Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Query: EC:2.7.7.49 (
reverse transcriptase
)
31,746
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
We utilized 2-aminoethyoxydiphenyl borane, an agent that blocks store-operated Ca(2+) entry, as well as an antisense approach to characterize endogenous Ca(2+) entry pathways in HEK-293 cells. The thapsigargin- and carbachol-induced, but not the 1-oleolyl-2-acytyl-sn-glycerol (OAG)-induced, entry was blocked by 2-aminoethyoxydiphenyl borane. Both
reverse transcriptase
-PCR and Western blot analyses demonstrated endogenous expression for HTRP1,
HTRP3
, and HTRP4 and specific suppression of mRNA levels and Trp protein levels in cells stably expressing antisense constructs. Expression of HTRP4 antisense inhibited 35% of the carbachol (CCh)-stimulated Ba(2+) entry and 46% of the OAG-stimulated Sr(2+) entry but in contrast had no effect on the thapsigargin-stimulated Ba(2+) or Sr(2+) entry.
HTRP3
antisense reduced, while HTRP1 antisense had no effect on, OAG-induced Sr(2+) entry. Of greater importance, HTRP4 antisense expression, but not
HTRP3
antisense expression, blocked the sustained Ca(2+) oscillations produced by low doses of CCh (15 microm), arguing that receptor-stimulated rather than store-operated channels are involved in these sustained oscillations. HTRP4 antisense also inhibited 75% of the arachidonic acid-induced Ca(2+) entry. In summary, these data suggest that HTRP4 proteins in HEK-293 cells, differing from
HTRP3
and HTRP1 proteins, do not serve as functional subunits of store-operated channels but do function as subunits for CCh- and OAG-stimulated channels. Furthermore, evidence is provided for the first time for the involvement of a Trp isoform (HTRP4) in the formation of the channel responsible for both arachidonic acid-induced Ca(2+) entry and the Ca(2+) entry needed to sustain long term Ca(2+) oscillations induced by low doses of carbachol.
...
PMID:The role of endogenous human Trp4 in regulating carbachol-induced calcium oscillations in HEK-293 cells. 1183 May 88