ライフサイエンスコーパス: stimulus-secretion coupling

1 metabolism play an important role in L cell stimulus-secretion coupling.

2 ta-cell function at the very latest stage of stimulus-secretion coupling.

3 tive importance of Epac and PKA to beta-cell stimulus-secretion coupling.

4 (2+) channels or subsequent events in Ca(2+) stimulus-secretion coupling.

5 that protein kinase C (PKC) participates in stimulus-secretion coupling.

6 nown whether there are additional effects on stimulus-secretion coupling.

7 KC) interacts at multiple sites in beta-cell stimulus-secretion coupling.

8 involved in the regulation of the beta-cell stimulus-secretion coupling.

9 of calcineurin results in similar defects on stimulus-secretion coupling.

10 al coupling, which translated into defective stimulus/secretion coupling.

11 ease in the ability of the ligand to mediate stimulus secretion coupling, although only small changes

12 ar Ca(2+) signaling remains at the center of stimulus secretion coupling and its regulation by inosit

13 ular Ca2+ signaling remains at the center of stimulus secretion coupling and its regulation has been

14 s in our understanding of both physiological stimulus-secretion coupling and the pathophysiology of a

15 stores are not of primary importance in the stimulus-secretion coupling, and furthermore, insulin os

16 ring rate reflects frequency-facilitation of stimulus-secretion coupling at the neurohypophysis.

17 To better understand how NCS-1 regulates stimulus-secretion coupling, bovine chromaffin cells wer

18 rectifier K+ channels can therefore suppress stimulus-secretion coupling by damping oscillations in m

19 he idea that glucose-induced disturbances of stimulus-secretion coupling by extramitochondrial metabo

20 rols, arguing against a ubiquitous beta cell stimulus-secretion coupling defect.

21 r this refractoriness involves alteration in stimulus-secretion coupling (desensitization) or results

22 en and glucose modulations, while monitoring stimulus-secretion coupling factors in real-time.

23 ase from acidic Ca(2+) storage organelles in stimulus-secretion coupling in beta cells.

24 udying, in real time, the dynamic aspects of stimulus-secretion coupling in beta-cells.

25 Stimulus-secretion coupling in bovine chromaffin cells w

26 as proposed that intracellular Ca2+ controls stimulus-secretion coupling in endocrine cells, and Katz

27 ne whether such regulation may contribute to stimulus-secretion coupling in islet cells, we used a re

28 Stimulus-secretion coupling in pancreatic exocrine cells

29 2+) release from intracellular stores during stimulus-secretion coupling in primary mouse pancreatic

30 ttle, have been proposed to be essential for stimulus-secretion coupling in the pancreatic beta-cell,

31 tude-encoded Ca2+ signal and Ca2+ influx for stimulus-secretion coupling in these nonexcitable cells.

32 l for immune cell function and may impact on stimulus-secretion coupling in wider cellular contexts.

33 phate (IP3) (one of the pathways involved in stimulus-secretion-coupling in mast cells), the differen

34 Here we describe stimulus-secretion coupling mechanisms in beta-cells and

35 ls appear to possess a broader repertoire of stimulus-secretion coupling modes than NHP terminals.

36 ins such as CDC42 is an obligate step in the stimulus-secretion coupling of nutrient-induced insulin

37 mastoparan effect acts at a "distal site" in stimulus-secretion coupling on one of the SNARE proteins

38 s pathway must remain intact for appropriate stimulus-secretion coupling, production of NADPH does no

39 The effects of glitazones on stimulus-secretion coupling (SSC) are poorly understood.

40 cannot account for alpha 2AAR suppression of stimulus-secretion coupling; thus, the D79N alpha 2AAR p

41 l transmitter of the glucose signal early in stimulus-secretion coupling to support the later stage o

42 This mode of stimulus-secretion coupling was labile and was seen only

43 Stimulus-secretion coupling was monitored with capacitan

44 ained in perifused islets, such that glucose stimulus-secretion coupling was potentiated.

45 To further elucidate Rab3D involvement in stimulus-secretion coupling, we examined the effect of C

46 dily explained by the classical mechanism of stimulus-secretion coupling, where exocytosis is synchro