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1 lecular pharmacogenetic studies of the human prostacyclin receptor.
2 even-transmembrane (TM) domains of the human prostacyclin receptor.
3 s were not similarly altered in mice lacking prostacyclin receptors.
4 /2, cyclooxygenase COX-1 (but not COX-2) and prostacyclin receptors.
5 he release of prostacyclin and activation of prostacyclin receptors.
6 the antagonists of EP4, prostaglandin D2, or prostacyclin receptors.
9 it failed to activate the recombinant human prostacyclin receptor and caused only minimal activation
10 ha, Csf1) were increased by treatment with a prostacyclin receptor antagonist and protein kinase A in
12 PGI2 binding to platelets was due to an anti-prostacyclin receptor antibody present in SCI plasma.
13 aining the structural integrity of the human prostacyclin receptor, as 7 of 12 extracellular and tran
16 induced phosphorylation of an epitope-tagged prostacyclin receptor (HAhIP) is mediated primarily by P
20 n = 1,761) to search for dysfunctional human prostacyclin receptor (hIP) variants, we recently discov
25 athways involving a cyclooxygenase-2 (COX-2)/prostacyclin receptor (IP receptor) autocrine loop and a
26 first intracellular loop (iLP1) of the human prostacyclin receptor (IP) and G alpha s protein have be
28 ellular loop (iLP1, residues 39-51) of human prostacyclin receptor (IP) was proposed to be involved i
34 e binding of [3H]prostaglandin E1, used as a prostacyclin receptor probe, showed the presence of one
35 ical approaches, we conclude that diminished prostacyclin receptor signaling may contribute, in part,
40 ion instigated further genetic screening for prostacyclin receptor variants on 1455 human genomic sam
41 in endothelial cells preferentially enhances prostacyclin receptor (versus other GPCR)-stimulated cAM
42 Using a naturally occurring mutation in the prostacyclin receptor, we report for the first time that
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