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1 and ERK1/2 activation through activation of beta-adrenergic receptor kinase 1.
2 t enhanced by simultaneous overexpression of beta-adrenergic receptor kinase 1.
3 nding peptide derived from the C terminus of beta-adrenergic receptor kinase 1 (50 microM) prevented
4 ed since the expression of the C terminus of beta-adrenergic receptor kinase 1, a Gbetagamma subunit-
5 tigation we demonstrate a novel finding that beta-adrenergic receptor kinase 1 and phosphoinositide 3
6 ein-coupled receptor kinases (GRKs) 2 and 3 (beta-adrenergic receptor kinases 1 and 2 (betaARK1 and -
7 nuated in transgenic mice overexpressing the beta-adrenergic receptor kinase-1, another member of the
12 vented by betaARK-ct, a peptide inhibitor of beta-adrenergic receptor kinase-1 (betaARK1) as well as
14 Expression of the betagamma-binding agents beta-adrenergic receptor kinase 1 (C-terminus, betaARK1C
15 by the Gbetagamma scavengers transducin and beta-adrenergic receptor kinase 1 carboxyl-terminal frag
17 lar regarding the roles of phospholamban and beta-adrenergic receptor kinase 1 in mediating the contr
20 ase form a cytosolic complex, which leads to beta-adrenergic receptor kinase 1-mediated translocation
21 blocked by the Gbetagamma-binding region of beta-adrenergic receptor kinase 1, suggesting that fast
22 verexpressing a carboxyl-terminal peptide of beta-adrenergic receptor kinase-1 that inhibits Gbetagam
23 vented, however, by the C-terminal region of beta-adrenergic receptor kinase 1, which sequesters Gbet
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