ライフサイエンスコーパス: GDF-9

1 nt BMP-15 (InvBMP-15) alone or together with GDF-9.

2 s not increased until 12 h after addition of GDF-9.

3 ep, i.e. I31D and S99I in BMP-15 and S77F in GDF-9.

4 is by itself, although less effectively than GDF-9 (3-fold vs. 6-fold increase over 24 h, respectivel

5 ne product, growth differentiation factor-9 (GDF-9), a member of the transforming growth factor-beta

6 fects on reporter gene activation induced by GDF-9, activin, or transforming growth factor-beta.

7 6 activity resembles BMP-15 but differs from GDF-9 activities.

8 Growth differentiation factor-9 (GDF-9), an oocyte-secreted member of the transforming gr

9 Interestingly, when GDF-9 and BMP-15 are co-expressed the processing of both

10 In contrast to the recent studies on GDF-9 and BMP-15, nothing is known about the biological

11 r than those of cells co-expressing wildtype GDF-9 and mutant BMP-15, suggesting a possible mechanism

12 dition of PGE(2) to cultures containing both GDF-9 and NS-398 overrides the NS-398 block in progester

13 15) and growth and differentiation factor-9 (GDF-9) are members of the transforming growth factor-bet

14 15) and growth and differentiation factor-9 (GDF-9) are oocyte-secreted factors that are critical loc

15 Here we show that, unlike BMP-15 and GDF-9, BMP-6 lacks mitogenic activity on rat granulosa c

16 Growth differentiation factor-9 (GDF-9), bone morphogenetic protein (BMP)-15, and BMP-6 a

17 d that Cox2 is a direct downstream target of GDF-9 but that progesterone synthesis required an interm

18 rate the first evidence that both BMP-15 and GDF-9 can form non-covalent homodimers when expressed in

19 Here we analyse ovaries from GDF-9-deficient female mice and demonstrate that primord

20 patterns, fully grown oocytes isolated from GDF-9-deficient mice progress to advanced stages of diff

21 cence microscopic analysis of follicles from GDF-9-deficient mice.

22 GDF-9 homozygous mutant mice indicates that GDF-9-deficient oocytes grow more rapidly than control o

23 gous ewes with a mutation in both BMP-15 and GDF-9 exhibit higher fertility than those having mutatio

24 yte follicles, indicative of aberrant BMP-15/GDF-9 expression, were observed in GCNF(fl/fl)Zp3Cre(+)

25 bound to DR0 elements within the BMP-15 and GDF-9 gene promoters and repressed their reporter activi

26 lly, while when both are co-expressed BMP-15/GDF-9 heterodimers are produced.

27 Analysis of follicles from GDF-9 homozygous mutant mice indicates that GDF-9-defici

28 cell aberrations suggest a critical role for GDF-9 in the regulation of growth in preantral follicles

29 Thus, GDF-9 induces an EP2 signal transduction pathway which a

30 nvBMP-15 is abolished, and the processing of GDF-9 is also severely impaired, suggesting that the het

31 Surprisingly, when GDF-9 is co-expressed, the processing and secretion of I

32 Thus, GDF-9 is the first oocyte-derived growth factor required

33 GDF-9 messenger RNA is synthesized only in the oocyte fr

34 ell lines, which express recombinant BMP-15, GDF-9, or both, and investigated whether they form homod

35 uggesting that the heterodimers of InvBMP-15/GDF-9 proproteins are not susceptible to proteolytic cle

36 culture system in which we added recombinant GDF-9, prostaglandins, prostaglandin receptor agonists,

37 ropose a novel hypothesis that a decrease in GDF-9 secretion may be involved in causing infertility i

38 GDF-9 stimulated Cox2 mRNA within 2 h, and PGE(2) within

39 NS-398, inhibitors of Cox2, block basal and GDF-9-stimulated progesterone synthesis.

40 In addition, GDF-9 stimulates EP2 mRNA synthesis by a prostaglandin-

41 e have produced recombinant human BMP-15 and GDF-9 that carry the mutations identified in those sheep

42 utant BMP-15 was co-expressed with wild-type GDF-9, the secretion of BMP-15 and GDF-9 was significant

43 s by regulating the expression of BMP-15 and GDF-9, to affect female fertility.

44 Moreover, when mutant GDF-9 was co-expressed with mutant BMP-15, the secretion

45 wild-type GDF-9, the secretion of BMP-15 and GDF-9 was significantly reduced, suggesting that the mec

46 BMP-15) and growth differentiation factor 9 (GDF-9), were up-regulated in GCNF(fl/fl)Zp3Cre(+) female

47 ily member, growth differentiation factor-9 (GDF-9), which is required for ovarian folliculogenesis.