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1 al neuroendocrine distribution of endogenous chromogranin A.
2 onserved N- and C-terminal regions of bovine chromogranin A.
3 gation properties as compared with wild-type chromogranin A.
4 0% of cells, and absence of chymotrypsin and chromogranin A.
5 related peptide, neurotensin, serotonin, and chromogranin A.
6 f chymotrypsin, and rare immunoreactivity to chromogranin A.
7 immunostaining for tau-2, synaptophysin, and chromogranin A.
8 n fragments, and was liberated from purified chromogranin A.
9 o label with antibodies specific for APP and chromogranin A.
10 EVSSKDAAE, which is a degradation product of chromogranin A.
11 euroendocrine cell markers Synaptophysin and Chromogranin A.
12 g, urinary catecholamines/metanephrines, and chromogranin A.
13 ed 2 neuroendocrine tumor markers, ASCL1 and chromogranin A.
14 of cells expressing the pan-endocrine marker chromogranin A.
15 and neuroendocrine markers synaptophysin and chromogranin A.
16 PA PET/CT results had higher values of serum chromogranin A (100% vs. 20%, P = 0.0003), serotonin, or
17              Among 37 patients with elevated chromogranin A, 26 (70%) achieved normalization or more
18                            Synthetic longer (chromogranin A(332-364)) and shorter (chromogranin A(344
19 trometry, a major catestatin form was bovine chromogranin A(332-364); identity of the peptide was con
20 alysis revealed two additional forms: bovine chromogranin A(333-364) and A(343-362).
21 strin (1031 pg/ml; reference value <108) and chromogranin A (337 U/L; reference value <36).
22 omaffin granules, with the major form, human chromogranin A(340-372), bounded by dibasic sites.
23 onger (chromogranin A(332-364)) and shorter (chromogranin A(344-364)) versions of catestatin each inh
24 tes highly O-glycosylated proteins including Chromogranin A, a key player in dense core granulogenesi
25                                        Serum chromogranin A, a marker for neuroendocrine tumors, is e
26 nase) blocked nicotinic or PMA activation of chromogranin A, although a dominant negative Ras mutant
27 s of the CT pulmonary angiographic findings, chromogranin A and 5-hydroxyindoleacetic acid levels wer
28                               Tumor markers (chromogranin A and 5-hydroxyindoleacetic acid) before an
29 levels of oxytocin and peptides derived from chromogranin A and B dramatically decreased in the PC1 K
30 proopiomelanocortin, protachykinins A and B, chromogranin A and B, and secretogranin II.
31 ically abolished regulated secretion of both chromogranin A and beta-endorphin in response to the usu
32                        GFI1 colocalizes with chromogranin A and calcitonin-gene-related peptide in em
33 nclude insulin and the two new autoantigens, chromogranin A and islet amyloid polypeptide, all protei
34                                        Thus, chromogranin A and its catestatin fragment may lie at th
35 eals that the interaction between fragmented chromogranin A and neuropilin-1 is required for tumor gr
36 a radioimmunoassays showed elevated gastrin, chromogranin A and normal levels of gastrin-releasing pe
37                                       Plasma chromogranin A and normetanephrine were the best tumor-m
38                     Staining is negative for chromogranin A and positive for bombesin, serotonin, neu
39 alize with secretory granule markers such as chromogranin A and Rab27b, whereas Myo5c tubules are lab
40 r panendocrine immunohistochemistry markers (chromogranin A and/or synaptophysin); 35% of NETs demons
41                                              Chromogranins A and B (CGA and CGB) are high capacity, l
42                                              Chromogranins A and B (CGA and CGB), the major proteins
43                                              Chromogranins A and B and secretogranin II are a family
44                                              Chromogranins A and B are high capacity, low affinity ca
45 ch activation, and secretory markers Mucin2, Chromogranin A, and Growth factor-independent 1 (Gfi1) w
46                Different amidation events on chromogranin A, and on peptides processed from proopiome
47 rade [poorly differentiated], respectively), chromogranin A, and proliferation index (Ki-67).
48                                              Chromogranin A appears to be the most useful serum marke
49  found extensive processing of catestatin in chromogranin A, as judged by catestatin radioimmunoassay
50 in positively for alpha-tubulin, mucins, and chromogranin A, as well as for endoderm transcription fa
51               In summary, common variants in chromogranin A associate with the risk of hypertensive E
52 t express typical LDCV proteins, transfected chromogranins A, B, and brain-derived neurotrophic facto
53 efore probed the role of the MAPK pathway in chromogranin A biosynthesis after secretory stimulation
54 ntestinal enteroendocrine cells positive for chromogranin A, but they had normal numbers of Paneth's,
55       We investigated the effects of a novel chromogranin A catecholamine release-inhibitory fragment
56 t, removing the C-terminal 90 amino acids of chromogranin A caused rerouting to the constitutive secr
57 ratin 20), acinar (chymotrypsin), and islet (chromogranin A) cell markers was performed to analyze th
58 ol as a well-known marker of stress loading, chromogranin A (CgA) and alpha-amylase (AA) are supposed
59 Results showed that proteolytic fragments of chromogranin A (CgA) and chromogranin B (CgB) represent
60  secretory vesicles of neuroendocrine cells, chromogranin A (CGA) and chromogranin B (CGB), have been
61  LDCV formation involves the granin proteins chromogranin A (CgA) and chromogranin B (CgB); CgA- and
62 nocarcinomas correlates with serum levels of chromogranin A (CgA) and drives treatment resistance.
63                                              Chromogranin A (CgA) and neuron-specific enolase (NSE) w
64     Immunohistochemical (IHC) measurement of chromogranin A (CgA) discriminates gastrointestinal (GI)
65                                  Previously, chromogranin A (CgA) has been shown to play a key role i
66 afficking of the regulated secretory protein chromogranin A (CgA) in PC12 cells.
67                                              Chromogranin A (CgA) is the major soluble protein in the
68             These conditions are reversed in Chromogranin A (CgA) knockout (CgA-KO) mice.
69                                              Chromogranin A (CgA) levels have previously been found t
70                                              Chromogranin A (CgA) may be critical for secretory granu
71 n active 21-residue peptide derived from the chromogranin A (CgA) precursor, and catestatin is secret
72             In neuroendocrine tumors (NETs), Chromogranin A (CgA) was considered acceptable as a biom
73 iated with increased cleavage of full-length chromogranin A (CgA), a circulating vasoregulatory neuro
74 ing and organ colonization were inhibited by chromogranin A (CgA), a protein present in variable amou
75 ctors to 125 species and observed that fecal chromogranin A (CgA), a protein secreted by enteroendocr
76 found that physiologic levels of circulating chromogranin A (CgA), a protein secreted by the neuroend
77  stores in which the Ca(2+) storage protein, chromogranin A (CGA), couples with InsP(3)-gated Ca(2+)
78 gnosis is established by elevation of plasma chromogranin A (CgA), serotonin, or urinary 5-hydroxyind
79 r Musashi-1 (Msi-1), neurogenin 3 (NEUROG3), chromogranin A (CgA), serotonin, peptide YY (PYY), oxynt
80                                              Chromogranin A (CgA), the major soluble protein in catec
81                                              Chromogranin A (CgA), which binds catecholamines for sto
82 cription of the major vesicular core protein chromogranin A (CgA).
83 secretion in endocrine cells is dependent on chromogranin A (CGA).
84 age product of the neuroendocrine prohormone chromogranin A (CgA).
85 n, increased tumor grade, and elevated serum chromogranin A (CgA).
86  cells, we show that SgIII is complexed with Chromogranin A (CgA).
87 e neuroendocrine (NE) markers calcitonin and chromogranin A (CgA).
88 the N- and C-terminal regions of circulating chromogranin A (CgA, CHGA), classically an antiangiogeni
89  and chemotherapy, presence of diabetes, and chromogranin-A (CgA) levels higher than 336 mug/L.
90                        The 2.5HIP (C-peptide-chromogranin A [CgA] HIP), recognized by the diabetogeni
91                                              Chromogranin A (CHGA) and its derived peptides, which ar
92 n C-peptide fragment fused to a peptide from chromogranin A (ChgA) and that endogenous 2.5HIP-reactiv
93 es, we have identified the peptide WE14 from chromogranin A (ChgA) as the antigen for highly diabetog
94 , which is a fusion of insulin C-peptide and chromogranin A (ChgA) fragments, and compared it with th
95                                              Chromogranin A (ChgA) has been identified as the antigen
96  Recent studies suggest an important role of chromogranin A (CHGA) in the regulated secretory pathway
97                                              Chromogranin A (ChgA) is an autoantigen for CD4(+) T cel
98                      The acidic glycoprotein chromogranin A (CHGA) is co-stored/co-secreted with cate
99                                              Chromogranin A (CHGA) is coreleased with catecholamines
100                    The secretory pro-hormone chromogranin A (CHGA) is densely packed into storage gra
101                     The secretory prohormone chromogranin A (CHGA) is overexpressed in essential hype
102 etermine whether the common variation at the chromogranin A (CHGA) locus increases susceptibility to
103                                      Whether chromogranin A (CHGA) polymorphisms predict end-organ co
104                                              Chromogranin A (CHGA) regulates catecholamine storage an
105                                              Chromogranin A (CHGA) regulates the storage and release
106                                              Chromogranin A (CHGA) triggers catecholamine secretory g
107  mimotope (BDC2.5(mim)) of islet autoantigen chromogranin A (ChgA) with or without calcitriol (1alpha
108                                              Chromogranin A (CHGA), a protein released from secretory
109 bal T1D serum proteomics analysis identified chromogranin A (CHGA), a T1D-autoantigen, as the top pro
110 mine release inhibitory peptide derived from chromogranin A (CHGA), and other CHGA- or chromogranin B
111 ied the beta cell secretory granule protein, chromogranin A (ChgA), as a new autoantigen in type 1 di
112 tide derived from the neuroendocrine protein chromogranin A (CHGA), is a functional AMP and is presen
113                                              Chromogranin A (Chga), which catalyzes formation and car
114                          Catestatin (CST), a chromogranin A (CHGA)-derived peptide, is a potent inhib
115                                              Chromogranin A (CHGA/Chga), a proprotein, widely distrib
116 esicular monoamine transporter (VMAT1,2) and chromogranin A (ChrgA), are also expressed in taste buds
117                                              Chromogranin A, chromogranin B, and secretogranin II, me
118 ocortin (POMC), provasopressin, prooxytocin, chromogranin A, chromogranin B, and secretogranin II.
119 ells revealed reciprocal changes in secreted chromogranin A COOH-terminal fragments (increased approx
120                                              Chromogranin A, coreleased with catecholamines by exocyt
121                       Point mutations of the chromogranin A CRE suggested that this element was neces
122              Here, we probed the role of the chromogranin A-derived peptide pancreastatin (PST: CHGA(
123                       Pancreastatin (PST), a chromogranin A-derived peptide, is a potent physiologica
124 orms of gastrin in each, and pyloric mucosal chromogranin A-derived peptides were investigated in the
125 nces in the concentration of pyloric mucosal chromogranin A-derived peptides were recorded between in
126                       Pancreastatin (PST), a chromogranin A-derived potent physiological dysglycemic
127 d secretion in both neuroendocrine cells and chromogranin A-expressing COS7 cells used as a simplifie
128 psies confirmed the presence of the virus in chromogranin A-expressing epithelial cells, as it does i
129                    Both the MAPK pathway and chromogranin A expression may be activated by cytosolic
130 ues representing subsequent recurrences, the Chromogranin A expression was lost, and the Ki-67 index
131                        Serum markers include chromogranin A for neuroendocrine tumors, pepsinogen I f
132 tely 71 and approximately 27 kD NH2-terminal chromogranin A fragments.
133               PACAP activated the endogenous chromogranin A gene by four- to fivefold.
134                             IGF-I stimulated chromogranin A gene expression by Northern blot analysis
135 led with assay of histidine decarboxylase or chromogranin A gene expression is useful in the assessme
136 ed whether PACAP regulates expression of the chromogranin A gene in PC12 rat chromaffin cells, so as
137 in, performance status, tumor burden, plasma chromogranin A (&gt;/=600 mug/L), neuron-specific enolase (
138              Tissue morphology, abundance of chromogranin A, gut hormones, alpha-defensin, mucin 2, N
139                                              Chromogranin A immunoblots revealed chromogranin A proce
140 tion was used to analyze the distribution of chromogranin A immunoreactive cells in serial sections o
141 injection, total insulin content and insulin:chromogranin A immunoreactivity were reduced by approxim
142          Therefore, the global deficiency of chromogranin A impairs recognition of the major diabetog
143 hemistry demonstrated a relative decrease of chromogranin A in processes (where regulated secretory v
144 retory granules, and stimulated secretion of chromogranin A increased 50%.
145 imulation of secretion in catecholamines and chromogranin A, indicating that secretion of solAPPcyt w
146  cells did not express defensin-5, Muc-2, or chromogranin A, indicating that they were not lineage co
147                             Hybrid-insulin C-chromogranin A (InsC-ChgA)-specific CD4(+) T cells skewe
148  Although various biomarkers including CHGA (Chromogranin A), INSM1 (Insulinoma-associated protein 1)
149               Specific endopeptidases cleave chromogranin A into biologically active peptide fragment
150               These results demonstrate that chromogranin A is a substrate for the endogenous endopro
151                   The catestatin fragment of chromogranin A is an endogenous inhibitor of nicotinic c
152                   The catestatin fragment of chromogranin A is an inhibitor of catecholamine release,
153                               This region of chromogranin A is extensively processed within chromaffi
154                                              Chromogranin A is released together with epinephrine and
155                                        Since chromogranin A is secreted along with catecholamines, we
156                                              Chromogranin A is the major soluble core component in se
157                                              Chromogranin A knock-out (Chga-KO) mice display increase
158                                              Chromogranin A knockout (Chga-KO) mice exhibit enhanced
159 are and characterise human EECs we generated chromogranin-A labelled organoids from duodenal and ilea
160 ng a greater than 50% reduction in the nadir chromogranin A level within the 1st year after treatment
161  estimated absorbed BM dose, elevated plasma chromogranin A level, baseline blood counts, and renal f
162           Her 5-hydroxyindoleacetic acid and chromogranin A levels were not elevated.
163                                              Chromogranin A levels were significantly higher in both
164 rmal, as were 5-hydroxyindoleacetic acid and chromogranin A levels.
165 on of PCl suggests that the action of PC1 on chromogranin A may be specific within the chromogranin/s
166  and calcitonin and suggest that the role of chromogranin A may be to stabilize an otherwise unstable
167                     This small domain within chromogranin A may contribute to a novel, autocrine, hom
168 owledge of cleavage sites of catestatin from chromogranin A may provide a useful starting point in an
169  function, e.g., histidine decarboxylase and chromogranin A messenger RNA abundance, in carcinoid tum
170  NH2-terminal fragment as well as the parent chromogranin A molecule accumulated, while an approximat
171 eprazole, VMAT2, histidine decarboxylase and chromogranin A mRNA abundance in gastric corpus, and pla
172                                              Chromogranin A mRNA responded to MAPK pathway manipulati
173                                              Chromogranin A mRNA showed a time-dependent 3.87-fold re
174 ng for mucosal 5-HT synthesis; P < 0.01] and chromogranin A (neuroendocrine secretion; P < 0.01), wit
175                       The baseline levels of chromogranin A, neuron-specific enolase, and multiple so
176               We also measured fasting serum chromogranin A, neuron-specific enolase, gastrin, glucag
177                            Elevated baseline chromogranin A, neuron-specific enolase, placental growt
178 n L-DsRed fusion protein with enkephalin and chromogranin A neuropeptides that are present in secreto
179 isense PC1 induction, an approximately 66-kD chromogranin A NH2-terminal fragment as well as the pare
180 hetic peptides spanning approximately 80% of chromogranin A, one (bovine chromogranin A344-364 [RSMRL
181 and neuroendocrine markers synaptophysin and chromogranin A (P < 0.0000001).
182                                  Fluorescent chromogranin-A positive EECs were purified and analysed
183               We report increased numbers of chromogranin A-positive (+), including orexigenic ghreli
184 as predominantly localized to epithelial and chromogranin A-positive endocrine cells.
185 et cell function while negatively regulating chromogranin A-positive enteroendocrine cell number.
186 inantly in intestinal epithelial cells, with chromogranin A-positive enteroendocrine cells (EECs) ide
187 otyping, including catecholamine production, chromogranin A precursor, and its catestatin product.
188          Chromogranin A immunoblots revealed chromogranin A processing, from both the NH2 and COOH te
189                                  A series of chromogranin A promoter 5' deletion mutant/luciferase re
190  markedly diminished trans-activation of the chromogranin A promoter by PACAP.
191 r was in linkage disequilibrium with 1 major Chromogranin A promoter haplotype, although promoter hap
192 cis, activation by the cascade maps onto the chromogranin A promoter proximal CRE, which is both nece
193 , and calcium-dependent signals map onto the chromogranin A promoter proximal CRE.
194 oximal CRE box is entirely necessary for the chromogranin A promoter response to PACAP.
195 kinase blocked the response of a transfected chromogranin A promoter to nicotine or protein kinase C
196 antagonist KCREB blocked the response of the chromogranin A promoter to nicotine, cAMP, or MAPK pathw
197 protein kinase C mapped principally onto the chromogranin A promoter's cAMP response element (TGACGTA
198 ltimately relays the secretory signal to the chromogranin A promoter's CRE box in cis.
199 tion in a fashion similar to the transfected chromogranin A promoter, in both direction and magnitude
200 n enhanced basal as well as IGF-I-stimulated chromogranin A promoter.
201 fection of pathway components stimulated the chromogranin A promoter.
202 we employed a novel mouse strain harboring a chromogranin A promoter/firefly luciferase reporter tran
203 e obtained with a transfected 1,200-bp mouse chromogranin A promoter/luciferase reporter construct.
204                                  Transfected chromogranin A promoter/luciferase reporter constructs w
205  the fluorescent protein Venus driven by the chromogranin-A promoter.
206           Generation of NOD mice lacking the chromogranin A protein (NOD.ChgA(-/-)) completely nullif
207  hypothesis, recombinant insulin, GAD65, and chromogranin A proteins were encapsulated within poly(d,
208 edistribution of desmoplakin, keratin 5, and chromogranin A proteins.
209 istochemistry for cytokeratins 7 and 20, and Chromogranin A-proteins which have a well described expr
210 his peptide blocked the inhibitory effect of chromogranin A proteolytic fragments on nicotinic-stimul
211 differentiation of thymocytes expressing the chromogranin A-reactive BDC-2.5 and BDC-10.1 TCRs or the
212 ay not be solely explained by the absence of chromogranin A reactivity.
213 atecholamine release, and was shared by this chromogranin A region from several species.
214 ced secretion, transcriptional activation of chromogranin A remained unaltered.
215 gen receptor, prostate specific antigen, and chromogranin A, respectively.
216 as associated with an objective biochemical (chromogranin A) response rate of 40%, and a radiologic r
217 sphatase and the regulated secretory protein chromogranin A resulted in an increased chromogranin sto
218 and-Factor[rs12829220] in the control group; Chromogranin-A[rs9658644], Cystatin-C[rs2424577] and Vit
219                          Plasma cortisol and chromogranin A showed a significant association that did
220         The frequencies of islet Ag-reactive chromogranin A-specific CD4(+) T cells and islet specifi
221  marker MTA1, the apoptotic marker NALP, and chromogranin A) that define gut neuroendocrine cell beha
222  biosynthesis of the major secreted protein (chromogranin A), that the activation is transcriptional,
223 secretion also activates the biosynthesis of chromogranin A, the major protein released with catechol
224 lls, we studied the biosynthetic response of chromogranin A, the major soluble protein co-stored and
225   Such coupling triggers the biosynthesis of chromogranin A, the precursor of catestatin.
226 ynthesis of just released catecholamines and chromogranin A, the precursor of the catecholamine relea
227 ization domain did not affect the sorting of chromogranin A to the regulated secretory pathway.
228                           Thus, PACAP-evoked chromogranin A transcription and catecholamine secretion
229 -binding protein CREB, blunted activation of chromogranin A transcription by nicotine, phorbol ester,
230               We conclude that activation of chromogranin A transcription by secretory stimulation in
231  receptor antagonist PACAP6-38 impaired both chromogranin A transcription or catecholamine secretion
232  Therefore, we propose that PACAP signals to chromogranin A transcription through the CRE in cis, and
233 bited both forskolin and PACAP activation of chromogranin A transcription, revealing that PACAP-induc
234 timuli influence exocytotic secretion versus chromogranin A transcription.
235 gene-3; stem (BMI1, nestin); and chromaffin (chromogranin A, tyrosine hydroxylase) markers similar to
236                                              Chromogranin A was identified as a promising marker for
237  a new phosphorylation site (S191) in bovine chromogranin A was identified.
238 eporter and the neuroendocrine-specific gene chromogranin A was induced 2-3.3-fold by insulin-like gr
239                Plasma levels of cortisol and chromogranin-A were determined.
240 easing peptide, neuron-specific enolase, and chromogranin-A) were analyzed in 50 patients commencing

 
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