ライフサイエンスコーパス: cGKII

1 cGKII and GluR1 form a complex in the brain, and cGKII i

2 cGKII was found to require the C2 amino group of cGMP an

3 Furthermore, a cGKII truncation mutant containing this autoinhibitory r

4 Acute cGKII inhibition significantly reduces LTP, whereas cGKI

5 I and GluR1 form a complex in the brain, and cGKII in this complex phosphorylates GluR1 at S845, a si

6 e of the roles and mechanisms of NO, CNP and cGKII signaling in cartilage and endochondral bone devel

7 Caco-2/Bbe cells overexpressing HA-NHE3 and cGKII, and in mouse ileum.

8 Because cGKII mediates the effects of heat-stable enterotoxins v

9 In this case, NHERF2 directly binds cGKII in the brush border to form an NHE3 complex, with

10 DZ2 C terminus, which binds NHE3, also bound cGKII.

11 ntified in which NHERF2 but not NHERF1 bound cGKII.

12 /H(+) exchanger NHE3 is acutely inhibited by cGKII/cGMP, but how cGKII inhibits NHE3 is unknown.

13 vation of type I cGK (cGKI) and type II cGK (cGKII) are differentially regulated by their cyclic nucl

14 cGMP/cGKII increased NHE3 phosphorylation at three sites (rab

15 cGMP/cGKII rapidly inhibited NHE3, which was associated with

16 er(663), all of which are necessary for cGMP/cGKII to inhibit NHE3.

17 We found that in cultured cGKII KO hippocampal neurons, cGKII-dependent phosphoryl

18 uggest distinct mechanisms of activation for cGKII and cGKI isoforms.

19 elated kinase, cGKI, does not compensate for cGKII KO.

20 for three phosphorylation sites in NHE3 for cGKII inhibition, and for phosphorylation of one of thes

21 ity of these residues was essential for full cGKII autoinhibition.

22 is acutely inhibited by cGKII/cGMP, but how cGKII inhibits NHE3 is unknown.

23 nlike the type I cGKs (cGKIalpha and Ibeta), cGKII autophosphorylation did not alter the basal activi

24 D binds to cGMP-dependent protein kinase II (cGKII) adjacent to the kinase catalytic site.

25 nstream mediators, cGMP-dependent kinase II (cGKII), has itself been shown to be essential for normal

26 udied mice lacking cGMP-dependent kinase II (cGKII), which phosphorylates GluA1, a subunit of AMPA re

27 we demonstrate that presynaptic cGK type II (cGKII) plays a major role in this process.

28 on of cGMP-dependent protein kinase type II (cGKII).

29 hosphate (cGMP)-dependent protein kinase II, cGKII, was tagged by retroviral insertions in two brain

30 II isozyme of cGMP-dependent protein kinase (cGKII), alanine was substituted for the conserved threon

31 at in cultured cGKII KO hippocampal neurons, cGKII-dependent phosphorylation of inositol 1,4,5-trisph

32 Activation of cGKII by cGMP increases the surface expression of AMPARs

33 or cyclic nucleotide-dependent activation of cGKII.

34 e residues responsible for autoinhibition of cGKII, Ala was substituted for basic residues (Lys(122),

35 ithin the putative pseudosubstrate domain of cGKII.

36 C(50) toward a constitutively active form of cGKII.

37 Inhibition of cGKII activity blocks the surface increase of GluR1 duri

38 esicle recycling, we found that knockdown of cGKII and/or the application of a cGK inhibitor reduced

39 y that the distinct activation mechanisms of cGKII and cGKI result from differences in the autophosph

40 A non-myristoylated mutant of cGKII did not support cGMP inhibition of NHE3.

41 dings describe an anti-proliferative role of cGKII in human glioma biology and would further explain

42 of the rapid and slow dissociation sites of cGKII was reversed relative to cGKI.

43 and allow the design of an isoform-specific cGKII inhibitor.

44 equired for cGMP inhibition of NHE3 and that cGKII must be bound both to the plasma membrane by its m

45 We conclude that cGKII controls the homeostatic balance of vesicle exocyt

46 onally, ultrastructural analysis showed that cGKII knockdown or inhibition favored the formation of e

47 lial lineage cell markers also suggests that cGKII induces differentiation of glioma cell lines.

48 s functional compensation for gene KO in the cGKII KO hippocampus.

49 urther explain the retroviral tagging of the cGKII gene during brain tumor formation in PDGF-induced

50 d suggested creating a truncated form of the cGKII protein.

51 All glioma cells transfected with the cGKII phosphorylate vasodilator-stimulated phosphoprotei

52 es of this truncation mutant are specific to cGKII when compared with cAMP-dependent protein kinase C

53 When cGKII was activated by cGMP analog treatment, Sox9 was p

54 Binding of GluR1 is increased when cGKII is activated by cGMP.

55 nsation for the LTP impairment observed when cGKII is acutely inhibited.

56 nhibition significantly reduces LTP, whereas cGKII KO mice show no LTP impairment.

57 e brush border to form an NHE3 complex, with cGKII also associating with the BB via its myristoylatio