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Titolo:
A NOVEL NEUROLOGICAL MUTANT MOUSE, YOTARI, WHICH EXHIBITS REELER-LIKEPHENOTYPE BUT EXPRESSES CR-50 ANTIGEN REELIN/
Autore:
YONESHIMA H; NAGATA E; MATSUMOTO M; YAMADA M; NAKAJIMA K; MIYATA T; OGAWA M; MIKOSHIBA K;
Indirizzi:
UNIV TOKYO,INST MED SCI,DEPT MOL NEUROBIOL,MINATO KU,4-6-1 SHIROKANEDAI TOKYO 108 JAPAN UNIV TOKYO,INST MED SCI,DEPT MOL NEUROBIOL,MINATO KU TOKYO 108 JAPAN KEIO UNIV,SCH MED,DEPT NEUROL,SHINJUKU KU TOKYO 160 JAPAN INST PHYS & CHEM RES,TSUKUBA LIFE SCI CTR,MOL NEUROBIOL LAB TSUKUBA IBARAKI 305 JAPAN KOCHI MED SCH,DEPT PHYSIOL,MED RES LAB,NANKO KU KOCHI 783 JAPAN
Titolo Testata:
Neuroscience research
fascicolo: 3, volume: 29, anno: 1997,
pagine: 217 - 223
SICI:
0168-0102(1997)29:3<217:ANNMMY>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
DIEKER LISSENCEPHALY GENE; CEREBELLUM; PROTEIN; ENCODES; SUBUNIT; NEURONS; MICE;
Keywords:
YOTARI; REELER; CEREBRAL CORTEX; CEREBELLAR CORTEX; MIGRATION; CR-50;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
26
Recensione:
Indirizzi per estratti:
Citazione:
H. Yoneshima et al., "A NOVEL NEUROLOGICAL MUTANT MOUSE, YOTARI, WHICH EXHIBITS REELER-LIKEPHENOTYPE BUT EXPRESSES CR-50 ANTIGEN REELIN/", Neuroscience research, 29(3), 1997, pp. 217-223

Abstract

We present yotari, a novel neurological mutant mouse whose mutation is transmitted in an autosomal recessive manner. The phenotype of yotari is very similar to that of reeler. yotari mutants are recognizable by their unstable gait and tremor and by their early deaths at around the time of weaning. The cerebella of homozygous yotari are hypoplasticand have no foliation. A molecular and a granular cell layer can be identified, but Purkinje cells are scattered throughout both the granular layer and white matter. The laminar structure of the cerebral cortex and the hippocampal formation are also distorted. To test whether the mutated gene in yotari is the reeler gene, reelin, yotari heterozygotes were mated with reeler homozygotes or heterozygotes. The absence of abnormal offspring indicated that the yotari gene is distinct from reelin. Furthermore, expression of mRNA and protein of reelin was verified by Northern blotting and immunohistochemistry using a CR-50 monoclonal antibody (mAb) which is specific to Reelin, the reelin gene product. Although the mutation of several genes, including cyclin-dependentkinase 5 (Cdk 5), p35 and LIS1, 45 kDa subunits of platelet-activating factor acetylhydrolase (PAF-AH) Ib, in Miller-Dieker lissencephaly syndrome (MDS) has been reported to cause abnormal laminar structure inthe brain, no abnormality was found in yotari by Western blotting with antibodies (Ab's) against these molecules. The close similarity of the phenotypes of yotari and reeler and the expression of reelin in yotari may suggest that the gene mutated in yotari encodes a molecule that is on the same signaling pathway as Reelin, the product of reelin. yotari will provide valuable clues to explore the molecular mechanism of neuronal migration and orderly laminar structure formation of the brain. (C) 1997 Elsevier Science Ireland Ltd.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 08/08/20 alle ore 07:40:25