1990 Fiscal Year Final Research Report Summary
Transmembrane Signaling System in Psoriatic Keratinocytes.
| Project/Area Number |
63570464
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Dermatology
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| Research Institution | Asahikawa Medical College |
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Principal Investigator |
IIZUKA Hajime Asahikawa Medical College Dept. Dermatology, Professor, 医学部, 教授 (90113513)
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| Co-Investigator(Kenkyū-buntansha) |
TSUTSUI Masato Asahikawa Medical Cellege Dept. Dermatology, Assistant, 医学部付, 助手 (10172032)
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| Project Period (FY) |
1988 – 1990
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| Keywords | Psoriasis / Adenylate cyclase / G protein / Protein kinase C / Calcium / Phorbol ester / Phospholipase C |
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| Research Abstract |
Recent evidence suggests that the breakdown of inositol phospholipids is an important transmembrane signalling system that is composed of two kinds of signals : the diacylglycerol (DAG) -protein kinase C signal, and the inositol trisphosphate - Ca^<++> signal. The system is activated in psoriatic hyperproliferative keratinocytes, which might be associated with the altered function of other transmembrane signaling systems such as the adenylate cyclase. The epidermal adenylate cyclase was shown to be modulated by various protein kinase C activators, which include tumor promoting phorbol esters. The modulation was similar to that of psoriatic involved epidermis. Despite the finding that the classical protein kinase C isozymes are activated by DAG and also by Ca^<++> at higher concentrations, the epidermal adenylate cyclase responses were modulated only by DAG-protein kinase C signal, but not by Ca^<++> signal. Our results indicate that the epidermal adenylate cyclase system is modulated by protein kinase C, which might be the novel Ca^<++>insensitive form of protein kinase C recently described by Kuroki and C -workers.
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Research Products
(14 results)
