戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 f Amh and Sox9, and a decline in Cyp19a1 and Foxl2.
2 egulation of ovarian regulators, Cyp19a1 and Foxl2.
3  mechanistic study of BPES and regulation of Foxl2.
4 duces, but not eliminates, the expression of Foxl2.
5 eam of the transcription start site (TSS) of Foxl2.
6 is dependent on an intact forkhead domain in FoxL2.
7  all consistent with an anti-testis role for Foxl2.
8 ce-specific chromatin remodeling activity in FOXL2.
9 vivo the poorly understood oncogenic role of FOXL2.
10 (p.C134W) affecting the transcription factor FOXL2.
11 al c.C402G (p.Cys134Trp) somatic mutation in FOXL2, a forkhead box family transcription factor import
12                                We identified FoxL2, a member of the forkhead family, as a candidate m
13                        Haploinsufficiency of FOXL2, a new forkhead transcription factor, causes bleph
14 ramming, as described in adult ovaries after Foxl2 ablation.
15                                      Pivotal Foxl2 action thus represses the male gene pathway at sev
16 kely be responsible for many BPES cases, how FOXL2 affects craniofacial development remain to be unde
17                     The female-related genes foxl2 and cyp19a1a were significantly increased in the g
18 sed CTNNB1, increased expression of WNT4 and FOXL2 and decreased expression of SRY and SOX9.
19     In this study, we explore the targets of FOXL2 and five nuclear receptors in murine primary folli
20 mice, and germ cell-depleted XX mice lacking Foxl2 and harboring a Kit mutation undergo partial femal
21          We confirmed the high prevalence of FOXL2 and KRAS mutations in granulosa cell tumors and in
22 ary silenced the female sex-maintenance gene Foxl2 and reprogrammed juvenile and adult granulosa cell
23 use Sertoli cells, even in adults, activates Foxl2 and reprograms Sertoli cells into granulosa cells.
24 precipitation assays confirm that endogenous FoxL2 and Smad3 are recruited to the intronic enhancer o
25 hese observations highlight a novel role for FoxL2 and suggest that it may function as a transcriptio
26 tations of the forkhead transcription factor FOXL2 are associated with and likely be responsible for
27                                 Mutations of FoxL2 are associated with the blepharophimosis/ptosis/ep
28                                    Dmrt1 and Foxl2 are conserved throughout vertebrates and Dmrt1-rel
29                Germline dominant variants in FOXL2 are responsible for blepharophimosis syndrome, whi
30 ot only do these results establish SMAD4 and FOXL2 as essential master regulators of Fshb transcripti
31                       A new study implicates FOXL2 as the first human gene required for the maintenan
32                      We have determined that FoxL2 binds to a forkhead-binding element (FKHB) located
33  adult-type granulosa cell tumors shows that FOXL2 C134W shifts the transcriptome towards a signature
34 ation of altered DNA-binding specificity for FOXL2(C134W) and identification of unique targets of FOX
35                                              FOXL2(C134W) associated with the majority of the FOXL2 w
36                          Our results suggest FOXL2(C134W) drives AGCT by altering the binding affinit
37 34W) and identification of unique targets of FOXL2(C134W) including SLC35F2, whose expression increas
38               A mechanistic understanding of FOXL2(C134W)-induced regulatory state alterations drives
39 chanisms, we engineered V5-FOXL2(WT)- and V5-FOXL2(C134W)-inducible isogenic cell lines and performed
40                               Interestingly, Foxl2+/C134W female mice had reduced fertility and devel
41 ce of additional driver mutations apart from FOXL2-C134W.
42 ves AGCT by altering the binding affinity of FOXL2-containing complexes to engage an oncogenic transc
43                       Differential timing of Foxl2 deletion, in embryonic versus adult mouse ovary, l
44                                              FoxL2 directly associates with Smad3 but not Smad2 or Sm
45                      Moreover, we found that FOXL2 directly modulates Esr2 expression through a newly
46                                              Foxl2 disruption thus provides a model for histogenesis
47 ectly from bipotential precursors, expresses Foxl2 early, and associates with cysts throughout the ov
48                                    Exogenous FoxL2 enhances SBE1-mediated transcription, and short ha
49                            DMRT1 can silence Foxl2 even in the absence of the testis-determining gene
50    Wave 1 follicles, lineage-marked by E16.5 Foxl2 expression in granulosa cells, reach preantral sta
51 r earlier, expresses Lgr5, but delays robust Foxl2 expression until after birth.
52                 Antagonism between Dmrt1 and Foxl2 for control of gonadal sex may therefore extend be
53 ds lacking the forkhead transcription factor Foxl2 form meiotic prophase oocytes, but then activate t
54                    Molecular analysis of the FOXL2 gene revealed the presence of 8 distinct mutations
55 K), LG volume, and molecular analysis of the FOXL2 gene.
56  patients were screened for mutations in the FOXL2 gene.
57 n typically associated with mutations in the FOXL2 gene.
58            In addition, forced expression of Foxl2 impairs testis tubule differentiation in XY transg
59 in combination with its DNA binding cofactor Foxl2 in gonadotrope cells, mice make essentially no FSH
60        This sheds a new light on the role of FOXL2 in ovarian maintenance and function.
61 transcription factor, DMRT1 in the testis or FOXL2 in the ovary.
62                               The absence of FOXL2 involvement emphasizes the importance of broad gen
63                                              FOXL2 is a lineage determining transcription factor in t
64           This association between Smad3 and FoxL2 is mediated by the MH2 domain of Smad3 and is depe
65                                We found that FOXL2 is required for normal gene regulation by steroid
66                     The transcription factor FOXL2 is required in ovarian somatic cells for female fe
67 ies, we created and characterized endogenous FOXL2 isogenic AGCT cells and an AGCT tumoroid biobank.
68                            Unexpectedly, the Foxl2 lineage tag also marked about 400 primordial folli
69                                              FoxL2 localizes to alpha-glycoprotein subunit- and folli
70 d biallelic deleterious variants in 6 genes, FOXL2, MAJIN, KASH5, SYCP2, MEIOB, and HFM1, in patients
71                             The discovery of FOXL2 may provide insight into the causes of idiopathic
72                     Altogether, we show that FOXL2 mobilizes estrogen signaling to establish a cohere
73     A newly generated mouse model carrying a FOXL2 mutation characteristic of adult-type granulosa ce
74 s incurable, but the mechanism of the unique FOXL2 mutation could confer therapeutic vulnerabilities.
75                                              FOXL2 mutations cause gonadal dysgenesis or premature ov
76 hogenic variant in the COLEC10 gene, with no FOXL2 mutations detected.
77                                  Features of Foxl2 null animals point toward a new mechanism of POF,
78 vel, RUNX1 occupancy overlaps partially with FOXL2 occupancy in the fetal ovary, suggesting that RUNX
79 ion of two ovarian somatic factors, Wnt4 and Foxl2, produces testis differentiation in XX mice, resul
80                                              Foxl2 promoter-driven knockout of Yap1 in ovarian granul
81  In the mouse ovary, oestrogen receptors and FOXL2 protect ovarian granulosa cells from transdifferen
82 hairpin RNA-mediated knockdown of endogenous FoxL2 protein compromises this effect in alphaT3-1 cells
83             Here we report that mice lacking Foxl2 recapitulate relevant features of human BPES: male
84                                We found that FOXL2 regulates more targets postnatally, through intera
85                 Interestingly, we found that FOXL2 repressed the testis-determining gene Sox9 both in
86 cell identity and combined loss of RUNX1 and FOXL2 results in masculinization of fetal ovaries.
87 tion of the female specific genes, including FOXL2, RSPO1, CYP19A1, WNT4, ERalpha and ERbeta, after o
88        Here, we comprehensively investigated FOXL2's role through a multi-omics approach to character
89 n the fetal ovary, suggesting that RUNX1 and FOXL2 target common sets of genes.
90 , coupled with genome-wide identification of FOXL2 targets and on-chromatin interacting partners in s
91 a mouse model harboring the C134W variant of FOXL2 to evaluate in vivo the poorly understood oncogeni
92 NX1 plays complementary/redundant roles with FOXL2 to maintain fetal granulosa cell identity and comb
93 s recruited on chromatin in the proximity of FOXL2 to maintain the ovarian pathway and to repress tes
94 termining decision is not final: loss of the FOXL2 transcription factor in adult granulosa cells can
95 nse point mutation c.402C>G (p.C134W) in the FOXL2 transcription factor is pathognomonic for adult-ty
96 d RAS/ERK1/2 signaling pathways and the FOXO/FOXL2 transcription factors.
97 ear the insertion site likely interacts with Foxl2 TSS.
98 , expression of only one somatic cell marker Foxl2 was reduced in ovaries at day 15.
99 2(C134W) associated with the majority of the FOXL2 wild-type DNA elements as well as a large collecti
100 In ovaries, gene expression of RSPO1, LIN28, FOXL2, WNT2B, and ETV5, were significantly higher than i
101  that the relative autonomy of the action of Foxl2, Wnt4 and additional ovarian factor(s) in the mous
102 o explore these mechanisms, we engineered V5-FOXL2(WT)- and V5-FOXL2(C134W)-inducible isogenic cell l

 
Page Top