibitor tofacitinib's success in the tr
115 -beta-induced Treg development, and inhibits Janus kinase 3-induced STAT5 phosphorylation, a transcri
117 et al. (2015) uncover multifaceted roles for janus kinase and microtubule-interacting protein 1 (JAKM
119 gh several signaling pathways, including the Janus kinase and signal transducer and activator (JAK-ST
120 gnal from the hub cells, which activates the Janus Kinase and Signal Transducer and Activator of Tran
122 by pathological activation of the JAK/STAT (Janus kinase and signal transducer and activator of tran
123 p38 mitogen-activated protein kinase (p38), Janus kinases and IL-6 have also shown some promising ef
124 eously secrete IL-17F and that inhibitors of Janus kinases and Signal transducer and activator of tra
126 s downstream of gp130 involved the classical Janus kinase family-signal transducer and activator of t
129 ort a model of nonhierarchical activation of Janus kinases in which one catalytically competent Jak i
130 ate antiviral receptor) and TYK2 (encoding a Janus kinase), in each case establishing a further serie
131 Other promising drugs focus on blockade of Janus kinase, inhibition of various chemokines, and biol
133 ggered Bcl-6 expression in MM cells, whereas Janus kinase inhibitor and STAT3 siRNA down-regulated Bc
139 Tofacitinib (CP-690,550) is a novel oral Janus kinase inhibitor that is being investigated as a t
140 Tofacitinib (CP-690,550) is a novel oral Janus kinase inhibitor that is being investigated for th
150 of the pathogenesis of vitiligo suggest that Janus kinase inhibitors may be a therapeutic option.
151 e results suggest that tofacitinib and other Janus kinase inhibitors may be effective in the treatmen
152 an agonist of the aryl hydrocarbon receptor, Janus kinase inhibitors, and commensal organisms also in
153 afety of ruxolitinib, a potent and selective Janus kinase (JAK) 1 and 2 inhibitor, as compared with t
157 ple signal-transduction pathways, among them janus kinase (JAK) 2-signal transducer and activator of
159 was recently shown to regulate Stat92E, the Janus kinase (JAK) and Signal transducer and activator o
160 Genetic alterations affecting members of the Janus kinase (JAK) family have been discovered in a wide
161 y administered pharmacological inhibitors of Janus kinase (JAK) family protein tyrosine kinases, down
163 cytokine-signaling inhibitor tofacitinib, a Janus kinase (JAK) inhibitor targeting JAK3 and JAK1.
164 Intriguingly, treatment of T cells with the Janus kinase (JAK) inhibitor tofacitinib disproportionat
166 oplasms (MPN) led to clinical development of Janus kinase (JAK) inhibitors for treatment of MPN.
167 ies on the mechanism of action of successful Janus kinase (Jak) inhibitors have revealed that, apart
169 iption 1 (STAT1), so we tested the effect of Janus kinase (JAK) inhibitors on STAT1 phosphorylation i
170 hod for identification of structurally novel Janus kinase (JAK) inhibitors predicted to bind beyond t
171 neoplasm-associated myelofibrosis, including Janus kinase (JAK) inhibitors, do not induce complete or
175 ransport, holo-RBP can activate STRA6-driven Janus kinase (JAK) signaling and downstream induction of
177 ells mediate alopecia areata in part through Janus kinase (JAK) signaling and that alopecia areata mi
178 rylation in AML leukemic blasts, the role of Janus kinase (JAK) signaling in primary AML compared wit
180 t clones with constitutive activation of the Janus kinase (JAK)- signal transducer and activator of t
182 d PD-L2, and promote their induction through Janus kinase (JAK)-signal transducer and activator of tr
185 hain (gamma(c)) cytokines signal through the Janus kinase (JAK)-signal transducer and activator of tr
186 tions that are either functionally linked to Janus kinase (JAK)-signal transducer and activator of tr
187 of R. conorii infection on the status of the Janus kinase (JAK)-signal transducer and activator of tr
190 clear factor-kappaB signaling pathway or the Janus kinase (JAK)-signal transducers and activators of
195 Because in various cells activation of the Janus kinase (JAK)/signal transducer and activator of tr
196 ent study was to investigate the role of the Janus kinase (JAK)/signal transducer and activator of tr
197 diabetes complications, such as elements of Janus kinase (JAK)/signal transducer and activator of tr
198 egulation of Jun N-terminal Kinase (JNK) and Janus Kinase (JAK)/Signal Transducer and Activator of Tr
200 ncubation with ToxB activated a proapoptotic Janus kinase (JAK)/signal transducer and activator of tr
202 Frequent mutations in cytokine receptor and Janus kinase (JAK)/signal transducer and activator of tr
204 leukaemia-initiation potential and activated Janus kinase (JAK)/signal transducers and activators of
206 n the pivotal RESPONSE study, ruxolitinib, a Janus kinase (JAK)1 and JAK2 inhibitor, was superior to
209 mutation leads to constitutive activation of Janus kinase (JAK)2 and contributes to dysregulated JAK
212 or hetero-dimeric cell surface receptors via Janus Kinase (JAK/TYK), or Receptor Tyrosine Kinase (RTK
213 results in activation of receptor-associated Janus kinases (Jak) and phosphorylation of STAT proteins
218 ansduces a signaling cascade mediated by the Janus kinase JAK2 and the transcription factors STAT3 an
221 /radixin/moesin domain-containing protein of Janus kinase (JAK2) as demonstrated by the reciprocal im
222 ese cytokines to their downstream effectors, Janus kinases (JAKs) and signal transducers and activato
231 s a key mechanism for the transactivation of Janus kinases (Jaks) bound at the intracellular receptor
234 TATs), essential functions of their upstream Janus kinases (JAKs) during postnatal development are le
237 ellular signal-regulated kinase (Erk)1/2 and janus kinases (Jaks), aberrant signal transducer and act
238 signaling molecules, including ERK, Akt, and Janus kinases (Jaks), especially those that mediate infl
239 orylated potentially on the basis of reduced Janus kinase-mediated inhibition of protein phosphatase
241 or molecules to make room for the associated Janus kinase molecules, while the self-rotation allows t
242 hocytes, PDE4, the histamine 4 receptor, and Janus kinase) or specifically itching (eg, NK1R inhibito
243 adhesion kinase, protein tyrosine kinase-2, Janus kinase, other focal adhesion-associated proteins,
246 b and ruxolitinib, which inhibit BCR-ABL and Janus kinases, respectively), significantly extends surv
247 N including utilization of the intracellular Janus kinase signal transducer and activator of transcri
249 n ALL, including tumor suppressors, Ras, and Janus kinase-signal transducer and activator of transcri
250 erization domain-like receptor signaling and Janus kinase-signal transducer and activator of transcri
251 a higher frequency of mutations outside the Janus kinase-signal transducer and activator of transcri
252 Mechanistically, loss of SH2B3 increases Janus kinase-signal transducer and activator of transcri
253 2V617F exerts its effects on cell growth via janus kinase-signal transducer and activator of transcri
254 nd the effects HEV has on IFN-alpha-mediated Janus kinase-signal transducer and activator of transcri
255 a stem cell niche by locally activating the Janus Kinase-Signal Transducer and Activator of Transcri
258 cells whose development is dependent on the Janus kinase-signal transducer and activator of transcri
259 cation after blocking the interferon-induced Janus kinase-signal transducer and activator of transcri
260 as the phosphoinositide 3-kinase (PI3K) and Janus kinase-signal transducer and activator of transcri
261 n Drosophila by the evolutionarily conserved Janus kinase-signal transducers and activators of transc
262 Combined, these data show that an IL-10/Janus kinase/signal transducer and activator of transcri
263 induce Bim in normal and ALPS T cells via a Janus kinase/signal transducer and activator of transcri
265 ays, such as TCRs, nuclear factor kappaB, or Janus kinase/signal transducer and activator of transcri
266 ingless-related integration site), JAK-STAT (Janus kinase/signal transducer and activator of transcri
267 cell-like diffuse cell lymphoma and enhanced Janus kinase/signal transducer and activator of transcri
268 e signature in CLL, containing components of Janus kinase/signal transducer and activator of transcri
269 grate toward the source by activation of the Janus kinase/signal transducer and activator of transcri
271 alone produced IL-2/IL-9, and the downstream Janus kinase/signal transducer and activator of transcri
273 origenic overgrowth by exploiting endogenous Janus kinase/signal transducer and activator of transcri
274 Conserved from humans to Drosophila, the Janus kinase/signal transducer and activators of transcr
276 Accumulating evidence points to a role for Janus kinase/signal transducers and activators of transc
277 erleukin-6 (IL-6) secretion, which activates Janus kinase/signal transducers and activators of transc
279 e that IL-4 up-regulates pIgR production via Janus kinase/signal transducers and activators of transc
281 ds of the Unpaired (Upd) family activate the Janus kinase/signal transducers and activators of transc
282 ignalling 3 (SOCS3), a negative regulator of Janus kinase/signal transducers and activators of transc
283 Mechanistically, IRS-1 deficiency promotes Janus kinase/signal transducers and activators of transc
285 ndent of IFNalpha, IFNbeta, IFNL1, IFNL2, or Janus kinase signaling via signal transducer and activat
287 late kinases known to activate Stat3 such as Janus kinases, Src kinase family members or receptor tyr
289 am transcriptional program and activates the Janus kinase-STAT signaling cascade and thus, by interfe
290 with the IL28B-T/T variant preactivates the Janus kinase-Stat signaling, leading to impaired HCV cle
293 iasis: (1) rapid attenuation of keratinocyte Janus kinase/STAT signaling; (2) removal of keratinocyte
294 MM cells is modulated, at least in part, via Janus kinase/STAT3 and canonical nuclear factor-kappaB p
296 rget three major cellular processes: (i) the Janus kinase/STAT5 pathway (ii) progenitor B-cell differ
297 y, binding of agonist to receptors activates Janus kinases that phosphorylate cytoplasmic STAT3 at ty
299 and stabilize the pseudokinase domain of the Janus kinase tyrosine kinase 2 (Tyk2), resulting in bloc
300 lated protein kinases, protein kinase B, and Janus kinase, which are activated by chemotherapeutics i
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