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Y Fuse

Publications and source records attributed to Y Fuse.

158 records · Page 9Linked to original sources
PubMedDate not supplied

A tyrosine-specific protein kinase inhibitor, alpha-cyano-3-ethoxy-4-hydroxy-5-phenylthiomethylcinnamamide, blocks the phosphorylation of tyrosine kinase substrate in intact cells.

Inhibition by alpha-cyano-3-ethoxy-4-hydroxy-5-phenylthiomethylcinnamamide (ST 638) of tyrosine-specific protein kinase was examined using epidermal growth factor (EGF)-treated A431 cells at the concentration of 25 to 100 microM. ST 638 had negligible effects on the growth and morphology of A431 cells and on EGF binding to its receptor, and subsequent down-regulation of the receptor. ST 638 specifically inhibited EGF-induced phosphorylation of tyrosine residues of whole cell proteins in a dose-dependent manner without affecting the phosphorylation of serine and threonine residues. ST 638 greatly inhibited the EGF-induced phosphorylation of lipocortin I at 25 microM, and yet had a negligible effect on the EGF-induced phosphorylation of EGF receptor. Neither the amount of [35S]methionine-labeled lipocortin I nor the serine/threonine phosphorylation level of fodrin beta-subunit was affected by the same concentration of ST 638. These results indicate that the phosphorylation of lipocortin I is not relevant to the transformation of A431 cells. In cell lines transformed by src or fgr oncogene encoding tyrosine kinase, ST 638 also inhibited phosphorylation of calpactin I (p36) without affecting that of the oncogene products. Two-dimensional polyacrylamide gel electrophoresis showed that ST 638 specifically inhibited the EGF-induced phosphorylation and dephosphorylation of cellular proteins in A431 cells.

Animals↗
PubMedDate not supplied

Reversible ischemic cerebrovascular disease associated with hyperleukocytosis in a patient with chronic myelogenous leukemia.

A 31-year-old man with chronic myelogenous leukemia in a chronic phase complicated with reversible ischemic cerebrovascular disease is described. Before therapy, the WBC count was 530.0 x 10(9)/l. Four days after initiation of busulfan, he rapidly developed disturbance of consciousness and right hemiplegia. Computerized tomography demonstrated the presence of multiple low density areas in the cerebrum. The symptoms were, however, completely relieved in accordance with the decrease in the WBC counts in 8 days. Repeated CT studies showed no abnormal findings after one month. The intracranial change was considered to be one of the manifestations of hyperleukocytic syndrome.

Adult↗