Disease relevance of Prl3d1

• Both recombinant Rcho-1 PL-I and PL-II proteins significantly stimulated the proliferation of lactogen-dependent rat Nb2 lymphoma cells and mouse mammary epithelial cells [1].

High impact information on Prl3d1

• In addition, overexpression of Hxt induced the differentiation of rat trophoblast (Rcho-1) stem cells as assayed by changes in cell adhesion and by activation of the placental lactogen-I gene promoter, a trophoblast giant cell-specific gene [2].
• In contrast, the negative HLH regulator, Id-1, inhibited Rcho-1 differentiation and placental lactogen-I transcription [2].
• The mouse homologue of the human PI-6 gene has been designated Spi3 and was mapped to chromosome 13 between the Pl1 and ctla2 alpha genes [3].
• Furthermore, PL-I and PL-Iv were synthesized at different times during gestation and by different cell types [4].
• Multiple PL-I and PL-Iv species were present in placental cytosol [4].

Biological context of Prl3d1

• We have isolated the gene encoding mouse placental lactogen-I and characterized the promoter region of this gene by transient and stable transfection [5].
• Given these results, we examined the original PL-I cDNA by PCR and nucleotide sequence analyses [1].
• The PL-I gene was localized to chromosome 17 of the rat genome, similar to other PRL family members [1].
• A complementary DNA (cDNA) library to differentiated Rcho-1 trophoblast cells was constructed and screened with probes to detect PL-I and PL-II [1].
• Antibodies to peripheral and interior antigens (P1, Pl1, Pl2, and lamin B) were used to immunolocalize nuclear matrix antigens in germinal vesicle oocytes, metaphase II oocytes, zygotes, two-cell-stage embryos, and eight-cell stage embryos [6].

Anatomical context of Prl3d1

• PL-I was synthesized by trophoblast giant cells during the first half of gestation, while PL-Iv was predominantly synthesized by spongiotrophoblast cells during the later stages of gestation [4].
• Specifically, the basic helix-loop-helix (bHLH) transcription factor Hand1 is essential for differentiation of trophoblast giant cells in mice and also regulates the promoter for the giant cell-specific hormone, placental lactogen I gene (Pl1) [7].
• The binding of recombinant mouse placental lactogen-I (mPL-Ir) to liver and ovarian membranes was investigated in virgin and pregnant mice [8].
• To determine whether the pituitary gland influences the concentration of mouse placental lactogen-I (mPL-I) in maternal serum, pregnant Swiss Webster mice were hypophysectomized or sham-operated on day 9 of gestation [9].
• Initiation of placental lactogen-I production by blastocysts growing on a two-dimensional surface and in hanging drops [10].

Associations of Prl3d1 with chemical compounds

• Two PRL-like glycoprotein hormone complexes were purified from the medium of cultured mouse conceptuses from day 10 of pregnancy: mouse placental lactogen-I (mPL-I) (29-32K), and mPL-I (36.5-42K) [11].
• Modulation of mouse placental lactogen-I secretion in vitro: effects of progesterone and mouse placental lactogen-II [12].
• Cyclic adenosine-3',5'-monophosphate stimulates mouse placental lactogen-I (mPL-I) secretion but inhibits mPL-II secretion at midpregnancy [13].
• Mouse placental lactogen-I (mPL-I), mPL-II, GH, and corticosterone concentrations were measured by RIA and related to hepatic GHR activity and serum GHBP concentration [14].

Regulatory relationships of Prl3d1

• The increase in the number of PLF-producing cells was accompanied by an increase in the number of cells expressing both PLF and mouse placental lactogen-I [15].
• Trophoblast giant cells ceased producing PL-I at midgestation and began expressing PL-II [16].
• The aim of this study was to determine whether transforming growth factor-alpha (TGF-alpha) regulates expression of mouse placental lactogen-I (mPL-I) and mPL-II at midpregnancy in vitro [17].

Other interactions of Prl3d1

• Oligonucleotides (20-23 bp) corresponding to regions of nucleotide homology between mouse PL-I (mPL-I) and rat PL-I (rPL-I) along with midgestation hamster placental RNA were used in 3' rapid amplification of cDNA ends (RACE) methodology to generate PRL-like cDNA [18].
• To determine whether lipopolysaccharides (LPS) regulate mouse placental lactogen-I (mPL-I), mPL-II, and mouse GHRF (mGHRF) secretion, mouse placental tissue from days 7, 9, and 12 of pregnancy was dispersed with collagenase and the purified trophoblast cells were cultured in a serum-free medium with or without LPS for 5 days [19].
• After 24 h, the medium was replaced with fresh medium with/or without mouse PRL (mPRL), mouse placental lactogen-I (mPL-I), mPL-II, mouse GH (mGH), IGF-I, and IGF-II, either alone or in combinations [20].
• Transforming growth factor-alpha regulates subpopulation of giant cells which secrete mouse placental lactogen-I (mPL-I) and/or mPL-II at midpregnancy [17].

Analytical, diagnostic and therapeutic context of Prl3d1

• Amino-terminal sequence analysis indicated that PL-Iv shared approximately 88% sequence identity with the amino terminus of PL-I [4].
• The primary objective of this study was to develop a cell culture system for assessing effects of putative secretagogues on mouse PL-I (mPL-I) secretion [12].
• PL-I mRNA expression was assessed by in situ hybridization, and expression of PL-I and PL-II protein was determined by immunocytochemical analysis [16].
• Pituitary-placental interaction: hypophysectomy modulates the secretion of mouse placental lactogen-I [9].
• Cytokines that use gp130 as a signal transducer stimulate mouse placental lactogen-I (mPL-I) but inhibit mPL-II production in vitro [21].

References