ライフサイエンスコーパス: JAK kinase

1 ypes identical to mutations in the Hopscotch/JAK kinase.

2 eceptor (IL-6R) also activates STAT3 through Jak kinase.

3 response to activation of the Drosophila Hop Jak kinase.

4 ssociated with a corresponding activation of JAK kinases.

5 interaction of some cytokine receptors with Jak kinases.

6 e cytokine family of receptors that activate JAK kinases.

7 but not on the enzymatic activity of Src or Jak kinases.

8 nt with activation of JAK2 in trans by other JAK kinases.

9 ved in tyrosine kinases and may be unique to Jak kinases.

10 uitment, and activation of the intracellular JAK kinases.

11 d activate certain STAT proteins, in lieu of JAK kinases.

12 s may be the primary functional attribute of JAK kinases.

13 cers and activators of transcription) by the Jak kinases.

14 eract with and form signaling complexes with Jak kinases.

15 res activation of receptor-associated Janus (Jak) kinases.

16 with imatinib together with an inhibitor of JAK kinases abrogates this resistance, suggesting that t

17 IRAK1 phosphorylation, NF-kappaB signalling, JAK kinase activation of STAT3, and secretion of IL-6, I

18 resulted in recovered JAK-STAT3 binding and JAK kinase activity after an initial reduction, although

19 SOCS-1 is a potent inhibitor of Jak kinase activity and of signaling initiated by severa

20 diated through altered JAK-STAT3 binding and JAK kinase activity and that this compensatory pathway a

21 In summary, optimal JAK kinase activity is a critical determinant of normal

22 JAK kinase activity is regulated by the adjacent pseudok

23 Inhibition of Jak kinase activity with Jak inhibitor I completely reve

24 Aberrations in JAK kinase activity, that may lead to derailment of one

25 in part to their inhibition of the requisite JAK kinase activity.

26 IL-2 signaling that functions by inhibiting Jak kinase activity.

27 ly had B-cell development/differentiation or JAK kinase alterations but had a high frequency (62%) of

28 es identical to those in the hopscotch (hop)/JAK kinase and marelle (mrl)/Stat92e mutations.

29 Agonist antiserum to TNFR1 induced Jak kinase and STAT protein phosphorylation.

30 rowth factor-beta and its signaling pathway (JAK kinase and STAT-6, Smad2/3, and Smad7) appear to pla

31 enotypes identical to those in the Hopscotch/JAK kinase and stat92E/STAT mutations.

32 ferons (IFNs) bind surface receptors, induce JAK kinases and activate STAT transcription factors to s

33 rget clinically relevant proteins, including JAK kinases and BET family members, with applications ex

34 kinase signaling through SRC family-TNK2 or JAK kinases and differential sensitivity to kinase inhib

35 IL-6 induced phosphorylation of JAK kinases and gp130, regardless of the proliferative r

36 glioblastoma by downregulating expression of JAK kinases and inhibiting activation of STAT3.

37 tly, acid 4 does not reach the intracellular JAK kinases and is inactive in cellular assays and in bl

38 regulation of cytokine-induced activation of Jak kinases and STAT transcription factors.

39 hich IFNaR1 mediates the interaction between JAK kinases and the STAT transcription factors.

40 ma, as determined by a lack of activation of jak kinases and the transcription factor, STAT1(alpha),

41 rosine phosphorylation of its receptors, two JAK kinases and three STAT transcription factors.

42 ss the phenotype of the hyperactive hopTum-1 Jak kinase, and recovered a mutation that meiotically ma

43 activation of CRLF2 expression, mutation of JAK kinases, and alterations of IKZF1 cooperate to promo

44 activation of Stat3 via the FGF receptor and JAK kinases, and pharmacological inhibition of MEK toget

45 ylation, TSLP was reported to not signal via JAK kinases, and the mechanism by which TSLP regulates S

46 less, a cytokine-like receptor; Hopscotch, a JAK kinase; and Stat92E, a STAT transcription factor.

47 In addition, JAK kinases appear to be essential for the phosphorylati

48 Our results show that none of the JAK kinases are constitutively phosphorylated by v-src o

49 Jak kinases are critical signaling components in hematop

50 Although Jak kinases are essential for initiating cytokine signal

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

52 istinct classes of cytokine receptors engage Jak kinases as primary effectors.

53 a type I cytokine receptor are important for Jak kinase association but also suggest that two IL-2Rbe

54 phorylation of STAT3 in MM cells by reducing Jak kinase autophosphorylation, and leads to down-regula

55 These findings establish that JAK kinase binding to betac requires the presence of thr

56 Furthermore, inhibition of Jak kinases by TGF-beta was associated with a decrease i

57 Activation of Jak kinases by TNF was associated with tyrosine phosphor

58 the dominant hop(Tum-l) mutation in the Hop Jak kinase causes leukemia-like and other developmental

59 mphoma B-cell line, expressed the four known Jak kinases constitutively tyrosine phosphorylated, with

60 need for development of better therapies for JAK kinase-dependent malignancies.

61 or (EpoR) mutants, we have demonstrated that Jak kinase-dependent signals initiated from the membrane

62 Furthermore, chemical inhibition of JAK kinases enhanced infection of stem cell-derived cult

63 The Jak kinases exhibit distinct cytokine receptor associati

64 Although Jak2 and other Jak kinase family members are phosphorylated on numerous

65 lines driven by similar fusions of the other JAK kinase family members.

66 Tyrosine kinase 2 (TYK2) is a member of the JAK kinase family of intracellular signalling molecules.

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

68 We show that Jak2 is the requisite Jak kinase for signaling by the LRb intracellular domain

69 In contrast, loss of JAK kinase function has been found to result in disease

70 t of this hypothesis, it has been found that JAK kinase function is required for optimal activation o

71 Evidence to date, indicates that JAK kinase function may integrate components of diverse

72 pro-B1 ALL had acquired somatic mutations in Jak kinase genes.

73 Thus, over-activation of JAK kinases has been implicated in tumorigenesis.

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

75 loss of function mutations in the Drosophila Jak kinase Hopscotch (Hop) to determine the role of Hop

76 flies wild-type and mutant for Dcr-2 or the JAK kinase Hopscotch to infections by seven RNA or DNA v

77 We demonstrate that the JAK kinase, Hopscotch, and the STAT DNA-binding protein,

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

79 may be important to re-evaluate the role of Jak kinases in other cytokine signaling pathways as well

80 studies have been conducted on the roles of Jak kinases in the hematopoietic cells, much less is kno

81 Tyk2 kinase and the hyperphosphorylation of Jak kinases in the motheaten cells that lack functional

82 To identify the pathways downstream of Jak kinases in v-Abl-mediated signaling, we examined the

83 ions and lipid elevations have occurred with JAK-kinase inhibition.

84 A Jak kinase inhibitor did not recapitulate this inhibitio

85 JAK kinase inhibitors have depressed leukemic T cell lin

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

87 Profiling of a set of Jak kinase inhibitors revealed kinase off-targets from n

88 f various solid tumors, including the use of JAK kinase inhibitors such as AZD1480.

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

90 .g. sphingosine-1-phosphate agonists and the JAK kinase inhibitors, have been proposed as potential t

91 .g. sphingosine-1-phosphate agonists and the JAK kinase inhibitors, have been proposed as potential t

92 ed IL-9-mediated tyrosine phosphorylation of JAK kinases, insulin receptor substrate-2, and signal tr

93 ired IL-9-induced cell growth, activation of JAK kinases, insulin receptor substrate-2, and STAT3 and

94 ociation but also suggest that two IL-2Rbeta-Jak kinase interactions are important for IL-2 signaling

95 nd interleukin-3) and that activation of the Jak kinase is necessary and sufficient for these effects

96 Our results suggest that the N-terminus of Jak kinases is critical for receptor binding, and is the

97 ms by which Jak2, the cognate LRb-associated Jak kinase, is regulated and mediates downstream signali

98 y be an important function attributed to the JAK kinases, it is certainly not the only function perfo

99 The JAK kinases JAK1, JAK2, JAK3, and TYK2 play key roles in

100 (IFN-gammaR2), and causes activation of two Jak kinases (Jak1 and Jak2).

101 It is interesting to note that JAK kinases (JAK1, JAK2, JAK3, and Tyk2) were not consis

102 oR) requires only one receptor chain and one Jak kinase (Jak2).

103 zation mediates the trans-phosphorylation of Jak kinases, Jaks phosphorylate receptors at tyrosine si

104 and Y510, suggesting that the role for this Jak kinase may extend beyond the Jak-STAT pathway.

105 In such a scenario, JAK kinases may be more crucial to phosphorylation of th

106 e phosphorylation of STAT3 and suggests that Jak kinases may not be required in this cascade.

107 These data suggest that Jak kinases may play an important role in v-Abl induced

108 ciated with myeloid cell proliferation while JAK kinases mediate the activation of Erk-2 pathway whic

109 of these diverse signaling cues from active JAK kinases, members of the Src-family kinases and STAT

110 The concerted action of JAK kinases, members of the Src-kinase family and STAT p

111 Pharmacologic inhibition of Jak kinases more selectively blocked EC sprouting behavi

112 of Bcl-XL protein levels is mediated by the Jak kinase pathway and is independent of other signaling

113 he target genes through which the Drosophila Jak kinase pathway regulates hemocyte development.

114 Signaling targets of Jak kinase pathways included members of the Bcl-2 family

115 dominant negative mutant vector at Tyr-701 (JAK kinase phosphorylation site) blocked the effect of I

116 However, mutations of Stat1 at Tyr-701 (JAK kinase phosphorylation site), Glu-428/429 (putative

117 n these cells, the v-Abl oncoprotein and the JAK kinases physically associate.

118 therefore likely to determine specificity of Jak kinase-receptor interactions.

119 The data support the concepts that Jak kinases regulate cell survival through their selecti

120 Jak/STAT signaling pathway, as inhibition of Jak kinases results in a loss of antiviral activity driv

121 on of multiple signaling cascades, involving Jak kinases, signal transducer and activator of transcri

122 Constitutive nuclear factor (NF)-kappaB and JAK kinase signalling promotes malignant cell survival i

123 ed the effects of dominant-negative forms of JAK kinases, STAT transcription factors, and Raf-1 in tr

124 Here, we describe the role of the IFN-Jak kinase-Stat (signal transducer and activator of tran

125 Jak kinase-Stat protein pathways play a critical role in

126 y IFNgamma, or pharmacological inhibition of JAKs, kinases that phosphorylate STATs, prevented the in

127 As SOCS-1 is a known potent inhibitor of Jak kinases, the mechanism by which v-Abl bypasses SOCS-

128 varying degrees of selectivity against other JAK kinases to address the requirement for TYK2 catalyti

129 V and ZIKV showed differential inhibition of Jak kinases upstream of STAT5, suggesting divergent coun

130 SOCS-1 regulation to constitutively activate Jak kinases was investigated.

131 35S-labeled Jak kinases were precipitated from a cell-free system an

132 litinib is a small-molecule inhibitor of the JAK kinases, which has been approved for the treatment o

133 BCR-ABL also activates JAK kinases, which may provide a mechanism for STAT acti

134 Our results associate Pyk2 and Jak kinases with the linkage of signals emanating from c

135 nhance tumorigenesis induced by an oncogenic JAK kinase without affecting JAK/STAT signaling.