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

1 rucial for pancreatic beta-cell function and stimulus secretion coupling.

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

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

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

5 (2+) channels or subsequent events in Ca(2+) stimulus-secretion coupling.

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

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

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

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

10 proline, which apparently enhances beta-cell stimulus-secretion coupling.

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

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

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

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

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

16 es that combines a spiking model, a model of stimulus-secretion coupling and a model of plasma cleara

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

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

19 The precise mechanisms of stimulus-secretion coupling, and its failure in Diabetes

20 e expression profile of proteins involved in stimulus-secretion coupling, as well as the function of

21 vide fundamental novel information regarding stimulus-secretion coupling at neuronal dendrites, and s

22 vide fundamental novel information regarding stimulus-secretion coupling at somatodendritic compartme

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

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

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

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

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

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

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

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

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

32 Stimulus-secretion coupling in bovine chromaffin cells w

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

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

35 oxidative respiration, a process central to stimulus-secretion coupling in mature beta cells.

36 voked Ca(2+) release is an important step in stimulus-secretion coupling in pancreatic B-cells, we pr

37 voked Ca(2+) release is an important step in stimulus-secretion coupling in pancreatic B-cells.

38 Stimulus-secretion coupling in pancreatic exocrine cells

39 2+) release from intracellular stores during stimulus-secretion coupling in primary mouse pancreatic

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

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

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

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

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

45 nadal feedback increases the efficacy of the stimulus-secretion coupling mechanisms, a phenomenon tha

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

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

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

49 for similar release sites, together encoding stimulus-secretion coupling over a large range of synapt

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

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

52 sodeoxycholic acid (TUDCA), acutely promoted stimulus-secretion coupling (SSC).

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

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

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

56 Stimulus-secretion coupling was monitored with capacitan

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

58 y pathways that may play a role in beta-cell stimulus-secretion coupling, we compared beta-cell and i

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

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