Search results for PTGDS

Showing 8 results out of 8

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Species

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Protein (1 results from a total of 1)

Identifier: R-HSA-2142814
Species: Homo sapiens
Compartment: endoplasmic reticulum membrane
Primary external reference: UniProt: PTGDS: P41222

DNA Sequence (1 results from a total of 1)

Identifier: R-HSA-9641066
Species: Homo sapiens
Compartment: nucleoplasm
Primary external reference: ENSEMBL: ENSG00000107317

Reaction (4 results from a total of 4)

Identifier: R-HSA-9692129
Species: Homo sapiens
Compartment: nucleoplasm, endoplasmic reticulum membrane
In the developing testis, the PTGDS gene is transcribed to yield mRNA and the mRNA is translated to yield PTGDS protein (inferred from mouse homologs). Transcription of PTGDS is directly activated by SOX9 (inferred from mouse homologs).
Identifier: R-HSA-9692154
Species: Homo sapiens
Compartment: nucleoplasm
SOX9 binds the promoter of the PTGDS gene (inferred from mouse homologs).
Identifier: R-HSA-2161620
Species: Homo sapiens
Compartment: endoplasmic reticulum membrane, endoplasmic reticulum lumen
Prostaglandin D2 (PGD2) is a structural isomer of prostaglandin E2 (PGE2). There is a 9-keto and 11-hydroxy group on PGE2 with these substituents reversed on PGD2. PGD2 is formed by two evolutionarily distinct, but functionally convergent, prostaglandin D synthases: lipocalin-type prostaglandin-D synthase aka Prostaglandin-H2 D-isomerase (PTDGS) and hematopoietic prostaglandin D synthase (HPGDS). One of the main differences between these two proteins is that HPGDS requires glutathione (GSH) for catalysis while PTDGS can function without this cofactor. Here, PTDGS promotes the isomerisation of prostaglandin H2 (PGH2) to prostaglandin D2 (PGD2) (Zhou et al. 2010).
Identifier: R-HSA-9690404
Species: Homo sapiens
Compartment: nucleoplasm
Subsequent to SRY expression in the gonadal ridge, the SOX9 gene is transcribed to yield mRNA and the mRNA is translated to yield SOX9 protein (Knower et al. 2011, Croft et al. 2018). SRY and NR5A1 (SF1) bound at the TES enhancer (Knower et al. 2011) and the eALDI enhancer (upstream of the TES enhancer, Croft et al. 2018) of the SOX9 gene initially activate transcription of SOX9 (Knower et al. 2011, Croft et al. 2018, and inferred from mouse homologs). Later, SOX9 and NR5A1 activate the TES enhancer, providing a mechanism for autoregulation (Knower et al. 2011). DMRT1, itself directly activated by SOX9, also directly activates SOX9 (inferred from mouse homologs). FGF9 acting through FGFR2 (inferred from mouse homologs) and Prostaglandin D2 (Malki et al. 2005), the product of PTGDS, activate SOX9 through less well characterized mechanisms.

Complex (1 results from a total of 1)

Identifier: R-HSA-9692114
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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