ライフサイエンスコーパス: FGF-3

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1 ypes depending on the levels of induction of FGF-3.

2 (TM) as well as the early mesodermal marker fgf-3.

3 to the pregnancy-dependent tumorigenesis of FGF-3.

4 means for understanding the diverse roles of FGF-3 and its interactions with hormones in mammary glan

5 terns of Hoxa-2, Hoxb-1, Hoxb-4, Krox-20 and FGF-3 as markers, we conclude that segmentation in the m

6 Int-2 was later designated FGF-3 based on sequence homology with other members of t

7 Since FGF-1 and FGF-3 can both activate one FGF receptor isoform (FGFR2

8 Zebrafish (Brachyodanio rerio) Fgf-3 cDNAs expressed in COS-1 cells give rise to the he

9 g inactivation of p53 and over-expression of Fgf-3, collaborate with Wnt-1 in leading to mammary tumo

10 The manifestations elicited by FGF-3 could be reversed by RU486 withdrawal.

11 FGF-3 does, however, appear to be required for a correct

12 nt induction of FGF-3 with induced levels of FGF-3 expression dependent on the levels of expression o

13 FGF-3 expression in the adult mouse lung resulted in two

14 To evaluate the effects of FGF-3 expression in the prostate and male reproductive t

15 High levels of FGF-3 expression resulted in diffuse alveolar type II ce

16 We present a first study that ectopic FGF-3 expression resulted in exuberant hyperplasia of al

17 Low levels of FGF-3 expression resulted in massive free alveolar macro

18 Taken together, we show that ectopic FGF-3 expression severely perturbs normal prostate devel

19 FGF-3, FGF-4, and FGF-8 were not detectable by RT-PCR in

20 The former suggest that FGF-3 from the hindbrain is required to induce formation

21 To characterize better FGF-3 function in postnatal mammary gland development an

22 ase-13 (MMP-13), fibroblast growth factor-3 (FGF-3), GADD45, and vascular endothelial growth factor (

23 Ectopic overexpression of FGF-3 in pubescent mammary glands elicited severe pertur

24 Expression of FGF-3 in the lens also resulted in developmental alterat

25 The expression of FGF-3 in the lens rapidly induced epithelial cells throu

26 circumvent these shortcomings, we expressed FGF-3 in the lungs under the control of the progesterone

27 e regulatory system to express conditionally FGF-3 in the mammary epithelium of transgenic mice.

28 rmalities of growth factors, such as HGF and FGF-3, in DR corneas.

29 A candidate for this signal is FGF-3 (Int-2), which is expressed in the hindbrain adjac

30 deed, co-expression of MMTV-Wnt-10b and MMTV-FGF-3/int-2 resulted in sterile offspring with highly di

31 persistence of mitogenic signal elicited by FGF-3 is crucial for the initiation, progression, and ma

32 These findings argue that FGF-3 is not required as an inductive signal for invagin

33 of the otocyst, while the latter imply that FGF-3 is required only in the later process of otocyst d

34 Fibroblast growth factor-3 (FGF-3) is a crucial developmental regulator.

35 rmations of the inner ear in kreisler and in FGF-3 knockout mice are similar, involving failure of th

36 , in vitro tests conflict with findings from FGF-3 knockout mice.

37 rgism between the stimulus from estrogen and FGF-3 mitogenic pathways was evident and likely contribu

38 FGF-3, originally named int-2, was discovered as an onco

39 dy marked out independently of any localized FGF-3 signal from r5 and r6.

40 in promoter was used to target expression of FGF-3 to the developing lens of transgenic mice.

41 we employed a bitransgenic system to target FGF-3 to these organs.

42 urthermore, transgenic lens cells expressing FGF-3 were able to induce the differentiation of neighbo

43 ed that showed ligand-dependent induction of FGF-3 with induced levels of FGF-3 expression dependent

44 protection analyses indicate that zebrafish Fgf-3 (ZFgf-3) is structurally analogous to the mouse ge

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