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1 sible mechanistic explanation for diminished catestatin.
2  diminished CHGA secretion and processing to catestatin.
3 he catecholamine release-inhibitory fragment catestatin.
4  polymorphisms in the amino acid sequence of catestatin.
5 nist chlorisondamine or the novel antagonist catestatin.
6 CgA that are utilized in the biosynthesis of catestatin.
7 ynthesis of chromogranin A, the precursor of catestatin.
8 ubstantially blocked in the adrenal gland by catestatin.
9 ry, nicotinic cholinergic antagonist peptide catestatin.
10 l transduction was specifically disrupted by catestatin.
11 esting diminished conversion of precursor to catestatin.
12  human Chga and exogenous injection of human catestatin, a CHGA-derived nicotinic cholinergic antagon
13                                  A model for catestatin action in the baroreceptor center of the nucl
14                                     And does catestatin antagonize secretion and transcription in viv
15                       Human, bovine, and rat catestatins (as well as substance P) had similar potenci
16 -dependent fashion, the nicotinic antagonist catestatin blocked agonist desensitization of both catec
17  cells was accompanied by the cosecretion of catestatin (CgA(344)(-)(364)) and variant peptide forms
18 A catecholamine release-inhibitory fragment, catestatin (chromogranin A344-364), on agonist-induced d
19  loci on chromosomes 4q35 and 5q34 affecting catestatin concentration (P = 3.40 x 10-30 for rs4253311
20  influenced CHGA secretion and processing to catestatin, confirming the mechanism of a novel trans-QT
21                                              Catestatin-containing polypeptides, demonstrated by anti
22 rocessing in HF and whether the CgA fragment catestatin (CST) may directly influence cardiomyocyte fu
23 e were treated with the CHGA-derived peptide catestatin (CST) that is deficient in these mice.
24                                              Catestatin (CST), a chromogranin A (CHGA)-derived peptid
25       In this study, we investigated whether catestatin (Cst), a peptide derived from the neuroendocr
26 desensitization by nicotinic agonists, since catestatin did not block desensitization of catecholamin
27 horter (chromogranin A(344-364)) versions of catestatin each inhibited catecholamine release from chr
28 es near unity suggested noncooperativity for catestatin effects on both nicotinic responses (secretor
29                On mass spectrometry, a major catestatin form was bovine chromogranin A(332-364); iden
30 lamine secretory granule biogenesis, and its catestatin fragment inhibits catecholamine release.
31                 Thus, chromogranin A and its catestatin fragment may lie at the nexus of nicotinic ch
32                                          The catestatin fragment of chromogranin A is an endogenous i
33                                          The catestatin fragment of chromogranin A is an inhibitor of
34               Knowledge of cleavage sites of catestatin from chromogranin A may provide a useful star
35                                          The catestatin Gly364Ser variant causes profound changes in
36 dentified a natural nonsynonymous variant of catestatin, Gly364Ser, that alters human autonomic funct
37                                We approached catestatin heritability using twin pairs, coupled with g
38            Loss of the physiological "brake" catestatin in Chga mice coupled with dysregulation of tr
39        Here we found extensive processing of catestatin in chromogranin A, as judged by catestatin ra
40               We established heritability of catestatin in twins from 2 continents.
41                             Heritability for catestatin in twins was 44% to 60%.
42 an CHGA haplotype in order to probe CHGA and catestatin in vivo.
43 is, necessary for catecholamine storage, and catestatin-induced inhibition of cholinergic-stimulated
44 the primary sequences of high molecular mass catestatin intermediates and peptides to define the prot
45                                 Secretion of catestatin intermediates from chromaffin cells was accom
46 icted that production of high molecular mass catestatin intermediates requires cleavage at the COOH-t
47 emonstrated the presence of 54-56 and 50 kDa catestatin intermediates that contain the NH(2) terminus
48                    The COOH termini of these catestatin intermediates were defined by the presence of
49 hese findings demonstrate that production of catestatin involves cleavage of CgA at paired basic and
50                             We conclude that catestatin is a highly potent, dose-dependent, noncompet
51                                              Catestatin is an active 21-residue peptide derived from
52    In chromaffin granules, the major form of catestatin is cleaved at dibasic sites, while smaller ca
53                             We conclude that catestatin is cleaved extensively in vivo, and the pepti
54 ts catecholamine release-inhibitory fragment catestatin is diminished, and low catestatin predicts au
55 from the chromogranin A (CgA) precursor, and catestatin is secreted from neuroendocrine chromaffin ce
56    However, it is notable that production of catestatin itself (CgA(344)(-)(364)) utilizes more unusu
57                                              Catestatin itself blocks stimulation of both secretion a
58 Linkage identified 3 regions contributing to catestatin, likely novel determinants of sympathochromaf
59 umans suggest a mechanism whereby diminished catestatin might increase the risk for hypertension.
60  and monobasic residues, necessary steps for catestatin peptide regulation of nicotinic cholinergic-i
61 HGA-derived catecholamine release-inhibitory catestatin peptides.
62 y incompletely blocked by chlorisondamine or catestatin, perhaps because of limited blood-brain barri
63 y fragment catestatin is diminished, and low catestatin predicts augmented adrenergic pressor respons
64 roduction, chromogranin A precursor, and its catestatin product.
65 f catestatin in chromogranin A, as judged by catestatin radioimmunoassay of size-fractionated chromaf
66             Natural allelic variation in the catestatin region was predicted to disrupt the coiled-co
67                Radioimmunoassay demonstrated catestatin release from the regulated secretory pathway
68 to normalcy was achieved by either exogenous catestatin replacement or humanization of Chga mice.
69 eceptor alpha/beta subunits and that crucial catestatin residues are likely to be identical across th
70               Peptide nicotinic antagonists (catestatins, substance P) were far more potent inhibitor
71  had elevated CHGA coupled with reduction in catestatin, suggesting diminished conversion of precurso
72 d a genome-wide association study for plasma catestatin, the catecholamine release inhibitory peptide
73                                         When catestatin variants were mixed in likely heterozygotic (
74 kallikrein cleaved recombinant human CHGA to catestatin, verified by mass spectrometry.
75                                        Human catestatin was cleaved in pheochromocytoma chromaffin gr
76 ogranin A344-364 [RSMRLSFRARGYGFRGPGLQL], or catestatin) was a potent, dose-dependent (IC50 approxima
77 etermines CHGA trafficking and processing to catestatin, we genotyped at positional candidate ATP6N1,
78                        Circulating levels of catestatin were lower among those with hypertensive ESRD
79 ontaining polypeptides, demonstrated by anti-catestatin western blots, of 54-56, 50, 32, and 17 kDa c
80 ogically active peptide fragments, including catestatin, which inhibits catecholamine release.

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