ライフサイエンスコーパス: v-Mos

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1 ogene, but not by the serine kinase oncogene v-MOS.

2 is the major in vivo phosphorylation site on v-Mos.

3 tudies, S34A but not S34E mutation inhibited v-Mos activity.

4 with alanine or glutamic acid in full-length v-Mos (an Env-Mos fusion protein that contains 31 additi

5 ed the major in vivo phosphorylation site on v-Mos as Ser-56, which is phosphorylated by cyclic AMP d

6 itions in cells conditionally transformed by v-mos but not in parental v-mos-transformed cells.

7 Efforts culminated in the case of Simkins v Moses H.

8 cyte lysates and repressed MKK activation by v-Mos in a coupled kinase assay.

9 the stability nor protein kinase activity of v-Mos (in which c-Mos residue Pro-2 becomes Pro-33) was

10 horylation at Ser-3 (equivalent to Ser-34 in v-Mos) is important for the interaction of c-Mos with it

11 56E mutation but not S56A mutation inhibited v-Mos kinase activity of both S34A and S34E mutants.

12 Results showing inhibition of v-Mos kinase activity of the S34E mutant by the S56E mut

13 The S56E but not the S56A mutation inhibited v-Mos kinase activity suggesting that Ser-56 phosphoryla

14 may also be regulated in the same manner as v-Mos kinase activity.

15 unit resulted in a significant inhibition of v-Mos kinase activity.

16 yclic AMP-dependent protein kinase (PKA ) on v-Mos kinase activity.

17 whose phosphorylation had been stimulated by v-mos kinase added to the lysate.

18 that the mechanism of in vivo inhibition of v-Mos kinase involves direct phosphorylation by PKA.

19 he inhibitory effect of the S34A mutation on v-Mos kinase suggesting that in c-Mos the corresponding

20 lation was not involved in the inhibition of v-Mos kinase.

21 acid (E) in different combinations, various v-Mos mutants were expressed in a rabbit reticulocyte ly

22 r-56 correlated with slower migration of the v-Mos protein during sodium dodecyl sulfate-polyacrylami

23 c-Mos), its mouse c-Mos equivalent version (v-Mos residues 32-374, hereafter referred to as Mos), an

24 Transduction of cells with v-mos resulted in an increase in micronucleus formation,

25 tutively activated by infecting cells with a v-mos retrovirus.

26 Because residues corresponding to both v-Mos Ser-34 and Ser-56 are evolutionarily conserved in

27 ation, we generated site-directed mutants of v-Mos that would mimic phosphorylation in terms of charg

28 at residue 56 did not affect the ability of v-Mos to autophosphorylate in vitro or, more importantly

29 alysis, we compared the expression of RNA in v-mos-transformed cells and their flat revertant and iso

30 own-regulated in serum starved, G1 arrested, v-mos-transformed cells as compared with quiescent NIH3T

31 ose expression is down-regulated in parental v-mos-transformed cells but which is expressed at a high

32 f AP-1 DNA binding activity in serum starved v-mos-transformed cells compared to very low amounts in

33 Furthermore, serum starved v-mos-transformed cells have elevated histone H1 kinase

34 The elevation of these complexes in arrested v-mos-transformed cells may be the cause of the transcri

35 Instead, G1-phase arrested v-mos-transformed cells stably express two E2F protein c

36 NIH3T3 cells is not present in serum starved v-mos-transformed cells.

37 lly transformed by v-mos but not in parental v-mos-transformed cells.

38 FR, cyclin A, and E2F1 seen in serum starved v-mos-transformed cells.

39 Serum deprived v-mos-transformed NIH3T3 cells are unable to enter a tru

40 Furthermore, v-mos-transformed NIH3T3 cells will undergo arrest of pr

41 r-263 phosphorylation, the Ala-263 mutant of v-Mos was not inhibited by forskolin treatment.

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