ライフサイエンスコーパス: CaM KIV

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1 Truncation mutant CaM-KK1-463 activated CaM-KIV and bound CaM similar to wild-type enzyme (CaM-K

2 direct phosphorylation of c-Jun by activated CaM-KIV, since transcription was blocked by a dominant-n

3 We have shown previously that activated CaM-KIV can activate the mitogen-activated protein kinas

4 odulin-dependent protein kinase IV activity (CaM KIV) and phosphorylation of c-AMP response element b

5 phosphorylation and activation of CaM-KI and CaM-KIV by CaM kinase kinase (CaM-KK), regulates transcr

6 hich phosphorylates and activates CaM-KI and CaM-KIV.

7 ndent protein kinases II and IV (CaM-KII and CaM-KIV).

8 ls, and is a direct target for antagonism by CaM KIV.

9 in CaM-KIV, which mediates its activation by CaM-KIV kinase, prevented activation of Elk-1, c-Jun, an

10 regulation of nuclear gene transcription by CaM-KIV.

11 n, we found that expression of a kinase-dead CaM-KIV construct in two cell lines inhibits IkappaB pho

12 onidine prevents hypoxia-induced increase in CaM KIV activity and CREB protein phosphorylation.

13 tion of the phosphorylation site (Thr196) in CaM-KIV, which mediates its activation by CaM-KIV kinase

14 affinity Ca(2+)/ATPase and prevent increased CaM KIV activity and CREB phosphorylation in the neurona

15 that calmodulin-dependent protein kinase IV (CaM KIV) antagonizes BMP signaling.

16 s of calmodulin-dependent protein kinase IV (CaM KIV) have not been previously investigated.

17 nous calmodulin-dependent protein kinase IV (CaM KIV) is required to negatively modulate hematopoieti

18 Ca2+/calmodulin-dependent protein kinase IV (CaM-KIV), as well as activation of c-Jun N-terminal kina

19 ion of CaM-KII with little effect on CaM-KI, CaM-KIV, CaM-KK, protein kinase A, or protein kinase C.

20 , we have transfected PC12 cells, which lack CaM-KIV, with constitutively active mutants of CaM kinas

21 e mechanism of hypoxia-induced activation of CaM KIV and CREB phosphorylation is nuclear Ca(2+) influ

22 n the other hand, constitutive activation of CaM KIV induces erythroid precursors to undergo apoptoti

23 lie this loss of erythrocytes: inhibition of CaM KIV activity causes commitment of hematopoietic prec

24 Thus, proper regulation of CaM KIV activity in nonhematopoietic tissues is essentia

25 embryogenesis and that strict regulation of CaM KIV activity is essential for normal primitive eryth

26 ce of neuronal nuclear Ca(2+) in the role of CaM KIV activation and CREB protein phosphorylation asso

27 lation or degradation and that expression of CaM-KIV augments hydrogen peroxide-induced IkappaB phosp

28 aM but activated a CaM-independent mutant of CaM-KIV in the absence of Ca2+/CaM.

29 y active mutants of CaM kinase kinase and/or CaM-KIV (CaM-KKc and CaM-KIVc, respectively).

30 ther endogenous or transfected CaM-KK and/or CaM-KIV activities.

31 Here, we show that CaM KIV transcripts are widely distributed during embryo

32 in ectodermal cells, while activation of the CaM KIV signaling pathway alters GATA-2 function posttra

33 These blood defects are observed even when CaM KIV activity is misregulated only in cells that do n

34 Xenopus embryos in which CaM KIV activity is either upregulated or inhibited show

35 ur data are consistent with a model in which CaM KIV inhibits BMP signals by activating a substrate,

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