High impact information on Prl8a5

• A PLP-C cDNA was used to identify dPRP cDNAs from a rat decidual cDNA library [1].
• NH2-terminal sequencing of the isolated decidual protein indicated that it shared significant sequence identity with the NH2 terminus of PLP-C [1].
• Six of the cysteine residues in PLP-C are located in positions homologous to the cysteines of pituitary prolactin (PRL) [2].
• Nucleotide sequence analysis of the PLP-C cDNA clone predicted a mature protein of 238 amino acids, including a 30-amino acid signal sequence [2].
• In this report, we describe the isolation and characterization of a full length cDNA clone for rat prolactin-like protein C (PLP-C) and describe the expression of PLP-C mRNA in the developing rat placenta [2].

Biological context of Prl8a5

• The clone was amplified from a 13.5-day-old mouse conceptus cDNA library by PCR using primers based on conserved regions of PLP-C sequences [3].
• In summary, overall high amino acid identity (79%), the locations of cysteine residues, and consensus sites for N-linked glycosylation between mouse and rat PLP-Cbeta clearly indicate that PLP-Cbeta is a bona fide member of the PLP-C subfamily [3].
• PLP-C mRNA was first detectable between days 13 and 14 of gestation, peaked by day 18 of gestation, and remained elevated until term [2].
• The PLP-C gene was localized to rat chromosome 17 [2].
• The predicted PLP-C amino acid sequence contains seven cysteine residues, three tryptophan residues, and two putative N-linked glycosylation sites [2].

Anatomical context of Prl8a5

• In situ hybridization analysis indicated that PLP-C mRNA was specifically expressed by spongiotrophoblast cells and some trophoblast giant cells in the junctional zone region of rat chorioallantoic placenta [2].
• Little is known about the mechanisms of: 1) biliary phosphatidylcholine (PC) secretion by the hepatocyte, 2) selectivity for biliary 1-palmitoyl-2-linoleoyl-PC (PLPC) secretion, and 3) exclusion of 1-stearoyl-2-arachidonyl-PC (SAPC) from bile [4].
• In contrast to conditioned medium, native PLP-B and PLP-C preparations failed to show any significant stimulation of endothelial cell migration [5].

Associations of Prl8a5 with chemical compounds

• The predicted protein shares 55-66% amino acid identity with mouse PLP-Calpha and rat PLP-D, PLP-H, PLP-Cv, and PLP-C and also contains 6 homologously positioned cysteine residues [3].
• Compared to bile acid depletion, infusion of each bile acid caused PLPC to decrease from 59% of bile PC to 48%, and SAPC to increase from 2.6% to 5% [4].
• This was done by intravenous injection of PLPC and SAPC labeled in the linoleate (14C) and arachidonate (3H) moieties [4].
• The melatonin agonist, chloromelatonin in culture media also decreased the levels of PL-Iv, PL-II and PLP-C mRNA [6].

Other interactions of Prl8a5

• Injected DA agonist, bromocriptine (in vivo) decreased PL-Iv, PLP-C and Pit-1 mRNA levels in the rat placenta [6].
• Temporally the increase in PLP-A expression preceded the increased expression of PLP-B (0.9 kb), PLP-C, and PL-Iv [7].

Analytical, diagnostic and therapeutic context of Prl8a5

• Northern blot analysis showed that the PLP-C cDNA clone specifically hybridized to a 1.0-kilobase mRNA [2].

References