Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.13 (protein kinase C)
 49,245 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thrombomodulin is an endothelial membrane anticoagulant protein that is a cofactor for protein C activation. We have evaluated the expression of thrombomodulin in cultured mouse hemangioma cells before and after treatment with phorbol myristate acetate (PMA), an agent that stimulates protein kinase C. We also isolated a cDNA encoding 481 amino acids of mouse thrombomodulin and the entire 3'-untranslated portion of its mRNA. The deduced amino acid sequence of mouse thrombomodulin is similar to those determined for human and bovine thrombomodulin. An S1 nuclease protection assay was used to measure thrombomodulin mRNA in hemangioma cells. The half-life for thrombomodulin mRNA was 8.9 +/- 1.8 h (S.D.) in cells treated with actinomycin D. Treatment with PMA had no effect on thrombomodulin mRNA levels. Thrombomodulin turnover was evaluated by immunoprecipitation of [35S]methionine-labeled thrombomodulin. The t1/2 was 19.8 +/- 3.9 h (S.D.); PMA treatment decreased the t1/2 to 10.9 +/- 1.1 h (S.D.) while increasing the rate of synthesis to a maximum of 190% of control. Protein C cofactor activity on hemangioma cells was reduced 35 +/- 4% by treatment with PMA within 30 min. This decrease was associated with a parallel decline in cell surface thrombomodulin antigen and with enhanced phosphorylation of thrombomodulin on serine residues. We conclude that thrombomodulin is phosphorylated in response to treatment of hemangioma cells with PMA which leads to decreased protein C cofactor activity and both increased degradation and synthesis of thrombomodulin.
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PMID:The structure and function of mouse thrombomodulin. Phorbol myristate acetate stimulates degradation and synthesis of thrombomodulin without affecting mRNA levels in hemangioma cells. 284 23

We report the unique case of a 69-year-old man with an extra-gastrointestinal stromal tumor (EGIST) in the lesser omentum. Based on the location of the tumor and the radiological findings, we made a provisional diagnosis of hepatic cavernous hemangioma in the lateral segment. However, after 5 years of follow-up, tumor growth was noted and the patient underwent a laparotomy. The tumor was located in the lesser omentum and resected en bloc with its fused lesser omentum and an adherent portion of the liver. The pathology results indicated an EGIST with microscopic proliferation of epithelioid cells in the lesser omentum; the tumor was immunohistochemically negative for KIT staining and positive for CD34 and PKC theta. Because of the rarity of mitotic figures and the low Ki-67 labeling, the tumor was diagnosed as a KIT-negative EGIST with a low malignant potential. The patient was followed up without receiving imatinib mesylate treatment and has remained free of any signs of recurrence for 26 months. The present case report describes a very rare lesser omental KIT-negative EGIST.
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PMID:A Case of KIT-Negative Extra-Gastrointestinal Stromal Tumor of the Lesser Omentum. 2285 55