Chromosomal localization of the human prostanoid receptor gene family

Duncan, Alessandra M.V.; Anderson, Linda; Funk, Colin D.; Abramovitz, Mark; Adam, Mohammed

doi:10.1016/0888-7543(95)80022-e

Cited by 31 publications

(17 citation statements)

References 14 publications

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“…This is consistent with the possibility that FP and EP3 receptors might have arisen as a result of duplication of a single ancestral gene. In contrast TP and EP1 receptors are syntenic on human chromosome 19 (50). Within this syntenic pair, both receptors signal via pertussis toxininsensitive Ca 2ϩ -coupled pathways (20,47).…”

Section: Discussionmentioning

confidence: 99%

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Characterization of a Rabbit Kidney Prostaglandin F2α Receptor Exhibiting Gi-restricted Signaling That Inhibits Water Absorption in the Collecting Duct

Hébert

Carmosino

Saito

et al. 2005

Journal of Biological Chemistry

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PGF 2␣ is the most abundant prostaglandin detected in urine; however, its renal effects are poorly characterized. The present study cloned a PGF-prostanoid receptor (FP) from the rabbit kidney and determined the functional consequences of its activation. Nuclease protection assay showed that FP mRNA expression predominates in rabbit ovary and kidney. In situ hybridization revealed that renal FP expression predominates in the cortical collecting duct (CCD Prostaglandin F 2␣ is a major prostaglandin excreted in urine (1) and is known to exert potent biological effects via its G protein-coupled cell membrane receptor designated the F-prostanoid (FP) 2 receptor (2-6). FP receptor mRNA is highly expressed along the genitourinary tract including ovary Ͼ uterus and kidney (7-9). Recent studies in mouse kidneys have shown that FP receptor expression is particularly abundant in the distal convoluted tubules and cortical collecting duct (10). The cellular and functional consequences of renal FP receptor activation in these renal epithelia have not been determined. Like PGE 2 (11), intravenous infusion of PGF 2␣ causes both a natriuresis and diuresis (4); however, because high concentrations of PGF 2␣ can cross-activate prostaglandin E 2 -EP3 receptors (12, 13), the molecular basis of PGF 2␣ -associated diuresis remains uncertain. The functional activity of PGE 2 in the rabbit collecting duct epithelium has been elucidated through use of the in vitro microperfused tubule (9, 14 -16); however, the effect of selective FP receptor activation in this segment has not previously been examined. The aim of the present study was to clone the rabbit FP receptor, determine its intrarenal distribution, and elucidate its functional activity in the kidney.

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Section: Discussionmentioning

confidence: 99%

“…It is notable that the FP and EP3 receptors are syntenic, residing in close proximity on chromosome 1 in humans (50) and chromosome 3 in mice (51). In addition, multiple C-terminal splice variants exist for both FP and EP3 receptors (52)(53)(54)(55).…”

Section: Discussionmentioning

confidence: 99%

Characterization of a Rabbit Kidney Prostaglandin F2α Receptor Exhibiting Gi-restricted Signaling That Inhibits Water Absorption in the Collecting Duct

Hébert

Carmosino

Saito

et al. 2005

Journal of Biological Chemistry

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“…A human homologue of the candidate for the Mom1 locus has been mapped to 1p35-p36.1 (Praml et al, 1995). Other genes or homologues to genes involved in cell growth and fidelity are: transcription factors, E2F2 on 1p36.11 (Lees et al, 1993), PAX7 on 1p36.1 (Vorobyov et al, 1997) and L-myc on 1p34.3 (Speleman et al, 1996); replication protein gene RPA2 on 1p35 (Ozawa et al, 1993); death receptor genes, TR2 (Kwon et al, 1997), TNFR2 (Kemper et al, 1991), DR3 (Bodmer et al, 1997) and DR5 (Wu et al, 1997), all on 1p36; other receptor genes, PTAFR on 1p34.3-p35 (Chase et al, 1996), TGFβR3 on 1p32-p33 (Johnson et al, 1995) and IL12Rβ2 on 1p31.2 (Yamamoto et al, 1997); prostaglandin receptors, PTGER3 on 1p31.2 and PTGFR on 1p31.1 (Duncan et al, 1995); tyrosine kinases, ECK on 1p36.1 (Sulman et al, 1997), LCK on 1p35 (Volpi et al, 1994) and JAK1 on 1p31.3-p32.3 (Modi et al, 1995); dual specific kinase ERK (Saito et al, 1995) on 1p36.1; repair protein genes, RAD54 on 1p32 (Rasio et al, 1997); and GADD45 on 1p31.1-p31.2 (Hey et al, 1996); cell cycle control proteins , 70 60 50 40 30 20 10 0 D1S243 D1S468 D1S214 D1S228 D1S507 D1S436 D1S201 D1S209 D1S216 D1S207 D1S488 D1S167 D1S435 70 60 50 40 30 20 10 0 A B %LOH %LOH D1S243 D1S468 D1S214 D1S228 D1S507 D1S436 D1S201 D1S209 D1S216 D1S207 D1S488 D1S167 D1S435 70 60 50 40 30 20 10 0 D %LOH D1S243 D1S468 D1S214 D1S228 D1S507 D1S436 D1S201 D1S209 D1S216 D1S207 D1S488 D1S167 D1S435 70 60 50 40 30 20 …”

Section: Discussionmentioning

confidence: 99%

“…A complex pattern of LOH and loss of all markers analysed is more frequently detected in lung and colorectal tumours than tumours of breast and kidney. The fraction of complete loss of chromosome 1p31-pter (all informative markers with LOH) was as following: testis, 0/30 (0%); breast, 6/238 (2.5%); kidney, 3/73 (4.1%); stomach, 2/38 (5.3%); thyroid, 1/14 (7.1%); colon/rectum, 14/109 (13%); lung, 9/63 (14%); ovaries, 5/31 (16%); endometrium, 5/25 (20%); and sarcoma, 3/14 (21% (Lahti et al, 1994) E2F2 1p36.11 (Lees et al, 1993) RIZ 1p36.1 (Vorobyov et al, 1996) PAX7 1p36.1 (Buyse et al, 1997) ECK 1p36.1 (Sulman et al, 1997) ERK 1p36.1 (Saito et al, 1995) MOM1 1p35-p36.1 (Praml et al, 1995) RPA2 1p35-p36.1 (Ozawa et al, 1993) CDC 42 1p35-p36 (Jensen et al, 1997) LCK 1p35 (Volpi et al, 1994) PTAFR 1p34.3-p35 (Chase et al 1996) MYCL1 1p34.3 (Speleman et al, 1996) TGFBR3 1p32-p33 (Johnson et al, 1995) RAD54 1p32 (Rasio et al, 1997) JAK1A 1p31.3-p32.3 (Modi et al, 1995) p18 (INK4C) 1p32 (Lapointe et al, 1996) IL12RB2 1p31.2 (Yamamoto et al, 1997) GADD45 1p31.1-31.2 (Hey et al, 1996) PTGER3 1p31.2 (Duncan et al, 1995) PTGER 1p31.1 (Duncan et al, 1995) SROs detected in the other three tumour types (Figure 4). A difference is also detected between the renal tumours and the other tumour types in the 1p32 region.…”

Section: Loss Of Heterozygosity At Chromosome 1pmentioning

confidence: 99%

Loss of heterozygosity at chromosome 1p in different solid human tumours: association with survival

et al. 1999

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SummaryThe distal half of chromosome 1p was analysed with 15 polymorphic microsatellite markers in 683 human solid tumours at different locations. Loss of heterozygosity (LOH) was observed at least at one site in 369 cases or 54% of the tumours. LOHs detected ranged from 30-64%, depending on tumour location. The major results regarding LOH at different tumour locations were as follows: stomach, 20/38 (53%); colon and rectum, 60/109 (55%); lung, 38/63 (60%); breast, 145/238 (61%); endometrium, 18/25 (72%); ovary, 17/31 (55%); testis, 11/30 (37%); kidney, 22/73 (30%); thyroid, 4/14 (29%); and sarcomas, 9/14 (64%). High percentages of LOH were seen in the 1p36.3, 1p36.1, 1p35-p34.3, 1p32 and 1p31 regions, suggesting the presence of tumour-suppressor genes. All these regions on chromosome 1p show high LOH in more than one tumour type. However, distinct patterns of LOH were detected at different tumour locations. There was a significant separation of survival curves, with and without LOH at chromosome 1p, in the breast cancer patients. Multivariate analysis showed that LOH at 1p in breast tumours is a better indicator for prognosis than the other variables tested in our model, including nodal metastasis.

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“…The genes encoding human, mouse, and rat EP4 have been mapped to chromosomes 5p13.1, 15, and 2q16 (Taketo et al, 1994;Duncan et al, 1995), respectively. The EP4 receptor is also present in nonmammalian vertebrates, such as chickens (Kwok et al, 2008) and zebrafish (Cha et al, 2006).…”

Section: A Cloningmentioning

confidence: 99%