ライフサイエンスコーパス: SAPK2

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1 imilar manner to SAPK1 (also termed JNK) and SAPK2 (also termed p38, RK, CSBP and Mxi2).

2 timulated stress-activated protein kinase-2 (SAPK2, also termed RK, p38, CSBP and Mxi2) and its downs

3 similar, although less pronounced effects of SAPK2 and ERK inhibition on hyperosmotic GADD153 inducti

4 on osmosignaling via SAPK2 and ERK, and that SAPK2 and ERK pathways have opposite effects on GADD exp

5 is partially dependent on osmosignaling via SAPK2 and ERK, and that SAPK2 and ERK pathways have oppo

6 hromaffin cells with acetylcholine activated SAPK2 and MAPKAP-K2, as well as p42/p44 MAP kinases and

7 SAP1, but SAPK3 was far less effective than SAPK2 in activating MAPKAP kinase-2 and MAPKAP kinase-3.

8 ncentrations similar to those that inhibited SAPK2 in vitro.

9 ctions previously attributed to SAPK1 and/or SAPK2 may be mediated by SAPK3 or SAPK4.

10 ctions previously attributed to SAPK1 and/or SAPK2 may be mediated by SAPK3.

11 SAPK2 may therefore contribute to the acetylcholine-indu

12 me residues phosphorylated by SAPK1, whereas SAPK2 only phosphorylated Thr69 and Thr71.

13 ated kinases 1 and 2 (ERK), SAPK1 (JNK), and SAPK2 (p38) are hyperosmotically activated in mIMCD cell

14 These results show for the first time that SAPK2/p38 plays an essential role in C2C12 cell differen

15 ing that a pathway involving PI 3-kinase and SAPK2/p38 was involved; translocation was unaffected by

16 findings, SB 203580 (a specific inhibitor of SAPK2/p38) or rapamycin (which blocks the activation of

17 horylation of stress-activated kinase-2/p38 (SAPK2/p38) was detected by immunocytochemistry.

18 of MAPKAP kinase-2 (an in vivo substrate of SAPK2/p38) was not only prevented by SB 203580 but also

19 t these events are dependent on PI 3-kinase, SAPK2/p38, and a nuclear phosphatase(s).

20 ted rapidly by SAPK4/p38delta, but poorly by SAPK2/p38, SAPK3/p38gamma, SAPK1/JNK or extracellular si

21 ctivated protein kinase (MAPK) family member SAPK2/p38, without significant activation of p42 MAPK an

22 d factor CREM-1 are stimulated by M-CSF in a SAPK2/p38-dependent manner.

23 sphatidylinositol 3-kinase (PI 3-kinase) and SAPK2/p38.

24 creased by 37.5% following inhibition of the SAPK2 pathway, whereas it was significantly increased (6

25 SAPK3 and SAPK2 phosphorylated a number of proteins at similar rat

26 Unlike SAPK2, SAPK3 was not inhibited by the drug SB 203580.

27 SAPK3 and SAPK2 were activated at similar rates in vitro by SAPKK3

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