Search results for FOXL2

Showing 7 results out of 7

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Species

Types

Compartments

Reaction types

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Protein (2 results from a total of 2)

Identifier: R-HSA-3968421
Species: Homo sapiens
Compartment: nucleoplasm
Primary external reference: UniProt: FOXL2: P58012
Identifier: R-HSA-3968395
Species: Homo sapiens
Compartment: nucleoplasm
Primary external reference: UniProt: FOXL2: P58012

DNA Sequence (1 results from a total of 1)

Identifier: R-HSA-9692247
Species: Homo sapiens
Compartment: nucleoplasm
Primary external reference: ENSEMBL: ENSEMBL:ENSG00000183770

Reaction (2 results from a total of 2)

Identifier: R-HSA-9692236
Species: Homo sapiens
Compartment: nucleoplasm
DMRT1 binds the FOXL2 gene and represses transcription of FOXL2, a promoter of ovary differentiation (inferred from mouse homologs).
Identifier: R-HSA-3968414
Species: Homo sapiens
Compartment: nucleoplasm
UBC9 and PIAS1 SUMOylate FOXL2 with SUMO1 (Kuo et al. 2009, Marongiu et al 2010, Georges et al. 2011). This modification changes its cellular localization, stability and transcriptional activity (Marongiu et al, 2010). SUMOylation localizes FOXL2 to PML bodies in the nucleus. SUMOylation is required for repression of transcription by FOXL2 at the StAR promoter and reduces transactivation by FOXL2 at the PER2 promoter. Hypophosphorylation of serine-33 correlates with SUMOylation and stablization of FOXL2, leading to enhanced transcriptional activation of TNF-R1, FAS, caspase 8, p21, and aromatase (Kim et al. 2014).

Complex (1 results from a total of 1)

Identifier: R-HSA-9692237
Species: Homo sapiens
Compartment: nucleoplasm

Pathway (1 results from a total of 1)

Identifier: R-HSA-9690406
Species: Homo sapiens
In humans, primordial germ cells (PGCs) are specified about 2 weeks after fertilization, a time before gastrulation (reviewed in Svingen and Koopman 2013, Mäkelä et al. 2019). PGCs are initially located extraembryonically and then migrate to colonize the gonadal ridges (genital ridges) of the embryo during the fifth week after fertilization. At this time, either ovaries and testes can originate from the gonadal ridges. That is, the cells of the gonadal ridges are initially bipotential and remain bipotential until about 42 days after conception, when transient expression of the SRY gene located on the Y chromosome in male embryos is initiated in some somatic cells of the gonadal primordium (reviewed in Sekido and Lovell-Badge 2013, Barrionuevo et al. 2013, Svingen et al. 2013, Mäkelä et al. 2019).
The transcription factors WT1, GATA4, ZFPM2 (FOG2), and the nuclear receptor NR5A1 (SF1) activate transcription of SRY (Shimamura et al. 1997, Hossain and Saunders 2001, De Santa Barbara et al. 2001, Miyamoto et al. 2008, and inferred from mouse homologs). SRY and NR5A1 then activate transcription of SOX9, one of the master regulators of testis development and maintenance (Knower et al. 2011, Croft et al. 2018, inferred from mouse homologs, reviewed in Gonen and Lovell-Badge 2019). Regulation of genes by SRY and then, when expression of SRY decreases, by SOX9 causes the specification of Sertoli cells that further organize formation of the testis by encasing the primordial germ cells in protocords, which then form fully developed testis cords.
SOX9 directly activates its own promoter to maintain SOX9 expression through development and into adulthood (Croft et al. 2018, and inferred from mouse homologs). SOX9 and GATA4 directly activate DMRT1 (inferred from mouse homologs), which maintains testis specification by maintaining expression of SOX9 and other testis-related genes. DMRT1 also acts to suppress ovarian specification by binding and repressing FOXL2 and WNT4 genes (inferred from mouse homologs). SOX9 directly activates FGF9 (inferred from mouse homologs), which acts via FGFR2 to maintain SOX9 expression, and PTGDS (inferred from mouse homologs), which converts Prostaglandin H2 to Prostaglandin D2, a critical hormone-like lipid that recruits supporting cells to Sertoli cells and acts indirectly to maintain SOX9 expression. SOX9, NR5A1, and GATA4 directly activate AMH (De Santa Barbara et al. 1998, and inferred from mouse homologs), an extracellular signaling molecule which causes regression of the Muellerian duct of the female reproductive system. SOX9 also directly activates many other genes, including DHH (Rahmoun et al. 2017, and inferred from mouse homologs), an intercellular signaling molecule required for testis formation.
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