caa a22 4500 397555288 CHVBK 20180308164800.0 cr unu---uuuuu 161202e199602 xx s 000 0 eng 10.1093/oxfordjournals.jbchem.a021242 doi (NATIONALLICENCE)oxford-10.1093/oxfordjournals.jbchem.a021242 Isolation and Characterization of Retinoic Acid-Inducible cDNA Clones in F9 Cells: A Novel cDNA Family Encodes Cell Surface Proteins Sharing Partial Homology with MHC Class I Molecules [Elektronische Daten] [Zhihua Zou, Midori Nomura, Yoshihiro Takihara, Teruo Yasunaga, Kazunori Shimada] Rae-1 cDNA is one of the retinoic acid (RA)-inducible cDNA clones in mouse embryonal carcinoma F9 cells. Rae-1 mRNAs were detected in mouse early embryos, but not in various tissues of adult mice. RAE-1 protein apparently consists of 253 amino acids and is likely to be a glycoprotein consisting of a leader sequence, an extracellular domain, a serine, threonine, proline-rich domain, and a transmembrane domain. Interestingly, it has a weak, but significant homology with major histocompatibility complex (MHC) class I molecules and was immunocytochemically identified as a cell surface protein. By determining partial nucleotide sequences of 17 Rae-1 cDNAs isolated from the RA-induced F9 cells, at least three different kinds of Rae-1 cDNAs were identified and were named Rae-lα, Rae-1β, and Rae-1γ cDNAs, respectively. As the overall nucleotide sequence homology among these three cDNAs was about 98%, they constitute a novel gene family which is likely to be involved in early mammalian embryogenesis. © by the Journal of Biochemistry Regular Papers nationallicence F9 cell nationallicence membrane glycoprotein nationallicence MHC class I molecule nationallicence RA-inducible gene nationallicence retinoic acid nationallicence Zou Zhihua Department of Medical Genetics, Division of Molecular Biomedicine, Research Institute for Microbial Diseases, Osaka University 3-1 Yamadaoka, Suita, Osaka 565 aut Nomura Midori Department of Medical Genetics, Division of Molecular Biomedicine, Research Institute for Microbial Diseases, Osaka University 3-1 Yamadaoka, Suita, Osaka 565 aut Takihara Yoshihiro Department of Medical Genetics, Division of Molecular Biomedicine, Research Institute for Microbial Diseases, Osaka University 3-1 Yamadaoka, Suita, Osaka 565 aut Yasunaga Teruo Genome Information Research Center, Osaka University 3-1 Yamadaoka, Suita, Osaka 565 aut Shimada Kazunori Department of Medical Genetics, Division of Molecular Biomedicine, Research Institute for Microbial Diseases, Osaka University 3-1 Yamadaoka, Suita, Osaka 565 aut The Journal of Biochemistry Oxford University Press 119/2(1996-02), 319-328 0021-924X 119:2<319 1996 119 jbchem https://doi.org/10.1093/oxfordjournals.jbchem.a021242 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1093/oxfordjournals.jbchem.a021242 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Zou Zhihua Department of Medical Genetics, Division of Molecular Biomedicine, Research Institute for Microbial Diseases, Osaka University 3-1 Yamadaoka, Suita, Osaka 565 aut NATIONALLICENCE 700 1- Nomura Midori Department of Medical Genetics, Division of Molecular Biomedicine, Research Institute for Microbial Diseases, Osaka University 3-1 Yamadaoka, Suita, Osaka 565 aut NATIONALLICENCE 700 1- Takihara Yoshihiro Department of Medical Genetics, Division of Molecular Biomedicine, Research Institute for Microbial Diseases, Osaka University 3-1 Yamadaoka, Suita, Osaka 565 aut NATIONALLICENCE 700 1- Yasunaga Teruo Genome Information Research Center, Osaka University 3-1 Yamadaoka, Suita, Osaka 565 aut NATIONALLICENCE 700 1- Shimada Kazunori Department of Medical Genetics, Division of Molecular Biomedicine, Research Institute for Microbial Diseases, Osaka University 3-1 Yamadaoka, Suita, Osaka 565 aut NATIONALLICENCE 773 0- The Journal of Biochemistry Oxford University Press 119/2(1996-02), 319-328 0021-924X 119:2<319 1996 119 jbchem Metadata rights reserved CC BY-NC-4.0 http://creativecommons.org/licenses/by-nc/4.0 nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-oxford