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D Takai

Publications and source records attributed to D Takai.

24 records · Page 2Linked to original sources
PubMed1994

Detection and characterization of muscle-specific nuclear proteins.

To identify nuclear proteins related to muscle tissue specificity, we tried to prepare antibodies recognizing muscle-specific nuclear proteins. Taking advantage of the autoimmunity of some nuclear proteins, we prepared an antiserum against chick muscle nuclear proteins by injecting protein components of the nuclei isolated from chick breast muscles into breast muscle. Three proteins, named p30, p32, and p37, were detected with the antiserum in a two-dimensional SDS-PAGE pattern of the isolated nuclei. P30 and p32 were not detected in the nuclei of liver, brain, cardiac muscle, or slow type skeletal muscle (anterior latissimus dorsi). They were detected in those of fast type skeletal muscle (pectoralis major and semitendinosus) and smooth muscle (gizzard) at all developmental stages examined. On serial fractionation of muscle cell nuclei, they were detected in a fraction obtained after DNase I treatment of the sample, suggesting that the proteins weakly bind to chromatin. A homology search of amino acid sequences showed that there is no known protein similar to p32.

Amino Acid Sequence↗
PubMed1993

Accumulation of mtDNA with a mutation at position 3271 in tRNA(Leu)(UUR) gene introduced from a MELAS patient to HeLa cells lacking mtDNA results in progressive inhibition of mitochondrial respiratory function.

A new mitochondrial DNA (mtDNA) mutation of tRNA(Leu)(UUR) at nucleotide position 3271 (MELAS3271) was determined to be involved in the pathogenic process of mitochondrial diseases MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) using intercellular transfer of patient-derived mtDNA to mtDNA-less HeLa cells (rho 0 HeLa cells). Cybrid clones containing imported mtDNA exclusively from a MELAS patient with MELAS3271 mtDNA were isolated, and the influence of MELAS3271 mtDNA on mitochondrial translation activity and mitochondrial respiratory complex I enzyme activity were examined. Accumulation of more than 87% MELAS3271 mutant mtDNA in the cybrid clones induced both low complex I activity and abnormal mtDNA-encoded polypeptide synthesis including at least complex I subunit ND6. suggesting involvement of the new MELAS-associated mutation in the pathogenesis.

Blotting, Southern↗
PubMed1990

Studies on the measurement of whole-body protein degradation in vivo in the chicken.

1. An attempt was made to develop a new in vivo method for measuring whole-body protein degradation rate in chickens within an hour. For this purpose, two amino acid fluxes, absorption and protein synthesis were inhibited almost completely, followed by the measurement of changes in radioactivity and pool size in free amino acid pool. 2. The results indicated that the degradation rate estimated by the present direct isotope dilution method was not significantly different from that obtained by an indirect calculation based on the difference between the synthesis and net accretion rates in chicks fed ad libitum an adequate diet. 3. A computer-aided simulation analysis demonstrated that under the present circumstances incomplete inhibition of amino acid fluxes, i.e. absorption and protein degradation, affected the estimate of fractional rate of whole-body protein degradation, ranging from 75 to 110% of the experimentally-determined value.

Amino Acids↗