ライフサイエンスコーパス: Janus kinase 2

1 nase), JNK (Jun N-terminal kinase), or JAK2 (Janus kinase 2).

2 on via a specific interaction with activated Janus kinase 2.

3 ic kidney 293T cells that express endogenous Janus kinase 2.

4 s could be reversed by administration of the Janus kinase 2/3 inhibitor tofacitinib, which blocks IL-

5 ating mutation (V617F) in the gene for JAK2 (Janus kinase 2), a tyrosine kinase utilized by hematopoi

6 Phase I clinical testing of inhibition of Janus kinase 2, active in vitro, began with several agen

7 tion of the redox-sensitive protein kinases (Janus kinase 2, Akt, and p38 mitogen-activated protein k

8 The high prevalence of the V617F mutation of Janus kinase 2 and associated mutations in myeloprolifer

9 rms of the relationship between dysregulated Janus kinase 2 and elevated blood counts.

10 r (MPL) to induce constitutive activation of Janus kinase 2 and signal transducer and activator of tr

11 support Epo-dependent cell growth or trigger Janus kinase 2 and STAT5 activation, even at concentrati

12 However, only IL-3 and IL-5 induced Janus kinase 2 and STAT5 phosphorylation.

13 ompounds are designed to bind selectively to Janus kinase 2 and the STAT3 Src homology-2 domain, whic

14 zed the response of bone to GH by increasing Janus kinase-2 and IGF-1R protein levels.

15 The V617F activating mutation of Janus kinase 2, and associated parallel mutations, is at

16 gulation of HMGB1 release through a TNF- and Janus kinase 2-dependent mechanism.

17 notypic consequence of the V617F mutation in Janus kinase 2 (encoded by JAK2), but the extent to whic

18 proliferation and constitutive activation of Janus kinase 2, ERK1, and ERK2.

19 ntly identified gain-of-function mutation in Janus kinase 2, found in the majority of patients with m

20 sis carry a gain-of-function mutation in the Janus kinase 2 gene (JAK2 V617F) that contributes to the

21 Somatic mutations in the Janus kinase 2 gene (JAK2) occur in many myeloproliferat

22 rimary myelofibrosis carry a mutation in the Janus kinase 2 gene (JAK2), and an additional 5 to 10% h

23 also mimicked apolipoproteins in activating Janus kinase 2; however, the M159D/E mutants were also a

24 123319 (AT(2) inhibitor), AG 490 (a specific Janus kinase 2 inhibitor), and genistein (a tyrosine kin

25 Compared with AG490, a well-characterized Janus kinase 2 inhibitor, curcumin was a more rapid (30

26 JAK2 (Janus kinase 2) is essential for cytokine receptor signa

27 y tyrosine phosphorylation and activation of Janus kinase-2 (Jak-2), Tyk-2, Stat3, and Stat4.

28 point mutation in the pseudokinase domain of Janus kinase 2 (JAK2 V617F).

29 uired gain-of-function V617F mutation in the Janus Kinase 2 (JAK2(V617F)) is the main mutation involv

30 etic deletion in the hematopoietic system of Janus kinase 2 (JAK2) abrogates initiation of myeloproli

31 Epo addition, the EpoR signaling through the Janus kinase 2 (JAK2) activates multiple pathways includ

32 es L253, I257, and W258, that is crucial for Janus kinase 2 (JAK2) activation and receptor signaling.

33 Using the chemical inhibitor of Janus kinase 2 (Jak2) activity, AG 490, and overexpressi

34 G also activates the growth-promoting enzyme janus kinase 2 (JAK2) and its latent signal transducers

35 channels in LH neurons via the activation of janus kinase 2 (JAK2) and of mitogen-activated protein k

36 an stimulate the tyrosine phosphorylation of Janus kinase 2 (JAK2) and other members of the JAK/signa

37 prevented the decrease of phosphorylation of Janus kinase 2 (JAK2) and phosphorylation of signal tran

38 nhibits interferon-gamma (IFN-gamma)-induced Janus kinase 2 (JAK2) and signal transducer and activati

39 sulting in a loss of downstream signaling by Janus kinase 2 (JAK2) and signal transducer and activato

40 GH triggered the tyrosine phosphorylation of Janus kinase 2 (Jak2) and STAT3 in neutrophils.

41 crovascular endothelial cell line-1 (HMEC-1) Janus kinase 2 (JAK2) and that the JAK2 inhibitor, AG-49

42 ndocytic AMR controls TPO expression through Janus kinase 2 (JAK2) and the acute phase response signa

43 he prolactin receptor (PRLR), its associated Janus kinase 2 (Jak2) and the signal transducer and acti

44 Enzymatic inhibitors of Janus kinase 2 (JAK2) are in clinical development for th

45 dermal growth factor receptor (EGFR) utilize Janus kinase 2 (JAK2) as a common signaling node to tran

46 Here, we investigated the role of Janus kinase 2 (JAK2) as a newly described intracellular

47 Inhibitors of Ca(2+)/calmodulin (CaM) and Janus kinase 2 (Jak2) attenuated this activation, wherea

48 The tyrosine kinase Janus kinase 2 (JAK2) binds to the majority of the known

49 The cytoplasmic tyrosine kinases Src and Janus kinase 2 (Jak2) both seem to be involved in the ac

50 Activation of Janus kinase 2 (JAK2) by chromosomal translocations or p

51 e receptor-like factor 2 (CRLF2) and mutated Janus kinase 2 (Jak2) cooperated in conferring cytokine-

52 Tyr(1007) residue in the activation loop of Janus kinase 2 (JAK2) has been shown to be essential for

53 The nonreceptor kinase Janus kinase 2 (JAK2) has garnered attention as a promis

54 to phosphatidylinositol 3-kinase and Akt via Janus kinase 2 (JAK2) in a cascade, which results in neu

55 s) is the acquisition of a V617F mutation in Janus kinase 2 (JAK2) in hematopoietic stem cells (HSCs)

56 ine kinase (IRTK) and leptin receptor (LEPR)-Janus kinase 2 (JAK2) in hypothalamic nuclei.

57 cotine activates the growth-promoting enzyme Janus kinase 2 (JAK2) in PC12 cells and that preincubati

58 ETE also induced tyrosine phosphorylation of Janus kinase 2 (Jak2) in VSMCs, and its inhibition subst

59 significantly blocked by the highly specific janus kinase 2 (JAK2) inhibitor alpha-cyano-(3,4-dihydro

60 tive to TG101348, a selective small-molecule Janus kinase 2 (JAK2) inhibitor.

61 ncreatic tumors were given gemcitabine and a Janus kinase 2 (JAK2) inhibitor; tumor growth was monito

62 Developing Janus kinase 2 (Jak2) inhibitors has become a significan

63 modifying agents (CMAs) but not hydroxyurea, Janus kinase 2 (JAK2) inhibitors, or low doses of interf

64 Janus kinase 2 (JAK2) is a central kinase in hematopoiet

65 Janus kinase 2 (JAK2) is associated with LEPRb and autop

66 quired for adequate basal signaling, whereas Janus kinase 2 (JAK2) is dispensable upstream of STAT3.

67 The Janus kinase 2 (Jak2) is essential for normal mammary gl

68 We recently found that activation of janus kinase 2 (JAK2) is essential for the Ang II-induce

69 The redox regulation of Janus kinase 2 (JAK2) is poorly understood, and there ar

70 ed to assess the effects of NADPH oxidase on Janus kinase 2 (JAK2) kinase, the low molecular weight-p

71 p24.1 amplification region also included the Janus kinase 2 (JAK2) locus.

72 e show that the protein-tyrosine kinase (TK) Janus kinase 2 (JAK2) modulates the apolipoprotein inter

73 "TET2-first patients"), patients in whom the Janus kinase 2 (JAK2) mutation was acquired first ("JAK2

74 Janus kinase 2 (JAK2) mutations define polycythemia vera

75 Second, when Janus kinase 2 (Jak2) phosphorylation was inhibited usin

76 eedforward loop in which p27pT157pT198 binds Janus kinase 2 (JAK2) promoting STAT3 (signal transducer

77 Expression of Janus kinase 2 (JAK2) R867Q and S755R/R938Q induced spon

78 We recently developed a Janus kinase 2 (Jak2) small molecule inhibitor called G6

79 Activating alleles of Janus kinase 2 (JAK2) such as JAK2(V617F) are central to

80 The tyrosine kinase Janus kinase 2 (JAK2) transduces signaling for the major

81 matic activating mutation (JAK2V617F) in the Janus kinase 2 (JAK2) tyrosine kinase in the myeloprolif

82 on of the phosphoinositol 3-kinase (PI3K) or Janus kinase 2 (Jak2) tyrosine kinase inhibitors abolish

83 tion in the JH2 autoinhibitory domain of the Janus kinase 2 (JAK2) tyrosine kinase was recently descr

84 iates signaling by activating the associated Janus kinase 2 (Jak2) tyrosine kinase, which promotes th

85 The Janus kinase 2 (JAK2) V617F mutation is the primary path

86 ostate cancer, a dominant-negative mutant of Janus kinase 2 (Jak2) was delivered by adenovirus to CWR

87 combined targeting of the BCR-ABL kinase and Janus kinase 2 (JAK2) with dasatinib and ruxolitinib, re

88 AG-490, a selective inhibitor of Janus kinase 2 (Jak2), also reduced the LPC-induced Sp1

89 After cotransfection of Ob-Rb, Janus kinase 2 (JAK2), and SHP-2 into 293T cells, leptin

90 8 inhibits tyrosyl phosphorylation of STAT3, Janus kinase 2 (JAK2), and Src.

91 anism that is dependent upon beta1 integrin, Janus kinase 2 (JAK2), and STAT3 but not EGFR.

92 Phosphorylated STAT3, phosphorylated Janus kinase 2 (JAK2), and suppressor of cytokine signal

93 growth factor beta receptor (PDGFbetaR), TEL/Janus kinase 2 (JAK2), and TEL/neurotrophin-3 receptor (

94 enerated by NADPH oxidase, the activation of Janus kinase 2 (JAK2), and the polyol pathway play impor

95 phospholipase C, Ca2+/calmodulin (CaM), and Janus kinase 2 (Jak2), but not by pertussis toxin or by

96 and are characterized by mutually exclusive Janus kinase 2 (JAK2), calreticulin (CALR), and myelopro

97 receptor-associated Janus kinase 1 (JAK1) or Janus kinase 2 (JAK2), concurrent with deletion of the w

98 Pacritinib (SB1518) is a Janus kinase 2 (JAK2), JAK2(V617F), and Fms-like tyrosin

99 s did not affect tyrosine phosphorylation of Janus kinase 2 (JAK2), Shc, signal transducer and activa

100 enhanced H(2)O(2)-induced phosphorylation of Janus kinase 2 (JAK2), signal transducer and activator o

101 (-/-) mice did not affect phosphorylation of Janus kinase 2 (JAK2), signal transducer and activator o

102 l and activates signaling molecules, such as Janus kinase 2 (JAK2), that optimize the lipid export ac

103 tracytoplasmic tyrosine kinases, essentially janus kinase 2 (JAK2), which regulates MPL stability and

104 culin (CALR) mutations have been reported in Janus kinase 2 (JAK2)- and myeloproliferative leukemia (

105 quires p53, we find that irinotecan inhibits Janus kinase 2 (JAK2)-signal transducer and activator of

106 red the human PRL-prolactin receptor (hPRLR)-Janus kinase 2 (JAK2)-signal transducer and activator of

107 PI3K-PDE3B-cAMP pathway interacting with the Janus kinase 2 (Jak2)-Stat3 pathway constitutes a critic

108 we demonstrated that inhibition of the IL-6-Janus kinase 2 (JAK2)-STAT3-calprotectin axis with FDA-a

109 uences of Stat1 deficiency on the effects of Janus kinase 2 (JAK2)-V617F in vivo by crossing mice exp

110 CIPs), and presence of the V617F mutation in Janus kinase 2 (JAK2).

111 sential thrombocythemia (ET) with nonmutated Janus kinase 2 (JAK2).

112 nonreceptor protein tyrosine kinases Lyn and janus kinase 2 (Jak2).

113 uperfamily members that bind to and activate Janus kinase 2 (JAK2).

114 short-interfering RNA-mediated knockdown of Janus kinase 2 (JAK2).

115 ting mutations of signaling proteins such as Janus kinase 2 (JAK2).

116 ffects are mediated by the activation of the Janus kinase 2 (Jak2)/signal transducer and activator of

117 Blockade of HGF/Met, Janus kinase 2 (JAK2)/STAT3 and TGF-beta1 signaling by s

118 ulated by retinoic acid 6" (STRA6), enhanced Janus kinase 2 (JAK2)/STAT5 cascade, up-regulated adenyl

119 The inclusion of a transgenic allele of Janus kinase 2 (JAK2)V617F resulted in acceleration of t

120 ross-talk between the signalling pathways of Janus kinase-2 (Jak2) and nuclear factor-kappaB (NF-kapp

121 various protein tyrosine kinases, including Janus kinase-2 (Jak2) and the insulin receptor.

122 Janus kinase-2 (JAK2) conveys receptor-binding signals b

123 The critical role of Janus kinase-2 (JAK2) in regulation of myelopoiesis was

124 Mutations in Janus kinase-2 (JAK2) occur in approximately 50% of pati

125 The tyrosine kinase, Janus kinase-2 (Jak2), plays a pivotal role in signal tr

126 receptor-associated protein tyrosine kinase janus-kinase 2 (JAK2) is essential for normal red cell d

127 ctor receptor [EGFr] inhibitor) and AG490 (a Janus kinase 2 [JAK2] inhibitor), SB203580 (a p38 inhibi

128 and downstream effectors of IL-13 signaling (Janus kinase-2 [JAK2] and signal transducer and activato

129 patients have a gain of function mutation in Janus kinase 2 (JAK2V617F), but little is known how JAK2

130 the epidermal growth factor receptor kinase, Janus kinase-2 kinase, and Src kinase did not block the

131 Mice with hepatocyte-specific deletion of Janus kinase 2 (L-JAK2 KO mice) develop spontaneous stea

132 The Janus kinase 2 mutation, JAK2617V>F, is myeloid neoplasm

133 AG490, a specific inhibitor for Janus kinase 2 of the IFN-gamma signaling pathway, dose-

134 lipopeptide did not affect the activation of Janus kinase 2 or its association with beta c.

135 Inhibition of Janus kinase 2 or SRC kinase signaling downstream of mut

136 x O1, extracellular signal-regulated kinase, Janus kinase 2, or signal transducers and activators of

137 d this required intact signaling through the Janus Kinase 2/phosphatidylinositol-4,5-bisphosphate 3-k

138 In addition, the rate of Janus kinase 2 phosphorylation, initiated through the th

139 tes the formation of a complex with IRS2 and Janus kinase 2, preventing IRS2 ubiquitination.

140 he phosphorylation of Lyn, the Epo receptor, Janus kinase 2, Signal Transducer and Action of Transcri

141 teins included constitutively phosphorylated Janus kinase 2, signal transducer and activator of trans

142 d PD-L2, and their further induction through Janus kinase 2-signal transducers and activators of tran

143 oid progenitors EPOR engagement of canonical Janus kinase 2/signal transducer and activator of transc

144 cyclin D1 through phosphoinositide 3-kinase, Janus kinase 2/signal transducer and activator of transc

145 ssion is mediated, at least in part, via the Janus kinase 2/signal transducers and activators of tran

146 The Janus kinase 2/signal transducers and activators of tran

147 aB pathway, however, IL-12 signaling through Janus kinase 2/Stat4 activation was markedly suppressed.

148 osine phosphorylation, and activation of the Janus kinase 2, STAT5, extracellular signal-regulated ki

149 An activating 1849G>T mutation of JAK2 (Janus kinase 2) tyrosine kinase was recently described i

150 ed IL-12-induced tyrosine phosphorylation of Janus kinase 2, tyrosine kinase 2, and STAT3 and STAT4 t

151 from polycythemia vera patients harboring a Janus kinase 2 V617F mutation in hematopoietic stem cell

152 ythropoietin (EPO), its receptor (EPOR), and janus kinase 2 were cloned; established to be essential