TY - JOUR
T1 - Molecular cloning of a novel apoptosis-related gene, human Nap1 (NCKAP1), and its possible relation to Alzheimer disease
AU - Suzuki, Takashi
AU - Nishiyama, Kazutoshi
AU - Yamamoto, Ayako
AU - Inazawa, Jyoji
AU - Iwaki, Toru
AU - Yamada, Takeshi
AU - Kanazawa, Ichiro
AU - Sakaki, Yoshiyuki
N1 - Funding Information:
We thank Dr. S. Kohsaka, Department of Neurochemistry, National Institute of Neuroscience, and Y. Misumi, Faculty of Medicine, Fukuoka University, for their generous gift of cell line and cDNA library, respectively. We also thank Dr. M. Ohashi, Faculty of Science, Nagoya University, for helpful discussion. This work was partly supported by a Grant-in-Aid for Scientific Research from the Ministry of Education, Science, Sports, and Culture, Japan and Grants from the Japan Science and Technology Corp.
PY - 2000/1/15
Y1 - 2000/1/15
N2 - Expression profiles of thousands of genes (cDNAs) were analyzed in sporadic Alzheimer disease (AD)-affected brains in comparison with normal subjects by using the high-density cDNA filter method and differential display analysis. Among 31 differentially expressed genes, one gene was found to be markedly depressed in AD-affected brains. A full-length (or nearly full-length) cDNA of the gene was isolated and sequenced. The cDNA turned out to be an orthologue of rat Nap1. The gene was thus designated human Nap1 (HGMW-approved symbol NCKAP1) and was mapped to human chromosome 2q32 by fluorescence in situ hybridization. Northern blotting and in situ hybridization studies showed that in brain, the gene is predominantly expressed in neuronal cells. Antisense oligo DNA of human Nap1 transcripts was found to induce apoptosis of neuronal cells. Based on these results, the possible role of human Nap1 in AD is discussed. (C) 2000 Academic Press.
AB - Expression profiles of thousands of genes (cDNAs) were analyzed in sporadic Alzheimer disease (AD)-affected brains in comparison with normal subjects by using the high-density cDNA filter method and differential display analysis. Among 31 differentially expressed genes, one gene was found to be markedly depressed in AD-affected brains. A full-length (or nearly full-length) cDNA of the gene was isolated and sequenced. The cDNA turned out to be an orthologue of rat Nap1. The gene was thus designated human Nap1 (HGMW-approved symbol NCKAP1) and was mapped to human chromosome 2q32 by fluorescence in situ hybridization. Northern blotting and in situ hybridization studies showed that in brain, the gene is predominantly expressed in neuronal cells. Antisense oligo DNA of human Nap1 transcripts was found to induce apoptosis of neuronal cells. Based on these results, the possible role of human Nap1 in AD is discussed. (C) 2000 Academic Press.
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U2 - 10.1006/geno.1999.6053
DO - 10.1006/geno.1999.6053
M3 - Article
C2 - 10673335
AN - SCOPUS:0034048704
VL - 63
SP - 246
EP - 254
JO - Genomics
JF - Genomics
SN - 0888-7543
IS - 2
ER -
