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anti-Human FOXL2 Antibodies:
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Human Polyclonal FOXL2 Primary Antibody for ChIP, ELISA - ABIN249959
Jamieson, Butzow, Andersson, Alexiadis, Unkila-Kallio, Heikinheimo, Fuller, Anttonen: The FOXL2 C134W mutation is characteristic of adult granulosa cell tumors of the ovary. in Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 2010
Show all 32 Pubmed References
Human Polyclonal FOXL2 Primary Antibody for IHC, ELISA - ABIN185040
Crisponi, Deiana, Loi, Chiappe, Uda, Amati, Bisceglia, Zelante, Nagaraja, Porcu, Ristaldi, Marzella, Rocchi, Nicolino, Lienhardt-Roussie, Nivelon, Verloes, Schlessinger, Gasparini, Bonneau, Cao, Pilia: The putative forkhead transcription factor FOXL2 is mutated in blepharophimosis/ptosis/epicanthus inversus syndrome. in Nature genetics 2001
Show all 3 Pubmed References
Human Polyclonal FOXL2 Primary Antibody for IF (p), IHC (p) - ABIN1715065
Cai, Sun, Li, Tsinkgou, Yu, Ying, Chen, Shi: Molecular mechanisms of enhancing porcine granulosa cell proliferation and function by treatment in vitro with anti-inhibin alpha subunit antibody. in Reproductive biology and endocrinology : RB&E 2015
Human Polyclonal FOXL2 Primary Antibody for FACS, WB - ABIN654125
Nakashima, Chung, Takahashi, Kamatani, Kawaguchi, Tsunoda, Hosono, Kubo, Nakamura, Zembutsu: A genome-wide association study identifies four susceptibility loci for keloid in the Japanese population. in Nature genetics 2010
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Cow (Bovine) Polyclonal FOXL2 Primary Antibody for WB - ABIN6746001
Ayllón, Cayla, García, Roncal, Fernández, Albar, Martínez, Rebollo: Bcl-2 targets protein phosphatase 1 alpha to Bad. in Journal of immunology (Baltimore, Md. : 1950) 2001
Cow (Bovine) Polyclonal FOXL2 Primary Antibody for WB - ABIN2777885
Tang, Wang, Lin, Sun, Wang, Yu: Mutation analysis of the FOXL2 gene in Chinese patients with blepharophimosis-ptosis-epicanthus inversus syndrome. in Mutagenesis 2006
The c.843_859dup17 frameshift mutation probably underlies the blepharophimosis-ptosis-epicanthus inversus type I in this Chinese pedigree
The research on the molecular pathogenesis of FOXL2 in BPES.
We observed no significant difference associated with POI in the patients when compared with a healthy control group (p > 0.05). Also, no exonic variants were found for the genes BMP15 and FOXL2 in the individuals tested
These results confirmed that FOXL2 disruption in KGN cells is associated with the cell cycle attenuation.
We detected two novel missense mutations, c.162G>T (p.Lys54Asn) and c.308G>A (p.Arg103His), in the FOXL2 gene; one in each of the study families. Bioinformatics did predict that the two mutations were likely damaging to protein function.
Thus, FOXL2C134W potentiates CYP19 expression in HGrC1 cells via enhanced recruitment of SMAD3 to a proximal FOX binding element.
In the present study, we analysed two Han Chinese families with BPES type I and identified two novel mutations (c.462_468del and c.988_989insG). Immunofluorescence and confocal microscopy revealed that the extended FOXL2, p.Ala330Glyfs*204, induced significant mislocalization and aggregation.
Three loci with high mutation frequencies, the 138665410 FOXL2 gene variant, the 23862952 MYH6 gene variant, and the 71098693 HYDIN gene variant were found to be significantly associated with sporadic Atrial Septal Defect (P<0.05); variants in FOXL2 and MYH6 were found in patients with isolated, sporadic Atrial Septal Defect (P<5x10-4).
We describe a girl and her father with isolated BPES without an intragenic mutation in FOXL2. MLPA of a FOXL2 enhancer region identified a small microdeletion at 234 kb upstream of FOXL2. This deletion fully includes the PISRT1 gene, a noncoding gene which is part of a cis-regulatory element of FOXL2
MiR-937 inhibits the proliferation and metastasis of gastric cancer cells by targeting FOXL2 via inactivation of PI3K/AKT signaling pathway. These results suggest that miR-937 may be a potential target for the treatment of gastric cancer.
This study demonstrated the existence of an AMH-FOXL2 relationship in hGCs. AMH is capable of increasing both gene and protein expression of FOXL2. Because FOXL2 induces AMH transcription, these ovarian factors could be finely regulated by a positive feedback loop mechanism to preserve the ovarian follicle reserve.
A novel FOXL2 indel mutation was identified in Chinese families with BPES. Our results expand the spectrum of known FOXL2 mutations and provide additional insight into the structure-function relationships of the FOXL2 protein.
The adult granulosa cell tumor (AGCT)-like components are likely to be tumor-like proliferations but not truly neoplastic AGCT. FOXL2 mutation testing may be useful in confirming an AGCT-like component.
This novel duplicate mutation (c.844_860dup17, p.His291Argfs*71) in FOXL2 was identified in a Chinese family with both types of BPES. These findings expand current knowledge of the mutation spectrum of the FOXL2 gene and confirmed the intrafamily phenotypic heterogeneity of BPES.
The study shows that half of granulosa theca cell tumors harbor the same FOXL2 mutation that characterizes adult granulosa cell tumors but there is no outcome evidence to guide whether mutation status should alter the classification of the tumor or the management of the patient.
The promoter of FOXL2 was successfully cloned and registered in Gen Bank, and a dual luciferase reporter (DLR) analysis demonstrated that the luciferase activity was significantly induced by the promoter of FOXL2. Subsequently, bioinformatics analysis indicated that FOXL2 may be regulated by STAT3.
This study demonstrated that the transactivation of FOXL2 driven by interactions between HMGA2 and pRb might exert critical effects on the metastases and EMT of chemoresistant gastric cancer. Blocking the HMGA2-FOXL2-ITGA2 pathway could serve as a new strategy for gastric cancer treatment.
A novel deletion mutation (C.634_641 del, CCCATGC) between the forkhead domain and the polyalanine domain was found, resulting in a frameshift mutation and a truncated protein.
FOXL2 had a sensitivity and specificity of 100% for all the cases of sex cord stromal tumors included in this study
Our results suggest that, in contrast to FOXL2 mutations in adult granulosa cell tumours (A-GCTs), DICER1 mutations in Sertoli-Leydig cell tumours (SLCTs) might be more useful for prognosis than for diagnosis.
comparison of FOXL2 genome-wide occupancy in the fetal ovary with testis-determining factor SOX9 genome-wide occupancy in the fetal testis revealed extensive overlaps, implying that antagonistic signals between FOXL2 and SOX9 occur at the chromatin level.
We found that endometrial cells expressing low FOXL2 levels, either endogenous or genetically manipulated, were associated with a higher attachment rate of mouse blastocysts. low-FOXL2 levels were associated with changes in the expression level of components of the Wnt/Fzd and apoptotic pathways, both of which are involved in uterine receptivity.
Testis determination involves FGFR2c-mediated repression of both the WNT4- and FOXL2-driven ovarian-determining pathways.
direct overexpression of Foxl2 decreased the expression of Sertoli cell-specific genes in primary Sertoli cells. Taken together, these results demonstrate that repression of beta-catenin (CTNNB1) signaling is required for lineage maintenance of Sertoli cells.
evidence that FOXL2 modulates Col1a2 transcription through interaction with a response element 65 Kb upstream of the transcription start site
Data indicate that a balance between supporting cell self-renewal and differentiation is maintained in the developing ovary by relative Wnt4 protein/beta-catenin and p27Kip1 protein (p27)/Forkhead box L2 (FOXL2) activities.
Data indicate that the hypothalamic-pituitary-gonadal axis controls expression of Foxl2 in pituitary gonadotropes primarily through positive feedback from ovarian hormones.
FOXL2 mobilizes estrogen signaling to establish a coherent feed-forward loop repressing Sox9.
Foxl2 has a crucial role in postnatal uterine maturation and could help to understand sub-fertility predisposition in women.
Results support FOXL2 as a master transcription factor in a spectrum of developmental processes, including growth, cartilage and bone formation. Its action overlaps that of SOX9, though they are antagonistic in female vs male gonadal sex determination but conjoint in cartilage and skeletal development.
Microarray expression profiling of whole adrenal mRNA from ovariectomized vs. intact mice demonstrated selective upregulation of gonadal-like genes including Spinlw1 and Insl3 in GDX-induced adrenocortical tumors of the mouse.
our results demonstrate the necessity of FOXL2 for proper FSH production in mice and implicate FOXL2 in integration of transcription factors at the level of the FSHbeta promoter.
Results show that a piggyBac insertion ~160 kb upstream of the transcription start site of Foxl2 partially disrupted its expression resulting in BPES (Blepharophimosis, ptosis, epicanthus inversus syndrome)-like conditions.
AMH is an endogenous target gene of FOXL2. AMH and FOXL2 collaboratively work to reserve ovarian follicles.
In this review, we focus on the role of four specific FOX factors (FOXD1, FOXL2, FOXO1 and FOXP3) in gonadotropin hormone production
When the Smad4 gene is ablated in combination with its DNA binding cofactor Foxl2 in gonadotrope cells, mice make essentially no FSH and females are sterile.
FOXL2 negatively regulates Sf1 expression by antagonizing WT1-KTS during early ovarian development in mice
Differential proximal promoter DNA methylation may contribute to cell- specific Foxl2 expression in some cellular contexts.
results demonstrate that miR-133b down-regulates Foxl2 expression in granulosa cells by directly targeting the 3'UTR
FOXL2 is required for FSH synthesis in vivo.
In vivo and in vitro experiments highlighted that neither interferon-tau nor FOXL2 were involved in transcriptional regulation of CAT, SOD1 and SOD2
involved in the regulation of endometrial tissue physiology
foxl2a and foxl2b cooperate to regulate zebrafish ovary development and maintenance, with foxl2b potentially having a dominant role in preventing the ovary from differentiating as testis, as compared to foxl2a.
Data show that cytochrome P450 enzymes Cyp17-I, Cyp11c1, Cyp19a1a and Cyp19a1b and one of their regulators forkhead protein Foxl2a were detected both in the testis and ovary.
Data indicate taht monocrotophos (MCP) exposure modulated gene expression of forkhead transcription factor gene L2 (foxl2), doublesex/mab-3 related transcription factor 1 (dmrt1), gonadal aromatase (cyp19a1a) and brain aromatase (cyp19a1b).
Effects of sexual steroids on the expression of foxl2 in Gobiocypris rarus
Xenopus W-linked DM-W induces foxl2 expression during ovary formation.
This gene encodes a forkhead transcription factor. The protein contains a fork-head DNA-binding domain and may play a role in ovarian development and function. Mutations in this gene are a cause of blepharophimosis syndrome and premature ovarian failure 3.
forkhead box protein L2
, forkhead transcription factor FOXL2
, pituitary forkhead factor
, putative transcription factor foxl2
, forkhead transcription factor L2
, forkhead box L2
, transcription factor FOXL2
, foxl2 protein
, fork-head box L2 transcription factor
, Forkhead box protein L2