ライフサイエンスコーパス: hypotonicity

1 d by exposure to hypotonic solutions (10-33% hypotonicity).

2 full activation of the cotransporter during hypotonicity.

3 the renin-angiotensin-aldosterone system and hypotonicity.

4 4, VR-OAC, TRP12, and VRL-2) is activated by hypotonicity.

5 pyrimidine uridine triphosphate (UTP) and by hypotonicity.

6 ICl(swell) activation by hypotonicity (240 mosm) was only partially inhibited by

7 Hypotonicity (25 %) failed to evoke any change in membra

8 Hypotonicity (50%) and mechanical stretch increased ATP

9 M) decreased both the inward and the outward hypotonicity-activated chloride current.

10 Hypotonicity also activated Ca2+ entry, which was requir

11 The response of ERK activation to hypotonicity also required Ca2+ entry and depended on ty

12 ed Ca2+ entry and loss of RVD in response to hypotonicity, although the extent of cell swelling was s

13 g site, rendered the channel unresponsive to hypotonicity and heat but responsive to 4alpha-phorbol 1

14 and negatively affect channel activation by hypotonicity and heat.

15 nEBP displayed nuclear export in response to hypotonicity and nuclear import in response to hypertoni

16 duction by EtOH of MT-I mRNA is secondary to hypotonicity, and (3) that hyperosmotic/hypertonic expos

17 ncreased transepithelial flux in response to hypotonicity are unknown.

18 , a key molecular model, can be activated by hypotonicity, but the mechanism of activation is unclear

19 ies and that AQP5 reduction by extracellular hypotonicity can be mediated by TRPV4.

20 id 4 (TRPV4), a cation channel responsive to hypotonicity, can also be activated by warm temperatures

21 eta-cells to hypotonic solutions (10 and 33% hypotonicity) caused an immediate increase in cell volum

22 l conditions and in response to secretin and hypotonicity, cysts from PCK rats expanded to a greater

23 om a hypertonic to isotonic medium (relative hypotonicity) decreased the membrane abundance of Slc26a

24 rtantly, point mutation of Tyr-253 abolished hypotonicity-dependent channel activity.

25 on of wild-type Lyn dramatically potentiated hypotonicity-dependent TRPV4 tyrosine phosphorylation wh

26 demonstrate that (i) activation of TRPV4 by hypotonicity depends on AQP5, not on cell swelling per s

27 Hypotonicity elicited a regulatory volume decrease (RVD)

28 xposure of salivary gland cells and acini to hypotonicity elicited an increase in cell volume and act

29 Lastly, knocking down TRPV4 impaired hypotonicity-evoked airway epithelial ATP release.

30 Importantly, hypotonicity-evoked ATP release from freshly excised tra

31 We find that hypotonicity facilitates TRPM7 at elevated intracellular

32 of HIV-transmitting leukocytes by its unique hypotonicity; however, the successful oral transmission

33 ormone analogue, dDAVP, resulted in systemic hypotonicity in trpv4-/- mice, despite the fact that the

34 Furthermore, hypotonicity increased the association and surface expre

35 chanosensitive ion channel blockers dampened hypotonicity-induced ATP release.

36 to hypertonicity-induced cell shrinkage and hypotonicity-induced cell swelling.

37 n by ClC-3 siRNA prevented the activation of hypotonicity-induced chloride currents, and arrested cel

38 nic acid (DIDS, 100 microM) also blocked the hypotonicity-induced current in a reversible manner.

39 mily with unknown function, as essential for hypotonicity-induced iodide influx.

40 V4 and that these channels were activated by hypotonicity-induced membrane stretch.

41 cells, which dominate our cultures, mediated hypotonicity-induced nucleotide release.

42 satrienoic acid is primarily responsible for hypotonicity-induced responses.

43 facilitates the time course and amplitude of hypotonicity-induced swelling and regulatory volume decr

44 s expressed on cholangiocyte cilia, and that hypotonicity induces an increase in intracellular Ca(2+)

45 For the hypotonic solution, we found that hypotonicity inhibited CFTR-mediated chloride secretion

46 ecomes dephosphorylated during incubation in hypotonicity, leading to a dramatic increase in KCC3 fun

47 Apart from its gating by hypotonicity, little is known about TRPV4 regulation.

48 F, we investigated the effects of hyper- and hypotonicity on ion transport processes.

49 The stimulatory effect of hypotonicity on K(+) flux is absent in wnk, fray, or Ncc

50 The influence of extracellular hypotonicity on the relationship between cell volume (V(

51 channels can be strongly activated by either hypotonicity or exposure to the potent agonist 4alphaPDD

52 higher, and it was not further increased by hypotonicity or inhibited by WNK3.

53 Hypotonicity potentiated ATP release into the apical and

54 Hypotonicity-promoted ATP release and dye uptake in prim

55 CCs are inactive and phosphorylated, whereas hypotonicity promotes their dephosphorylation and activa

56 Admixtures with excessive hypotonicity (sodium = 103 mEq/L), in contrast, decrease

57 3-T991A/T1048A could be further activated by hypotonicity, suggesting that additional phosphorylation

58 RVD) over a period comparable to that of the hypotonicity-triggered increase in Isc.

59 The tracheobronchial ASL hypotonicity was hypothesized to reflect collection-indu

60 iggered by increased tubular flow or by bath hypotonicity, were approximately three-fold greater when

61 ctional manner; TonEBP activity decreases in hypotonicity, whereas it increases in hypertonicity.

62 on-selective channel is gated by exposure to hypotonicity within the physiological range.