ライフサイエンスコーパス: PI turnover

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1 in or formyl-Met-Leu-Phe receptor-stimulated PI turnover.

2 somers of PBG were equipotent in stimulating PI turnover.

3 cology of the h-TM cell FP-receptor-mediated PI turnover and [Ca(2+)](i) mobilization was defined usi

4 FP-receptor-mediated PI turnover and [Ca(2+)](i) mobilization were measured i

5 5HT and its analogues stimulated PI turnover and [Ca2+]i mobilization in h-TM cells from

6 ane-1,3-dicarboxylic acid, it fails to block PI turnover and changes in spike adaptation stimulated b

7 the key dimensionless group, the ratio of 3' PI turnover and diffusion rates, can be estimated within

8 tropic glutamate receptors (mGluRs) activate PI turnover and thereby trigger intracellular calcium re

9 uR) agonist 1S,3R ACPD was used to stimulate PI turnover and to determine the E(MAX) for each rat.

10 of receptor-mediated phosphatidylinositide (PI) turnover and intracellular Ca(2+) release.

11 s: enhanced PI 3-kinase activity, reduced 3' PI turnover, and possibly slow/constrained 3' PI diffusi

12 e chain reaction (RT-PCR), phosphoinositide (PI) turnover, and intracellular Ca2+ ([Ca2+]i) mobilizat

13 onist potencies of the PG analogues from the PI turnover assays in h-TM cells correlated well with PI

14 led (formyl-Met-Leu-Phe) receptor-stimulated PI turnover by 50-100% in PHM1, HeLa, COSM6, and RBL-2H3

15 er assays in h-TM cells correlated well with PI turnover data obtained from the cloned human ciliary

16 AT1aR), ligand binding decreased by 60% and PI turnover decreased by 69%.

17 5-HT3 receptors) dose-dependently stimulated PI turnover in fronto-cingulate cortical slices.

18 0 antagonized the (+/-)-fluprostenol-induced PI turnover in these cells (K(i) = 2.56 +/- 0.62 micro M

19 se-dependently stimulated phosphoionositide (PI) turnover in fronto-cingulate cortical slices.

20 However, although phosphoinositide (PI) turnover in response to BK by Y131A and Y131S proved

21 In addition, we report that 3' PI turnover is not affected by PDGF receptor signaling i

22 evelopmental decline in glutamate-stimulated PI turnover is well correlated with the decline in exper

23 ty of signal transduction pathways including PI turnover, MAP kinase activation, and PI 3-kinase acti

24 The results show that PI turnover mediated by the mGluRs was blunted in the ag

25 The decrease in mGluR-mediated PI turnover occurred without changes in the protein leve

26 from WT with respect to either BK-activated PI turnover or arachidonic acid release.

27 nse in muscarinic stimulation of hippocampal PI turnover that we previously found in this same study

28 gible, the YAYA mutant returned BK-activated PI turnover to wild type (WT).

29 The magnitude of the decrement in PI turnover was also significantly correlated with age-r

30 Maximal phosphoinositide (PI) turnover was examined in the hippocampus of young an

31 In contrast, PI turnover with YSYS remained unresponsive to BK.

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