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Query: EC:3.6.3.1 (
Mg2+-ATPase
)
1,484
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Saponin-treated liver cells and a microsomal fraction were used to characterize the mechanism of the Ca2+ release induced by different bile acids. The saponin-treated cells accumulated 0.8-1 nmol/mg of protein of the medium Ca2+ in a nonmitochondrial, high affinity, and inositol (1,4,5)-trisphosphate (
Ins(1,4,5)P3
)-sensitive Ca2+ pool. Three of five bile acids tested, lithocholate and the conjugates taurolithocholate and taurolithocholate sulfate, released 85% of the Ca2+ pool within 45-60 s and with ED50 from 16 to 28 microM.
Ins(1,4,5)P3
released 80% from the same Ca2+ pool with an ED50 of 0.3 microM. The Ca2+-
Mg2+-ATPase
inhibitor vanadate (1 mM) had no effect on the Ca2+ released by the bile acids and
Ins(1,4,5)P3
. The
Ins(1,4,5)P3
-binding antibiotic neomycin (1 mM) and the receptor competitor heparin (16 micrograms/ml) abolished the releasing effect of
Ins(1,4,5)P3
but had no effect on the bile acid-mediated Ca2+ release. The 45Ca2+ accumulated by the microsomal fraction (8 nmol of 45Ca2+/mg of protein) was released by the bile acids within 45-90 s and with an ED50 of 17 microM. In contrast, the bile acids had no effect on the Ca2+ permeability of other natural and artificial membranes. The resting 45Ca2+ influx of intact cells (0.45 nmol/mg of protein/min), the 45Ca2+ accumulated by mitochondria (2-13 nmol of 45Ca2+/mg of protein), and the 45Ca2+ trapped in sonicated phosphatidylcholine vesicles (5 mM 45Ca2+) were not altered by the different bile acids. These results suggest that the Ca2+ release initiated by lithocholate and its conjugates results from a direct action on the Ca2+ permeability of the
Ins(1,4,5)P3
-sensitive pool. It is not mediated by
Ins(1,4,5)P3
or via activation of the
Ins(1,4,5)P3
receptor, and it is specific for the membrane of the internal pool.
...
PMID:Characteristics of bile acid-mediated Ca2+ release from permeabilized liver cells and liver microsomes. 278 15