Disease relevance of Prl3b1

• 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].
• PRL and placental lactogen (PL) stimulate beta-cell proliferation and insulin gene transcription in isolated islets and rat insulinoma cells, but the roles of the lactogenic hormones in islet development and insulin production in vivo remain unclear [2].
• PE(-/-) mice, ELP(-/-) mice, and mice missing both P- and L-selectins (PL(-/-)) show drastic reductions in leukocyte rolling and in extravasation of neutrophils in thioglycollate-induced peritonitis [3].
• The prolactin-like effect of hGH in these mice probably induced female sterility, and milk could therefore not be obtained [4].
• MATERIALS AND METHODS: To determine whether irradiation-induced inflammatory cytokine levels influenced the recovery of tumors following single fraction irradiation, mice with orthotopic Lewis Lung Carcinoma (3LL) tumors received MnSOD-PL treatment 24 hours after tumor implantation and 24 hours prior to irradiation [5].

High impact information on Prl3b1

• Interleukin 6 inhibits mouse placental lactogen II but not mouse placental lactogen I secretion in vitro [6].
• Placental-specific expression from the mouse placental lactogen II gene promoter [7].
• A prolactin-like molecule has also been found in mouse splenocytes and a human B-lymphoblastoid cell line [8].
• There are three types of PL-containing giant cells in mouse placental cell cultures: cells that contain either mPL-I or mPL-II and cells that contain both hormones [9].
• Epidermal growth factor stimulates mouse placental lactogen I but inhibits mouse placental lactogen II secretion in vitro [9].

Chemical compound and disease context of Prl3b1

• To determine whether a slowly proliferating population of cells in the lung was responsible for initiation of fibrosis and was altered by MnSOD-PL therapy, 20 Gy total lung-irradiated mice were examined at serial time points for bromodeoxyuridine (BrdU) uptake in sites of cell division [10].

Biological context of Prl3b1

• The molecule had 77% nucleotide sequence homology with mouse proliferin-related protein (mPRP) and somewhat less homology (approximately 60%) with hamster, rat, and mouse PRL or placental lactogens (PL) [11].
• In humans a five-gene cluster on chromosome 17 contains two growth hormone (GH) and three placental lactogen (PL) genes [12].
• 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].
• Immunoreactive PL-II-producing giant cells were detected first on Day 10 of gestation, continuing on Day 11 of gestation [13].
• The two new clones show 62 and 39% overall homology with each other at the levels of nucleotide and amino acid sequences, respectively. bPLP-I, bPLP-II, placental lactogens, prolactins (PRLs), and other prolactin-like proteins isolated from cow, mouse, and rat share 7 common amino acid residues [14].

Anatomical context of Prl3b1

• Expression of a prolactin-like factor in preneoplastic and neoplastic mouse mammary gland and cells [15].
• Regulation of the production of a prolactin-like protein (MRP/PLF) in 3T3 cells and in the mouse placenta [16].
• Immunocytochemical detection of prolactin or prolactin-like immunoreactivity in epididymis of mature male mouse [17].
• Identification of prolactin-like proteins synthesized by normal murine lymphocytes [18].
• The lipolytic effects of mouse placental lactogen II, mouse prolactin, and mouse growth hormone on adipose tissue from virgin and pregnant mice [19].

Associations of Prl3b1 with chemical compounds

• Co-localization of placental lactogen-I, placental lactogen-II, and proliferin in the mouse placenta at midpregnancy [20].
• The influence of thyroxine, growth hormone and prolactin alone and in combination on the production of prolactin-like activity by splenocytes from Snell dwarf mice [21].
• Further, the phospholipase A effect was nonadditive to the prolactin-like effects produced by the cyclic GMP, prostaglandin F2alpha or arachidonic acid [22].
• Substitution of serine for cysteine-51, which prevents formation of the large disulfide loop, results in a protein equivalent to placental lactogen II in receptor-binding activity; however, this mutant protein is not mitogenic in an assay for lactogenic hormones [23].
• Modulation of mouse placental lactogen-I secretion in vitro: effects of progesterone and mouse placental lactogen-II [24].

Physical interactions of Prl3b1

• Mutant forms of mouse placental lactogen-II (PL-II) have been generated to assess the role of specific amino acid residues and protein regions in binding to the PRL receptor and in mitogenic activity [25].

Regulatory relationships of Prl3b1

• Trophoblast giant cells ceased producing PL-I at midgestation and began expressing PL-II [13].

Other interactions of Prl3b1

• Individual cells contained both PLF and placental lactogen II [26].
• Additionally, both recombinant Rcho-1 PL-I and PL-II proteins are biologically active [1].
• Interestingly, the effects of PL on the GE appear to require the absence of PR and prior exposure to IFN tau [27].
• In eggs collected at the pronuclear stage and cultured to the late two-cell stage in the presence of alpha-amanitin, the matrix morphology was altered for Pl1 and Pl2. alpha-Amanitin had no affect on the distribution of P1 or lamin B antigens [28].
• Saponin effects of prolactin-like stimulation of ornithine decarboxylase activity in mouse mammary gland explants [29].

Analytical, diagnostic and therapeutic context of Prl3b1

• PL-I mRNA expression was assessed by in situ hybridization, and expression of PL-I and PL-II protein was determined by immunocytochemical analysis [13].
• Gel filtration studies of serum samples revealed that PL and GHLA in the hamster, mouse and rat had different elution volumes, whereas, in the remaining species, the two activities co-eluted [30].
• In both strains, a midpregnancy peak in prolactin-like activity was detected by a radioreceptor assay but not by the mPL RIA [31].
• In the medium conditioned by HTS-1 cells, the presence of secretory form of PL and IFNtau was confirmed by Western blotting [32].
• HTS-1 cells express placental lactogen (PL) and interferon-tau (IFNtau), as confirmed by immunocytochemistry, Western blotting and RT-PCR analysis [32].

References