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1 s to DEA/NO, atrial natriuretic peptide, and C-type natriuretic peptide.
2 t of recent advances with a special focus on C-type natriuretic peptide.
4 tic peptide acts primarily on the artery and C-type natriuretic peptide acts predominantly on the vei
5 rophy and pathologic calcification, and with C-type natriuretic peptide, an essential factor in endoc
6 om these vessels, the pattern of response to C-type natriuretic peptide and atrial natriuretic peptid
7 donors was mimicked by 2 cGMP analogues and C-type natriuretic peptide and blocked by a specific inh
8 racrine signaling by extracellular peptides (C-type natriuretic peptide and EGF receptor ligands) mai
9 r affinity for [125I]-DNP binding sites than C-type natriuretic peptide and the natriuretic peptide r
11 pulmonary vasculature to atrial, B-type, and C-type natriuretic peptides (ANP, BNP, and CNP) during a
15 ions of atrial natriuretic peptide (ANP) and C-type natriuretic peptide (CNP) are elaborated by membr
18 ently, CD-NP, a chimeric peptide composed of C-type natriuretic peptide (CNP) fused to the C-terminal
20 te important roles for nitric oxide (NO) and C-type natriuretic peptide (CNP) in the regulation of ca
21 Both atrial natriuretic peptide (ANP) and C-type natriuretic peptide (CNP) increased the accumulat
27 he binding of atrial natriuretic peptide and C-type natriuretic peptide (CNP) to the guanylyl cyclase
28 be coimmunoprecipitated with Galpha(i), and C-type natriuretic peptide (CNP) treatment induced trans
29 domain of the mammalian receptor (GC-B) for C-type natriuretic peptide (CNP) was fused to the cataly
30 uced by atrial natriuretic peptide (ANP) and C-type natriuretic peptide (CNP), activators of particul
31 ial-specific deletion of Nppc, which encodes C-type natriuretic peptide (CNP), and determined that th
33 Activating mutations in the receptor for C-type natriuretic peptide (CNP), guanylyl cyclase B (GC
35 GMP signaling pathway composed of the ligand C-type natriuretic peptide (CNP), its receptor, the guan
36 r S-nitroso-N-acetylpenicillamine (SNAP) and C-type natriuretic peptide (CNP), reduced TNF-alpha-indu
37 t marked elevations of cyclic GMP induced by C-type natriuretic peptide (CNP), the ligand of GC-B, bl
38 ngest candidate therapy employs an analog of C-type natriuretic peptide (CNP), which antagonizes the
50 ic peptides, atrial natriuretic peptide, and C-type natriuretic peptide evoked fluorescence resonance
51 markedly increased by natriuretic peptides (C-type natriuretic peptide >> atrial natriuretic peptide
52 muscle cells cultured from these vessels to C-type natriuretic peptide in comparison with atrial nat
54 ocytochemically localized atrial, brain, and C-type natriuretic peptide-like immunoreactivity (ANP-LI
55 L658F, Y708C, R776W, and G959A) bound (125)I-C-type natriuretic peptide on the surface of cells but f
56 clase B is the receptor for a small peptide (C-type natriuretic peptide) produced locally in many dif
58 l value) was more effective than 1 microM of c-type natriuretic peptide (three-fold increase in cycli
59 se with the discovery that administration of C-type natriuretic peptide to achondroplastic mice ameli
60 by daily injection of a recombinant form of C-type natriuretic peptide to post-natal pups for 18 day
61 ase in cyclic GMP in response to 1 microM of C-type natriuretic peptide vs. six-fold increase in cycl
63 the order ANP > brain natriuretic peptide >> C-type natriuretic peptide) was also similar to that of
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