ライフサイエンスコーパス: HCK

1 HCK represents a novel target for therapeutic developmen

2 HCKs grown in vitro were stimulated with IL-1alpha, TNF-

3 HCKs incubated with TNF-alpha, IL-1alpha, or IFN-gamma r

4 factor SPIB or EHF is sufficient to activate HCK-dependent apical-to-basolateral transcytosis of thes

5 However, CDK2 and HCK kinase in complex with other flavone inhibitors such

6 Mutated MYD88 triggers BTK, IRAK1/IRAK4, and HCK growth and survival signaling, whereas CXCR4 mutatio

7 is significantly enhanced in both HCECs and HCKs in response to either IL-1alpha or TNF-alpha stimul

8 Cultures of HCECs and HCKs were stimulated with either human recombinant IL-1a

9 e more potent HCK inhibitor A419259, blocked HCK activation and induced apoptosis in mutated MYD88 WM

10 an activating function in cells coexpressing HCK p59.

11 Here we find that high HCK levels correlate with reduced survival of colorectal

12 In addition, in HCK cell over-expressing LEDGF, the levels of hINV mRNA

13 IP-10 synthesis is induced in HCKs by IL-1alpha, TNF-alpha, and IFN-gamma.

14 ast, induction of I-TAC and MIG synthesis in HCKs requires costimulation with IFN-gamma and either IL

15 tein tyrosine kinases, including JAK1, JAK3, HCK, epidermal growth factor receptor kinase, and insuli

16 l simian virus 40-transformed keratinocytes (HCK), was transactivated by LEDGF significantly.

17 determine whether human corneal keratocyte (HCKs) in culture synthesize these chemokines in response

18 ss levels between human corneal keratocytes (HCKs), fibroblasts (HCFs) and keratoconus cells (HKCs).

19 FAE model, we show that the tyrosine kinase HCK regulates apical-to-basolateral transcytosis of non-

20 lls show enhanced hematopoietic cell kinase (HCK) transcription and activation, and that HCK is activ

21 SRC family kinase hematopoietic cell kinase (HCK) triggers hematological malignancies as a tumor cell

22 s increased levels of the src-family kinases HCK and FGR.

23 We show here that the SFKs LYN, HCK, or FGR are overexpressed and activated in AML proge

24 ted that expression and/or activation of LYN/HCK occurs during disease progression.

25 ted MYD88 expressing WM cells with a mutated HCK gatekeeper greatly increased the half maximal effect

26 sing LEDGF, but not detectable in the normal HCK cells or HCK cells transfected with vector.

27 at hINV protein is found in the cytoplasm of HCK cells over-expressing LEDGF, but not detectable in t

28 Exposure of HCK to IL-1alpha stimulated a 10-fold increase in ENA-78

29 iologically important, as over-expression of HCK with LEDGF increases the expression of the endogenou

30 and IL-6 transcription, whereas knockdown of HCK reduced survival and attenuated BTK, phosphoinositid

31 r study supports the specific requirement of HCK p59 and FGR src-family kinases for FCRL4-mediated im

32 Treatment of HCKs with IFN-gamma activated STAT1 and, in combination

33 or STAT1 by IFN-gamma receptors expressed on HCKs was determined by Western blot analysis.

34 ut not detectable in the normal HCK cells or HCK cells transfected with vector.

35 xpression of IL-10 in the presence of FGR or HCK p59 in response to CpG, but increased levels of IFN-

36 Ibrutinib and the more potent HCK inhibitor A419259, blocked HCK activation and induce

37 ing epidermal turn-over rate, and protecting HCKs against stress.

38 is is only inducible in IL-1alpha-stimulated HCKs.

39 (HCK) transcription and activation, and that HCK is activated by interleukin 6 (IL-6).

40 Docking and pull-down studies confirmed that HCK was a target of ibrutinib.

41 The findings support that HCK expression and activation is triggered by mutated MY

42 on tyrosine residues in the presence of the HCK p59 or FGR.

43 so blocked adenosine triphosphate binding to HCK, whereas transduction of mutated MYD88 expressing WM

44 ed on the crystal structures of PP1 bound to HCK and N(6)-(benzyl)-ADP bound to c-Src (T338G).

45 Over-expression of mutated MYD88 triggers HCK and IL-6 transcription, whereas knockdown of HCK red

46 ctivated the TGF-beta/Smad3 pathway, whereas HCK knockdown inhibited it.