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  • Mice  (2)
  • American Association for the Advancement of Science (AAAS)  (2)
  • American Institute of Physics (AIP)
  • American Society of Hematology
  • National Academy of Sciences
  • Springer
  • Springer Nature
Collection
Publisher
  • American Association for the Advancement of Science (AAAS)  (2)
  • American Institute of Physics (AIP)
  • American Society of Hematology
  • National Academy of Sciences
  • Springer
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  • 1
    Publication Date: 1997-08-01
    Description: Mice lacking the gene encoding the receptor for prostaglandin F2alpha (FP) developed normally but were unable to deliver normal fetuses at term. Although these FP-deficient mice showed no abnormality in the estrous cycle, ovulation, fertilization, or implantation, they did not respond to exogenous oxytocin because of the lack of induction of oxytocin receptor (a proposed triggering event in parturition), and they did not show the normal decline of serum progesterone concentrations that precedes parturition. Ovariectomy at day 19 of pregnancy restored induction of the oxytocin receptor and permitted successful delivery in the FP-deficient mice. These results indicate that parturition is initiated when prostaglandin F2alpha interacts with FP in ovarian luteal cells of the pregnant mice to induce luteolysis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sugimoto, Y -- Yamasaki, A -- Segi, E -- Tsuboi, K -- Aze, Y -- Nishimura, T -- Oida, H -- Yoshida, N -- Tanaka, T -- Katsuyama, M -- Hasumoto, K -- Murata, T -- Hirata, M -- Ushikubi, F -- Negishi, M -- Ichikawa, A -- Narumiya, S -- New York, N.Y. -- Science. 1997 Aug 1;277(5326):681-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiological Chemistry, Faculty of Pharmaceutical Sciences, Kyoto University, Kyoto 606, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9235889" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Corpus Luteum/*metabolism ; Dinoprost/*metabolism ; Female ; Gene Targeting ; Heterozygote ; Homozygote ; *Labor, Obstetric ; Male ; Mice ; Mice, Inbred C57BL ; Ovariectomy ; Oxytocin/biosynthesis/pharmacology ; Pregnancy ; Progesterone/blood ; Receptors, Oxytocin/biosynthesis ; Receptors, Prostaglandin/genetics/*metabolism ; Uterine Contraction/drug effects ; Uterus/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 1995-05-12
    Description: A gene from human chromosome 11p11.2 was isolated and was shown to suppress metastasis when introduced into rat AT6.1 prostate cancer cells. Expression of this gene, designated KAI1, was reduced in human cell lines derived from metastatic prostate tumors. KAI1 specifies a protein of 267 amino acids, with four hydrophobic and presumably transmembrane domains and one large extracellular hydrophilic domain with three potential N-glycosylation sites. KAI1 is evolutionarily conserved, is expressed in many human tissues, and encodes a member of a structurally distinct family of leukocyte surface glycoproteins. Decreased expression of this gene may be involved in the malignant progression of prostate and other cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dong, J T -- Lamb, P W -- Rinker-Schaeffer, C W -- Vukanovic, J -- Ichikawa, T -- Isaacs, J T -- Barrett, J C -- CA 58236/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1995 May 12;268(5212):884-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institute of Health, Research Triangle Park, NC 27709, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7754374" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD/chemistry/*genetics/physiology ; Antigens, CD82 ; Base Sequence ; Biological Evolution ; *Chromosomes, Human, Pair 11 ; Gene Expression ; *Genes, Tumor Suppressor ; Humans ; Male ; Membrane Glycoproteins/chemistry/*genetics/physiology ; Mice ; Mice, SCID ; Molecular Sequence Data ; Neoplasm Metastasis/*genetics ; Prostatic Neoplasms/*genetics/pathology ; *Proto-Oncogene Proteins ; Rats ; Transfection ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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