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1 f Amh and Sox9, and a decline in Cyp19a1 and Foxl2.
2  mechanistic study of BPES and regulation of Foxl2.
3 duces, but not eliminates, the expression of Foxl2.
4 eam of the transcription start site (TSS) of Foxl2.
5 is dependent on an intact forkhead domain in FoxL2.
6 egulation of ovarian regulators, Cyp19a1 and Foxl2.
7  all consistent with an anti-testis role for Foxl2.
8                                We identified FoxL2, a member of the forkhead family, as a candidate m
9                        Haploinsufficiency of FOXL2, a new forkhead transcription factor, causes bleph
10 ramming, as described in adult ovaries after Foxl2 ablation.
11                                      Pivotal Foxl2 action thus represses the male gene pathway at sev
12 kely be responsible for many BPES cases, how FOXL2 affects craniofacial development remain to be unde
13                     The female-related genes foxl2 and cyp19a1a were significantly increased in the g
14     In this study, we explore the targets of FOXL2 and five nuclear receptors in murine primary folli
15 mice, and germ cell-depleted XX mice lacking Foxl2 and harboring a Kit mutation undergo partial femal
16          We confirmed the high prevalence of FOXL2 and KRAS mutations in granulosa cell tumors and in
17 ary silenced the female sex-maintenance gene Foxl2 and reprogrammed juvenile and adult granulosa cell
18 use Sertoli cells, even in adults, activates Foxl2 and reprograms Sertoli cells into granulosa cells.
19 precipitation assays confirm that endogenous FoxL2 and Smad3 are recruited to the intronic enhancer o
20 hese observations highlight a novel role for FoxL2 and suggest that it may function as a transcriptio
21 tations of the forkhead transcription factor FOXL2 are associated with and likely be responsible for
22                                 Mutations of FoxL2 are associated with the blepharophimosis/ptosis/ep
23                                    Dmrt1 and Foxl2 are conserved throughout vertebrates and Dmrt1-rel
24 ot only do these results establish SMAD4 and FOXL2 as essential master regulators of Fshb transcripti
25                       A new study implicates FOXL2 as the first human gene required for the maintenan
26                      We have determined that FoxL2 binds to a forkhead-binding element (FKHB) located
27                                              FoxL2 directly associates with Smad3 but not Smad2 or Sm
28                      Moreover, we found that FOXL2 directly modulates Esr2 expression through a newly
29                                              Foxl2 disruption thus provides a model for histogenesis
30                                    Exogenous FoxL2 enhances SBE1-mediated transcription, and short ha
31                            DMRT1 can silence Foxl2 even in the absence of the testis-determining gene
32                 Antagonism between Dmrt1 and Foxl2 for control of gonadal sex may therefore extend be
33 ds lacking the forkhead transcription factor Foxl2 form meiotic prophase oocytes, but then activate t
34                    Molecular analysis of the FOXL2 gene revealed the presence of 8 distinct mutations
35 K), LG volume, and molecular analysis of the FOXL2 gene.
36  patients were screened for mutations in the FOXL2 gene.
37            In addition, forced expression of Foxl2 impairs testis tubule differentiation in XY transg
38 in combination with its DNA binding cofactor Foxl2 in gonadotrope cells, mice make essentially no FSH
39        This sheds a new light on the role of FOXL2 in ovarian maintenance and function.
40 transcription factor, DMRT1 in the testis or FOXL2 in the ovary.
41                                              FOXL2 is a lineage determining transcription factor in t
42           This association between Smad3 and FoxL2 is mediated by the MH2 domain of Smad3 and is depe
43                                We found that FOXL2 is required for normal gene regulation by steroid
44                                              FoxL2 localizes to alpha-glycoprotein subunit- and folli
45                             The discovery of FOXL2 may provide insight into the causes of idiopathic
46                     Altogether, we show that FOXL2 mobilizes estrogen signaling to establish a cohere
47                                              FOXL2 mutations cause gonadal dysgenesis or premature ov
48                                  Features of Foxl2 null animals point toward a new mechanism of POF,
49 ion of two ovarian somatic factors, Wnt4 and Foxl2, produces testis differentiation in XX mice, resul
50 hairpin RNA-mediated knockdown of endogenous FoxL2 protein compromises this effect in alphaT3-1 cells
51             Here we report that mice lacking Foxl2 recapitulate relevant features of human BPES: male
52                 Interestingly, we found that FOXL2 repressed the testis-determining gene Sox9 both in
53 tion of the female specific genes, including FOXL2, RSPO1, CYP19A1, WNT4, ERalpha and ERbeta, after o
54 termining decision is not final: loss of the FOXL2 transcription factor in adult granulosa cells can
55 d RAS/ERK1/2 signaling pathways and the FOXO/FOXL2 transcription factors.
56 ear the insertion site likely interacts with Foxl2 TSS.
57 , expression of only one somatic cell marker Foxl2 was reduced in ovaries at day 15.
58 In ovaries, gene expression of RSPO1, LIN28, FOXL2, WNT2B, and ETV5, were significantly higher than i
59  that the relative autonomy of the action of Foxl2, Wnt4 and additional ovarian factor(s) in the mous

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