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Biomedical subjects

M Kamijo

Publications and source records attributed to M Kamijo.

47 records · Page 3Linked to original sources
PubMed1989

Phosphorylation of the tumor suppressor gene RB protein by M-phase specific histone H1 kinase.

We have noted the presence of the consensus amino acid sequence for phosphorylation by M-phase specific histone H1 kinase in six sites of the tumor suppressor gene retinoblastoma (RB) protein and determined whether or not RB protein is, in fact, phosphorylated by this kinase. Highly purified enzyme was used for this purpose. Human cell extracts immunoprecipitated with anti-RB antiserum as well as RB proteins expressed in Escherichia coli cells were shown to be phosphorylated by this kinase in vitro. Synthetic peptides for the six expected sites were also phosphorylated. These results suggest the possibility that the function of RB protein is regulated by CDC2 kinase. We also noted the presence of putative phosphorylation sites by H1 kinase in a homologous region between the RB gene and L1 family repetitive sequences.

Amino Acid Sequence↗
PubMedDate not supplied

Nerve fiber regeneration following axotomy in the diabetic biobreeding Worcester rat: the effect of ARI treatment.

Diabetic neuropathy is characterized by progressive nerve fiber degeneration resulting in nerve fiber loss. In order to examine what role impaired nerve fiber regeneration may play in the progressive net nerve fiber loss, spontaneously diabetic biobreeding Worcester (BB/W) rats were subjected to sciatic nerve axotomy at 6 weeks of diabetes. Myelinated nerve fiber regeneration was examined morphologically and morphometrically at various time points following axotomy. The data were compared with those of axotomized control rats and diabetic rats treated with an aldose reductase inhibitor (ARI) from 1 week after onset of diabetes. Diabetic rats showed a significant attenuation of nerve fiber regeneration during the first 6 weeks following axotomy, which was normalized at 4 months postaxotomy. ARI treatment resulted in an initial burst of supranormal regeneration, which was normalized at 4 months postaxotomy. Impaired nerve fiber regeneration in diabetic rats was associated with a marked delay in preceding Wallerian degeneration and decreased phagocytic activity by macrophages, changes not demonstrated in ARI-treated diabetic rats. We propose that the impaired nerve fiber regeneration in the diabetic BB/W rat may, in part, be the result of impaired recruitment and/or function of macrophages necessary for the initiation of normal nerve fiber regeneration. The corrective effects of ARI treatment on the regenerative ability of diabetic peripheral nerve suggest that an activated polyol pathway may impact on both intrinsic and extrinsic mechanisms governing nerve fiber regeneration.

Aldehyde Reductase↗
PubMedDate not supplied

Nodal Na(+)-channel displacement is associated with nerve-conduction slowing in the chronically diabetic BB/W rat: prevention by aldose reductase inhibition.

Chronic nerve conduction showing in experimental diabetic neuropathy has been associated with decreased nodal Na+ permeability and an ultrastructurally identifiable loss of axo-glial junctions, which comprise the paranodal voltage channel barrier separating nodal Na+ channels from paranodal K+ channels. In human and experimental diabetic neuropathy these structural changes of the paranodal apparatus correlate closely with the nerve conduction defect. The present immunocytochemical study of the alpha-subunit of the Na+ channel examined whether the breach of the voltage channel barrier may account for a shift in the distribution of Na+ channels explaining decreased nodal Na+ permeability. Biobreeding Wistar (BB/W) rats diabetic for 4-8 months showed a progressive redistribution of nodal Na+ channels across the paranodal barrier into the paranodal and internodal domains which was associated with chronic nerve conduction slowing. The present data suggest that structural damage to the paranodal barrier system in diabetic nerve facilitates the lateral displacement of Na+ channels from the nodal axolemma thereby diminishing their nodal density and the nodal Na+ permeability associated with the chronic nerve conduction defect in experimental diabetes. These abnormalities were prevented by the treatment with an aldose reductase inhibitor, belonging to a class of drugs that, in neuropathic patients, improves nerve-conduction velocity and repairs axo-glial dysjunction of the paranodal apparatus.

Aldehyde Reductase↗
PubMedDate not supplied

Preference of human cdc2 kinase for peptide substrate.

Human cyclin B1-bound cdc2 kinase phosphorylated the threonine residue in the sequence -Thr-Pro-Lys-Lys-Ala- but hardly phosphorylated it in the sequence -Thr-Pro-Lys-Ala-Lys. The sequence -Thr-Pro-Ala-Pro-Lys-, as found in p53 protein, was also phosphorylated by this enzyme, but less efficiently than in the sequence described above. When the threonine residue in -Thr-Pro-Lys-Lys-Ala- was changed to a serine or a tyrosine residue, the enzyme phosphorylated the serine, but not the tyrosine residue. Changing the lysine next to the proline to alanine reduced its efficiency as a substrate. The peptide, Ala-Ala-Ala-Ala-Lys-Thr-Pro-Ala-Lys-Ala-Ala, containing the -Thr-Pro-Ala-Lys- sequence, but not the other lysine residues, was not used as a substrate by the kinase.

Amino Acid Sequence↗