Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Methionine starvation causes changes in the protein pattern of HL-60 promyelocytic leukemia cells as observed by two-dimensional electrophoresis. One group of proteins is apparently modified, appearing in new positions. A further series of proteins, including several principal nuclear polypeptides, is substantially diminished. The morphology of a fraction of the cells in the culture changes concomitantly, with condensation and fragmentation of the nucleus and eventual remolding of the cell to a "grape-cluster" appearance. Similar effects are produced by a DNA methylation inhibitor, 5-azacytidine, but not by various other toxic agents tested. A defect in DNA methylation, either by depletion of S-adenosyl-L-methionine (the methyl donor) or by inactivation of the relevant enzyme, may be responsible. The T-lymphoblastoid line CCL-119 and the histiocytic lymphoma line U-937 also show these effects, but most fibroblast, epithelial, and lymphoblastoid lines do not. These changes can be largely prevented in each of the three susceptible lines by prior treatment with the tumor promoter, phorbol myristate acetate (PMA), an agent known to cause differentiation in at least two of the lines. The results thus suggest interesting relationships between methionine metabolism, protein and structural changes in the cell nucleus, and PMA-induced cell differentiation.
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PMID:Protein-pattern changes and morphological effects due to methionine starvation or treatment with 5-azacytidine of the phorbol-ester-sensitive cell lines HL-60, CCL-119, and U-937. 620 32

The KCNQ gene family, whose members encode Kv7 channels, belongs to the voltage-gated potassium (Kv) channel group. The roles of this gene family have been widely investigated in nerve and muscle cells. In the present study, we investigated several characteristics of Kv7.5, which is strongly expressed in the canine osteosarcoma cell line, CCL-183. Serum starvation upregulated Kv7.5 expression, and the Kv7 channel opener, flupirtine, attenuated cell proliferation by arresting cells in the G0/G1 phase. We also showed that Kv7.5 knockdown helps CCL-183 cells to proliferate. In an effort to find an endogenous regulator of Kv7.5, we used mithramycin A to reduce the level of the transcription factor Sp1, and it strongly inhibited the induction of Kv7.5 in CCL-183 cells. These results suggest that the activation of Kv7.5 by flupirtine may exert an anti-proliferative effect in canine osteosarcoma. Therefore, Kv7.5 is a possible molecular target for canine osteosarcoma therapy.
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PMID:Serum starvation-induced voltage-gated potassium channel Kv7.5 expression and its regulation by Sp1 in canine osteosarcoma cells. 2443 41