inostamycin and erbstatin

inostamycin has been researched along with erbstatin* in 4 studies

Reviews

2 review(s) available for inostamycin and erbstatin

Article	Year
[Modulators of oncogene product functions]. Tanpakushitsu kakusan koso. Protein, nucleic acid, enzyme, 1993, Volume: 38, Issue:11 Topics: Bacteria; Fungi; Furans; GTP-Binding Proteins; Hydroquinones; Lovastatin; Monophenol Monooxygenase; Oncogene Proteins; Phenols; Phosphatidylinositols; Plants; Ribonucleosides	1993
[Biological activity of oncogene function inhibitors isolated from microorganisms]. Seikagaku. The Journal of Japanese Biochemical Society, 1992, Volume: 64, Issue:3 Topics: Acyl Coenzyme A; Animals; Bacteria; Furans; Genistein; Hydroquinones; Isoflavones; Lovastatin; Oncogene Proteins; Phosphatidylinositols; Protein-Tyrosine Kinases	1992

Other Studies

2 other study(ies) available for inostamycin and erbstatin

Article	Year
[Study of the novel compounds modulating signal transduction system from microbial origin]. The Japanese journal of antibiotics, 2001, Volume: 54, Issue:3 Topics: Animals; Apoptosis; Bacterial Physiological Phenomena; Furans; Humans; Hydroquinones; Phosphatidylinositols; Protein Tyrosine Phosphatases; Protein-Tyrosine Kinases; Signal Transduction; Streptomyces	2001
Inhibition of EGF-induced cytoskeletal change in A431 cells by inhibitors of phosphatidylinositol turnover. Drugs under experimental and clinical research, 1992, Volume: 18, Issue:1 Expression of epidermal growth factor (EGF) receptor is often increased in various human carcinomas. Therefore, inhibition of the EGF/EGF receptor-induced signaling pathway may help to suppress these carcinomas. In the presence of Ca2+, EGF induces elongation of A431 cells in approximately 30 min. The cell elongation was shown to be accompanied by a reorganization of actin filaments. These phenotypical changes were specifically inhibited by a tyrosine kinase inhibitor, erbstatin, and inhibitors of phosphatidylinositol (PI) turnover such as psi-tectorigenin and inostamycin. The amount of filamentous actin was increased by EGF, which was also inhibited by these compounds. Long-term treatment of A431 cells with EGF induced the disappearance of cytoskeleton and aggregation of the cells, which was again inhibited by the PI turnover inhibitors. Thus tyrosine kinase and phosphatidylinositol turnover inhibitors were shown to inhibit the signaling pathways of EGF-induced cytoskeletal organization of A431 cells. Topics: Actins; Calcium; Carcinoma; Cell Aggregation; Cytoskeleton; Epidermal Growth Factor; Furans; Humans; Hydroquinones; Isoflavones; Microscopy, Phase-Contrast; Phosphatidylinositols; Protein-Tyrosine Kinases; Tumor Cells, Cultured	1992

Article

Year

[Study of the novel compounds modulating signal transduction system from microbial origin].

The Japanese journal of antibiotics, 2001, Volume: 54, Issue:3

Topics: Animals; Apoptosis; Bacterial Physiological Phenomena; Furans; Humans; Hydroquinones; Phosphatidylinositols; Protein Tyrosine Phosphatases; Protein-Tyrosine Kinases; Signal Transduction; Streptomyces

2001

Inhibition of EGF-induced cytoskeletal change in A431 cells by inhibitors of phosphatidylinositol turnover.

Drugs under experimental and clinical research, 1992, Volume: 18, Issue:1

Expression of epidermal growth factor (EGF) receptor is often increased in various human carcinomas. Therefore, inhibition of the EGF/EGF receptor-induced signaling pathway may help to suppress these carcinomas. In the presence of Ca2+, EGF induces elongation of A431 cells in approximately 30 min. The cell elongation was shown to be accompanied by a reorganization of actin filaments. These phenotypical changes were specifically inhibited by a tyrosine kinase inhibitor, erbstatin, and inhibitors of phosphatidylinositol (PI) turnover such as psi-tectorigenin and inostamycin. The amount of filamentous actin was increased by EGF, which was also inhibited by these compounds. Long-term treatment of A431 cells with EGF induced the disappearance of cytoskeleton and aggregation of the cells, which was again inhibited by the PI turnover inhibitors. Thus tyrosine kinase and phosphatidylinositol turnover inhibitors were shown to inhibit the signaling pathways of EGF-induced cytoskeletal organization of A431 cells.

Topics: Actins; Calcium; Carcinoma; Cell Aggregation; Cytoskeleton; Epidermal Growth Factor; Furans; Humans; Hydroquinones; Isoflavones; Microscopy, Phase-Contrast; Phosphatidylinositols; Protein-Tyrosine Kinases; Tumor Cells, Cultured

1992