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1 plex stabilization related to the associated Janus kinases.
2 ciated signal transduction machinery such as Janus kinases.
3 ockade of IL-12 and IL-23; and inhibition of Janus kinases.
4 we discovered that miR-373 directly targets Janus kinase 1 (JAK1) and IFN-regulating factor 9 (IRF9)
5 f the FERM and SH2-like domains of the human Janus kinase 1 (JAK1) bound to a fragment of the intrace
6 enes encoding interferon-receptor-associated Janus kinase 1 (JAK1) or Janus kinase 2 (JAK2), concurre
7 mutations, including activating mutations of Janus kinase 1 (JAK1), in 9.1% of patients and provides
10 In phase 2 studies, baricitinib, an oral Janus kinase 1 and 2 inhibitor, reduced disease activity
13 malignancies, alone or in combination with a Janus kinase 1 inhibitor (itacitinib) or chemotherapy (r
15 efficacy of multiple doses of the selective Janus kinase 1 inhibitor upadacitinib in patients with m
16 nd safety of upadacitinib, an oral selective Janus kinase 1 inhibitor, in a randomized trial of patie
20 validation of one of these candidates, Jak1 (Janus kinase 1), a tyrosine kinase of the nonreceptor ty
21 Finally, we determined that inhibition of Janus kinase 1, inhibition of Glycogen synthase kinase 3
22 TYK2-dependent IL-12 and IL-23 signaling and Janus kinase 1-dependent signaling in cells expressing t
23 ase 2 study for the treatment of MF with the Janus kinase 1/2 (JAK1/2) inhibitor momelotinib (MMB) de
26 agues report their results on the use of the Janus kinase 1/2 (JAK1/2) inhibitor ruxolitinib in murin
29 ) transcription factor and the JAK1/2-STAT3 (Janus Kinase 1/2 - Signal Transducer and Activator of Tr
30 n of STAT1 signaling with the small-molecule Janus kinase 1/2 inhibitor ruxolitinib in vitro and in v
36 lso evaluated the efficacy of tofacitinib (a Janus kinase 1/3 inhibitor) in 5 patients with severe, l
37 treatment with tofacitinib citrate, an oral Janus kinase 1/3 inhibitor, resulted in significant repi
38 notypic consequence of the V617F mutation in Janus kinase 2 (encoded by JAK2), but the extent to whic
40 uired gain-of-function V617F mutation in the Janus Kinase 2 (JAK2(V617F)) is the main mutation involv
41 etic deletion in the hematopoietic system of Janus kinase 2 (JAK2) abrogates initiation of myeloproli
42 prevented the decrease of phosphorylation of Janus kinase 2 (JAK2) and phosphorylation of signal tran
43 nhibits interferon-gamma (IFN-gamma)-induced Janus kinase 2 (JAK2) and signal transducer and activati
44 sulting in a loss of downstream signaling by Janus kinase 2 (JAK2) and signal transducer and activato
45 ndocytic AMR controls TPO expression through Janus kinase 2 (JAK2) and the acute phase response signa
46 dermal growth factor receptor (EGFR) utilize Janus kinase 2 (JAK2) as a common signaling node to tran
48 imerization and revealed that the associated Janus kinase 2 (JAK2) dimerizes through its pseudokinase
51 ortant axis in memory CD8(+) T cells couples Janus kinase 2 (JAK2) hyperactivation to the phosphoryla
52 s) is the acquisition of a V617F mutation in Janus kinase 2 (JAK2) in hematopoietic stem cells (HSCs)
54 ncreatic tumors were given gemcitabine and a Janus kinase 2 (JAK2) inhibitor; tumor growth was monito
57 "TET2-first patients"), patients in whom the Janus kinase 2 (JAK2) mutation was acquired first ("JAK2
59 eedforward loop in which p27pT157pT198 binds Janus kinase 2 (JAK2) promoting STAT3 (signal transducer
62 on of the phosphoinositol 3-kinase (PI3K) or Janus kinase 2 (Jak2) tyrosine kinase inhibitors abolish
64 combined targeting of the BCR-ABL kinase and Janus kinase 2 (JAK2) with dasatinib and ruxolitinib, re
67 and are characterized by mutually exclusive Janus kinase 2 (JAK2), calreticulin (CALR), and myelopro
68 receptor-associated Janus kinase 1 (JAK1) or Janus kinase 2 (JAK2), concurrent with deletion of the w
70 tracytoplasmic tyrosine kinases, essentially janus kinase 2 (JAK2), which regulates MPL stability and
71 culin (CALR) mutations have been reported in Janus kinase 2 (JAK2)- and myeloproliferative leukemia (
72 red the human PRL-prolactin receptor (hPRLR)-Janus kinase 2 (JAK2)-signal transducer and activator of
73 we demonstrated that inhibition of the IL-6-Janus kinase 2 (JAK2)-STAT3-calprotectin axis with FDA-a
74 uences of Stat1 deficiency on the effects of Janus kinase 2 (JAK2)-V617F in vivo by crossing mice exp
79 patients have a gain of function mutation in Janus kinase 2 (JAK2V617F), but little is known how JAK2
80 r (MPL) to induce constitutive activation of Janus kinase 2 and signal transducer and activator of tr
82 rimary myelofibrosis carry a mutation in the Janus kinase 2 gene (JAK2), and an additional 5 to 10% h
85 x O1, extracellular signal-regulated kinase, Janus kinase 2, or signal transducers and activators of
86 a selective inhibitor of Janus kinase 1 and Janus kinase 2, potently suppresses cytokine signaling i
88 d PD-L2, and their further induction through Janus kinase 2-signal transducers and activators of tran
89 s could be reversed by administration of the Janus kinase 2/3 inhibitor tofacitinib, which blocks IL-
90 cyclin-dependent kinase inhibitor), AT9283, (Janus kinase 2/3 inhibitor), ispinesib (kinesin spindle
91 d this required intact signaling through the Janus Kinase 2/phosphatidylinositol-4,5-bisphosphate 3-k
92 oid progenitors EPOR engagement of canonical Janus kinase 2/signal transducer and activator of transc
96 tokine receptor superfamily that signals via Janus kinase-2-signal transducer and activator of transc
98 SGs was prevented through the activation of Janus kinase 3 (JAK3) by the vitamin K3 analog menadione
99 yromonas gingivalis enhances the activity of Janus kinase 3 (JAK3) in innate immune cells, and subseq
100 NK cells on SIV infection, use was made of a Janus kinase 3 (JAK3) inhibitor that has previously been
104 microarray-based analyses and showed reduced Janus kinase 3 (JAK3) phosphorylation upon activation.
105 mitogen-activated protein kinase (MAPK), and Janus kinase 3 (JAK3) signaling are necessary for F. tul
107 r of cell lines, and the results showed that Janus kinase 3 (JAK3) was with reduced expression in the
109 receptor common gamma chain cytokines and a Janus kinase 3 (JAK3)-dependent pathway in malignant T c
110 ctions during obesity are because of loss of Janus kinase 3 (JAK3)-mediated tyrosine phosphorylation
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
116 et al. (2015) uncover multifaceted roles for janus kinase and microtubule-interacting protein 1 (JAKM
118 by pathological activation of the JAK/STAT (Janus kinase and signal transducer and activator of tran
119 gnal from the hub cells, which activates the Janus Kinase and Signal Transducer and Activator of Tran
122 p38 mitogen-activated protein kinase (p38), Janus kinases and IL-6 have also shown some promising ef
123 eously secrete IL-17F and that inhibitors of Janus kinases and Signal transducer and activator of tra
125 s downstream of gp130 involved the classical Janus kinase family-signal transducer and activator of t
130 ort a model of nonhierarchical activation of Janus kinases in which one catalytically competent Jak i
131 ate antiviral receptor) and TYK2 (encoding a Janus kinase), in each case establishing a further serie
132 or TNF or targeting cytokine signalling via Janus kinase inhibition in the treatment of COVID-19.
133 Other promising drugs focus on blockade of Janus kinase, inhibition of various chemokines, and biol
148 activity of IFN-gamma and oncostatin M, and Janus kinase inhibitors appear to be an effective treatm
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
155 tivation of STAT3 by inhibiting the upstream Janus kinase (JAK) 1 or JAK2 or by STAT3 knockdown was f
160 y administered pharmacological inhibitors of Janus kinase (JAK) family protein tyrosine kinases, down
161 tential of IL-7 as a clinical target using a Janus kinase (JAK) inhibitor and an IL-7-blocking antibo
164 cytokine-signaling inhibitor tofacitinib, a Janus kinase (JAK) inhibitor targeting JAK3 and JAK1.
165 Intriguingly, treatment of T cells with the Janus kinase (JAK) inhibitor tofacitinib disproportionat
167 oplasms (MPN) led to clinical development of Janus kinase (JAK) inhibitors for treatment of MPN.
168 ies on the mechanism of action of successful Janus kinase (Jak) inhibitors have revealed that, apart
170 iption 1 (STAT1), so we tested the effect of Janus kinase (JAK) inhibitors on STAT1 phosphorylation i
171 hod for identification of structurally novel Janus kinase (JAK) inhibitors predicted to bind beyond t
173 neoplasm-associated myelofibrosis, including Janus kinase (JAK) inhibitors, do not induce complete or
177 ransport, holo-RBP can activate STRA6-driven Janus kinase (JAK) signaling and downstream induction of
178 ells mediate alopecia areata in part through Janus kinase (JAK) signaling and that alopecia areata mi
179 rylation in AML leukemic blasts, the role of Janus kinase (JAK) signaling in primary AML compared wit
182 t clones with constitutive activation of the Janus kinase (JAK)- signal transducer and activator of t
185 d PD-L2, and promote their induction through Janus kinase (JAK)-signal transducer and activator of tr
186 c cytokines via inhibition of the downstream Janus kinase (JAK)-signal transducer and activator of tr
187 F-kappaB) to the nucleus, signalling via the Janus kinase (JAK)-signal transducer and activator of tr
189 ass I cytokine receptor that signals via the Janus kinase (JAK)-signal transducer and activator of tr
190 SGs) occurs upon activation of the canonical Janus kinase (JAK)-signal transducer and activator of tr
192 clear factor-kappaB signaling pathway or the Janus kinase (JAK)-signal transducers and activators of
195 Frequent mutations in cytokine receptor and Janus kinase (JAK)/signal transducer and activator of tr
198 Because in various cells activation of the Janus kinase (JAK)/signal transducer and activator of tr
199 ent study was to investigate the role of the Janus kinase (JAK)/signal transducer and activator of tr
200 diabetes complications, such as elements of Janus kinase (JAK)/signal transducer and activator of tr
201 egulation of Jun N-terminal Kinase (JNK) and Janus Kinase (JAK)/Signal Transducer and Activator of Tr
202 mor-derived factors induce activation of the 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
217 In a phase 2 trial, ruxolitinib, a selective Janus kinase (JAK1 and JAK2) inhibitor, showed potential
219 ansduces a signaling cascade mediated by the Janus kinase JAK2 and the transcription factors STAT3 an
221 ese cytokines to their downstream effectors, Janus kinases (JAKs) and signal transducers and activato
233 TATs), essential functions of their upstream Janus kinases (JAKs) during postnatal development are le
238 ated kinases (ERKs), protein kinase B (Akt), Janus kinases (JAKs), and signal transducer activator of
239 signaling molecules, including ERK, Akt, and Janus kinases (Jaks), especially those that mediate infl
241 orylated potentially on the basis of reduced Janus kinase-mediated inhibition of protein phosphatase
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 cells whose development is dependent on the Janus kinase-signal transducer and activator of transcri
250 cation after blocking the interferon-induced Janus kinase-signal transducer and activator of transcri
251 as the phosphoinositide 3-kinase (PI3K) and Janus kinase-signal transducer and activator of transcri
252 n ALL, including tumor suppressors, Ras, and Janus kinase-signal transducer and activator of transcri
253 a higher frequency of mutations outside the Janus kinase-signal transducer and activator of transcri
254 Mechanistically, loss of SH2B3 increases Janus kinase-signal transducer and activator of transcri
255 2V617F exerts its effects on cell growth via janus kinase-signal transducer and activator of transcri
258 highly recurrent oncogenic mutations in the Janus kinase-signal transducer and activator of transcri
259 erization domain-like receptor signaling and Janus kinase-signal transducer and activator of transcri
260 n Drosophila by the evolutionarily conserved Janus kinase-signal transducers and activators of transc
261 d BALF ILs and cytokines including Jak-STAT (Janus kinases-signal transducer and activator of transcr
263 origenic overgrowth by exploiting endogenous Janus kinase/signal transducer and activator of transcri
264 Combined, these data show that an IL-10/Janus kinase/signal transducer and activator of transcri
265 induce Bim in normal and ALPS T cells via a Janus kinase/signal transducer and activator of transcri
267 , ruxolitinib, an inhibitor of IFN-triggered Janus kinase/signal transducer and activator of transcri
268 ays, such as TCRs, nuclear factor kappaB, or Janus kinase/signal transducer and activator of transcri
269 ingless-related integration site), JAK-STAT (Janus kinase/signal transducer and activator of transcri
270 cell-like diffuse cell lymphoma and enhanced Janus kinase/signal transducer and activator of transcri
271 e signature in CLL, containing components of Janus kinase/signal transducer and activator of transcri
272 tiviral response by activating the JAK/STAT (Janus kinase/signal transducer and activator of transcri
273 flammatory gene sets such as IL-6/JAK/STAT5 (Janus kinase/signal transducer and activator of transcri
274 Conserved from humans to Drosophila, the Janus kinase/signal transducer and activators of transcr
275 Mechanistically, IRS-1 deficiency promotes Janus kinase/signal transducers and activators of transc
277 Accumulating evidence points to a role for Janus kinase/signal transducers and activators of transc
278 erleukin-6 (IL-6) secretion, which activates Janus kinase/signal transducers and activators of transc
280 e that IL-4 up-regulates pIgR production via Janus kinase/signal transducers and activators of transc
284 ts of IL22 were prevented with inhibitors of Janus kinase signaling to signal transducer and activato
285 ndent of IFNalpha, IFNbeta, IFNL1, IFNL2, or Janus kinase signaling via signal transducer and activat
289 late kinases known to activate Stat3 such as Janus kinases, Src kinase family members or receptor tyr
291 am transcriptional program and activates the Janus kinase-STAT signaling cascade and thus, by interfe
292 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
295 rget three major cellular processes: (i) the Janus kinase/STAT5 pathway (ii) progenitor B-cell differ
296 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