Disease relevance of Ptgir

• Prostaglandin E and prostacyclin receptor expression in tumor and host tissues from MCG 101-bearing mice: a model with prostanoid-related cachexia [1].
• Augmented cardiac hypertrophy in response to pressure overload in mice lacking the prostaglandin I2 receptor [2].
• Translocation of alpha subunits of stimulatory guanine nucleotide-binding proteins through stimulation of the prostacyclin receptor in mouse mastocytoma cells [3].
• To prove that prostaglandin I2 (PGI2) is a major prostaglandin involved in bradykinin-induced exudation, we examined carrageenin- or bradykinin-induced paw edema in prostacyclin receptor-deficient mice (IPKO) [4].

High impact information on Ptgir

• To examine this issue, we cross-bred atherosclerosis-prone apoE-deficient mice with mice deficient in either the TXA receptor (TP) or the PGI receptor (IP) [5].
• Decreased susceptibility to renovascular hypertension in mice lacking the prostaglandin I2 receptor IP [6].
• In contrast, the prostacyclin receptor (IP) mediates the inhibitory effect of higher PGE2 concentrations [7].
• The deduced amino acid sequence has a high degree of similarity with the mouse PGI receptor and the EP2 subtype of the PGE receptor, which together form a subgroup of the prostanoid receptors [8].
• Protein kinase A-mediated phosphorylation of serine 357 of the mouse prostacyclin receptor regulates its coupling to G(s)-, to G(i)-, and to G(q)-coupled effector signaling [9].

Biological context of Ptgir

• A functional cDNA for a mouse prostacyclin receptor was isolated from a mouse cDNA library by reverse transcription polymerase chain reaction and hybridization screening [10].
• Investigation of the effect of the farnesyl protein transferase inhibitor R115777 on isoprenylation and intracellular signalling by the prostacyclin receptor [11].
• Two types of prostacyclin receptor coupling to stimulation of adenylate cyclase and phosphatidylinositol hydrolysis in a cultured mast cell line, BNu-2cl3 cells [12].
• Considering a prostacyclin receptor targeting analgesic agent usually had bleeding action and to appraise the bleeding risk, the in vivo tail bleeding time of 1.30mmol/kg 3a-t receiving mice was found to be ranged from 116.3+/-8.2s to 120.3+/-9.2s, which was substantially equal to that (117.8+/-8.4s to 119.0+/-8.6s) of NS receiving mice [13].
• In contrast, the membrane fraction had the binding site specific for PGE2 and PGE1, which was distinct from the prostacyclin receptor [14].

Anatomical context of Ptgir

• PPAR delta functions as a prostacyclin receptor in blastocyst implantation [15].
• 1 To evaluate the role of prostaglandin I(2) (PGI(2)) in allergic inflammation, allergic responses in the airway, skin and T cells were studied in mice lacking the receptor for PGI(2) (the prostanoid IP receptor) through gene disruption [16].

Associations of Ptgir with chemical compounds

• 7,7-Difluoroprostacyclin derivative, AFP-07, a highly selective and potent agonist for the prostacyclin receptor [17].
• 6. PGE2, PGF2alpha, butaprost (an EP2 agonist) and cicaprost (a PGI receptor agonist) did not affect the nociceptin-induced allodynia [18].
• The persistent response in EP(2) nulls suggests involvement of prostaglandin E(2) receptor subtype 4 and/or prostacyclin receptor (IP) [19].
• Although TEI-3356 is an isocarbacyclin analogue, it showed low affinity for the prostacyclin receptor [20].
• Prostacyclin receptor-independent inhibition of phospholipase C activity by non-prostanoid prostacyclin mimetics [21].

Physical interactions of Ptgir

• Identification of a prostacyclin receptor coupled to the adenylate cyclase system via a stimulatory GTP-binding protein in mouse mastocytoma P-815 cells [14].

Other interactions of Ptgir

• Ptgdr mapped to proximal Chr 14, Ptgfr mapped to distal Chr 3, Ptgerepl mapped to middle Chr 8, and Ptgir mapped to proximal Chr 7 [22].

Analytical, diagnostic and therapeutic context of Ptgir

• To examine this issue, we backcrossed mice lacking the PGI receptor (IP) to the DBA/1J strain and subjected them to collagen-induced arthritis (CIA) [23].
• In situ hybridization studies of prostacyclin receptor mRNA expression in various mouse organs [24].

References