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1 actor in insulin-secreting beta-cell tumors (insulinomas).
2 y severe hypoglycemic events or diagnoses of insulinoma.
3 patient, there was no radiologic evidence of insulinoma.
4 tumor stroma in a mouse model of pancreatic insulinoma.
5 a successful hand-assisted enucleation of an insulinoma.
6 n pancreatic neuroendocrine tumors including insulinoma.
7 glycaemia especially in suppression tests of insulinoma.
8 or MR imaging) was not able to localize the insulinoma.
9 rs (insulinomas), and also in human sporadic insulinomas.
10 endin-4 ((111)In-DTPA-exendin-4) to identify insulinomas.
11 a may overlap with those in patients without insulinomas.
12 rgical resection of histologically confirmed insulinomas.
13 consistent, abnormal methylation pattern in insulinomas.
14 his difference was present in all nine human insulinomas.
15 he understanding of the molecular biology of insulinomas.
16 est in ileal NETs and may also be helpful in insulinomas.
17 eatic beta-cell mass and detection of benign insulinomas.
18 n to be highly efficient in the detection of insulinomas.
19 s feasible and sensitive in detecting benign insulinomas.
20 ucagonlike peptide-1 receptor-overexpressing insulinomas.
22 d 44 pancreatic primary tumors, including 12 insulinomas, 28 nonfunctioning endocrine tumors, and fou
26 cted pharmacological approaches in the mouse insulinoma-6 (Min6) cell line, we demonstrate that eleva
27 NMDAR-mediated signaling was observed in rat insulinoma 832/13 cells and in human beta-cells, indicat
28 that insulin 2 (Ins2) mRNA expression in rat insulinoma 832/13 cells is markedly increased by wild-ty
29 the RIP1-Tag2 model are well-differentiated insulinomas, a subset of tumors had lost multiple marker
31 for dosimetry studies estimating the maximum insulinoma absorbed dose that could be achieved without
32 small microparticles, mainly EXO, from mouse insulinoma and examined their activities to stimulate th
33 correctly identified 48 of 49 patients with insulinoma and excluded the diagnosis in 64 of 65 contro
34 arlier, we had cloned IG20 cDNA from a human insulinoma and had shown that IG20/MADD can encode six d
38 abeling in human IAPP transgenic mice, human insulinoma and pancreas from humans with and without T2D
39 lanoma, lung carcinoma and pancreatic B-cell insulinoma and provide evidence that loss of pericyte FA
40 differential expression of proteins between insulinoma and their paired tissues by proteomic analysi
41 rigenesis; miR-204 is primarily expressed in insulinomas and correlates with immunohistochemical expr
42 ations include preoperative visualization of insulinomas and discrimination between focal and diffuse
46 TPA-exendin-4 SPECT/CT correctly detected 19 insulinomas and four additional positive lesions (two is
48 offer higher sensitivity in the detection of insulinomas and imaging of beta-cell mass in diabetic pa
49 fore seems to be a general characteristic of insulinomas and is estimated to contribute about 90% to
50 st cancers, colorectal cancer, melanoma, and insulinoma) and other diseases including vascular defect
51 ckdown, in MEN1-associated beta cell tumors (insulinomas), and also in human sporadic insulinomas.
54 cid decarboxylase 65 (GAD65) autoantibodies, insulinoma antigen 2 (IA2) autoantibodies, and diabetes.
61 a subunits was detected in betaTC3 and NIT-1 insulinomas as well as in primary islets, with integrin
65 d decarboxylase (65-kDa isoform; GAD65), and insulinoma-associated Ag-2 (IA-2), and peptides were elu
66 antibodies (IAA), GAD autoantibodies (GADA), insulinoma-associated antigen 2 autoantibodies (IA-2A),
67 antibodies to glutamic acid decarboxylase or insulinoma-associated antigen 2, or diabetes were observ
70 acid decarboxylase autoantibodies (GADA) and insulinoma-associated antigen-2 autoantibodies (IA-2A) w
71 for insulin, glutamic acid decarboxylase, or insulinoma-associated antigen-2 autoantibodies on 2 cons
73 form of glutamic acid decarboxylase (GAD65), insulinoma-associated protein 2 (IA-2), and zinc transpo
74 ecific for either known autoantigens (GAD65, insulinoma-associated protein 2 (IA2), IA2beta/phogrin,
75 antibodies to insulin (IAAs), GAD65 (GADAs), insulinoma-associated protein 2 (IA2As), and ZnT8 (ZnT8A
76 ere hypoglycemia nor positivity to GAD65 and insulinoma-associated protein 2 antibodies was associate
77 posttransplant autoantibodies (GAD antibody, insulinoma-associated protein 2 antigen, zinc transporte
79 oform of glutamic acid decarboxylase), IA-2 (insulinoma-associated protein IA-2) or insulin, alone or
80 onses to beta-cell autoantigens (proinsulin, insulinoma-associated protein, and GAD65 peptides) were
81 cell autoantibodies, insulin autoantibodies, insulinoma-associated protein-2 autoantibodies, and GAD
83 nsulin, glutamic acid decarboxylase, and the insulinoma-associated-2 (IA-2) molecule were analyzed us
87 n fatty acyl-carnitines promoted IS from rat insulinoma beta-cells (INS-1) as well as primary mouse i
88 up B, the presence of low-Km hexokinase-I in insulinoma beta-cells (not in adjacent islets) was revea
89 effect of carbidopa on (18)F-FDOPA uptake in insulinoma beta-cells and an insulinoma xenograft model
91 n1 knockout mice develop multiple pancreatic insulinomas, but this occurs many months after loss of b
92 of exendin-4 derivatives for the imaging of insulinomas by high-resolution PET at early or late time
93 ions for reducing beta-cell proliferation in insulinomas by inhibiting phospho-HLXB9 or its interacti
97 3C6]glucose, was compared in four clonal rat insulinoma cell 1-derived cell lines with varying degree
98 -O-(thio)triphosphate binding and INS1 832-3 insulinoma cell cAMP assays, BETP enhanced GLP-1(9-36)-N
99 the production of free radicals, induces rat insulinoma cell death by activation of a non-selective c
100 a cell line (PANC-1) and the endocrine human insulinoma cell line (CM) were applied for in vitro (11)
101 hermore, addition of monomeric IAPP to a rat insulinoma cell line (INS-1) resulted in decreased cell
102 in the pancreatic beta-cell line MIN6 (mouse insulinoma cell line 6) and islets of Langerhans that ag
103 LAG fusion protein was expressed in an INS-1 insulinoma cell line and then adsorbed to an anti-FLAG m
104 kdown of PTPMT1 expression in the pancreatic insulinoma cell line INS-1 832/13 alters the mitochondri
108 cruited to the insulin promoter in the mouse insulinoma cell line MIN6 when cells are switched from h
109 ee genetically modified strains of the mouse insulinoma cell line MIN6, each of which expressed key i
112 B2 can be phosphorylated in Rin cells (a rat insulinoma cell line) and cultured chromaffin cells, but
116 sing the highly glucose-sensitive 832/13 rat insulinoma cell line, we demonstrated that glucose regul
123 lysis on the four most widely studied rodent insulinoma cell lines and defined their flow cytometric
124 ency of adenovirus-mediated gene transfer in insulinoma cell lines and rat islets and 2) the rapidity
125 the hazards of interpreting data from rodent insulinoma cell lines as modeling normal cell cycle prog
126 cell proliferation in three different rodent insulinoma cell lines by arresting the cells in G2/M pha
127 lthough many studies using rodent islets and insulinoma cell lines have been performed to determine t
130 t-negative interference of SEL1L function in insulinoma cell lines severely impairs, whereas overexpr
134 ic condition, obestatin augments GSIS in rat insulinoma cells (INS-1) and in pancreatic islets from g
136 (Prolastin, human) were observed when murine insulinoma cells (MIN6) were exposed to tumor necrosis f
137 he expression profiles of glucose-responsive insulinoma cells 45 min after the addition of glucose, K
139 , and overexpression of iPLA(2)beta in INS-1 insulinoma cells amplifies, glucose-stimulated insulin s
140 y that enables the study of granule aging in insulinoma cells and beta-cells of knock-in mice through
141 echanism, we overexpressed human IAPP in rat insulinoma cells and freshly isolated human islets.
143 in NAD(P)H autofluorescence in both betaTC3 insulinoma cells and islets in a manner consistent with
144 reased IRS-2 protein expression in INS-1/832 insulinoma cells and mouse islets, whereas IRS-2 mRNA le
146 APK is activated by phosphorylation in INS-1 insulinoma cells and mouse pancreatic islets, that this
147 mall interfering RNA specific for pdx-1 into insulinoma cells and pancreatic islets to diminish endog
149 is transiently activated by nitric oxide in insulinoma cells and rat islets following IL-1 treatment
150 both in vitro and in vivo approaches (mouse insulinoma cells and SPL-deficient mice), that SPL is a
151 are remarkably similar to those observed for insulinoma cells and suggest that this family of non-sel
152 CAP proteins were present in the nucleus of insulinoma cells and that endogenous INSM1 protein was c
153 itor thapsigargin induces apoptosis in INS-1 insulinoma cells and that this is inhibited by a bromoen
154 MS4 and MS6) were examined using 832/13 rat insulinoma cells as well as rodent and human islets.
155 previously reported that apoptosis of INS-1 insulinoma cells due to thapsigargin-induced ER stress w
156 s issue, we initially demonstrated that MIN6 insulinoma cells express functional M3Rs and that RGS4 w
157 solated rat pancreatic islets, whereas INS-1 insulinoma cells expressed only EDG-1, -2, -3, and -5 mR
159 tion (gammaH2AX formation) in rat islets and insulinoma cells in a nitric oxide- and ATM-dependent ma
160 kine-resistant cell lines by growth of INS-1 insulinoma cells in iteratively increasing concentration
161 Recordings of Kv2.1 currents from INS-1 insulinoma cells incubated with AA (5 mum) and subjected
162 ckdown of Pdx1 gene expression in mouse MIN6 insulinoma cells induced apoptotic cell death with an in
164 retrograde transport in isolated islets and insulinoma cells mimicked the phenotype of Asna1(beta-/-
165 ria from liver, pancreatic islets, and INS-1 insulinoma cells or adding glucose to intact INS-1 cells
166 ne expression was knocked down in mouse MIN6 insulinoma cells resulting in apoptotic cell death that
167 n, and short interfering RNA to PDX1 in Min6 insulinoma cells results in the induction of normally un
168 d with GG-labeled encapsulated mouse betaTC6 insulinoma cells returned to normal within 1 week after
169 LA(2)beta) activity in pancreatic islets and insulinoma cells suggest that iPLA(2)beta participates i
170 tion of iPLA(2)beta in pancreatic islets and insulinoma cells suppresses, and overexpression of iPLA(
172 rin expression in human pancreas and in MIN6 insulinoma cells was studied by Western blot, PCR, confo
174 ulated in vitro by chronic culture of 832/13 insulinoma cells with high concentrations of free fatty
175 KN93 reduced arachidonate release from INS-1 insulinoma cells, and both inhibit insulin secretion.
176 aling significantly reduces proliferation of insulinoma cells, and expression of Hedgehog signaling t
177 glucose dependent insulin secretion in NIT-1 insulinoma cells, and high insulin expression in the pre
178 th rat and human pancreatic islets and INS-1 insulinoma cells, and its attachment to cellular protein
179 ed p125 tyrosine phosphorylation in beta-TC3 insulinoma cells, beta-HC9 cells, and in freshly isolate
180 e peroxynitrite generation by rat islets and insulinoma cells, either with or without phorbol 12-myri
181 most potent GHRH agonist MR403 was tested on insulinoma cells, isolated rat islets, and adrenal beta-
182 extrans to study insulin granule dynamics in insulinoma cells, normal mouse islets, and primary pancr
185 ed in electrophysiological recordings of rat insulinoma cells, which are known to express K(V)2 chann
207 ulin mRNA was increased more than 50-fold in insulinomas compared with normal islets, and this differ
210 t the pathway level that the majority of the insulinomas display mutations, copy number variants and/
211 alculations to estimate the maximum absorbed insulinoma dose that could be achieved if exendin were t
215 days after injection for the demarcation of insulinomas from the kidneys represent current limitatio
218 d targeted sequencing revealed that 14 of 43 insulinomas harbored the identical somatic mutation in t
221 using distinct clinical endocrine syndromes (insulinoma [hypoglycemia], gastrinoma [Zollinger-Ellison
222 eath, dedifferentiation, or the formation of insulinomas if cooverexpressed with Bcl-xL, an inhibitor
224 TA-exendin-4 PET/CT correctly identified the insulinoma in 4 of 4 patients, whereas (111)In-DOTA-exen
226 vity, pericytes on capillary-size vessels in insulinomas in RIP-Tag2 transgenic mice expressed both d
228 tently, siRNA-mediated Shp2-knockdown in rat insulinoma INS-1 832/13 cells resulted in decreased insu
230 tion of RESP18HD upon exocytosis of SGs from insulinoma INS-1 cells is associated with cleavage of it
231 ntic vacuoles were also observed in cultured insulinoma INS-1 cells upon CRISPR/Cas9-mediated removal
233 binding to the extracellular surface of rat insulinoma INS-1E cells that stably expressed a tagged h
236 tudy demonstrates that lactogens protect rat insulinoma (INS-1) cells and primary mouse beta cells ag
237 in both primary mouse beta-cells and in rat insulinoma (INS-1) cells, indicating a direct effect on
238 independent robustly glucose-responsive rat insulinoma (INS-1-derived) cell lines and in primary rat
247 at understanding the molecular complexity of insulinoma may be a valuable approach to diabetes drug d
248 ant with increased translation efficiency in insulinomas might explain how these tumours maintain hig
249 suppression of Pdx1 increases death of mouse insulinoma MIN6 beta-cells associated with dissipation o
252 this study, microarray analysis of the mouse insulinoma MIN6 cell line revealed that the transcriptio
253 -induced dynamic Zn(2+) secretion from mouse insulinoma MIN6 cells and primary mouse and human pancre
254 trated that down-regulation of Nck1 in mouse insulinoma MIN6 cells results in faster dephosphorylatio
255 his study, we introduced an shRNA into mouse insulinoma MIN6 cells to deplete Pdx1 and found that exp
259 that decrease insulin secretion from murine insulinoma MIN6B1 cells in response to the GLP-1 analog
261 D3 overexpression protected the NOD-derived insulinoma NIT-1 cell line from cytokine-induced apoptos
262 se 1/2 and nuclear factor-kappaB pathways in insulinoma NIT-1 cells, and inhibitors of either pathway
265 ed the weak transfer of ZnT8 reactivity from insulinomas or primary beta-cells to APC for presentatio
266 rom excessive beta-cell proliferation (e.g., insulinoma) or insufficient beta-cell mass (e.g., diabet
270 ar scintigraphic (111)In-exendin images of 5 insulinoma patients were used for dosimetry studies esti
271 secretion by perifused fragments of 10 human insulinomas permitted their subdivision into three funct
274 Recent biochemical diagnostic guidelines for insulinomas require demonstration of hypoglycemia with i
277 perplasia) and one false negative (malignant insulinoma) result was identified in separate patients b
278 ionality would suppress proliferation of rat insulinoma (Rin) cells comparably to wild-type Cx37 (Cx3
279 tumor-associated Ag in spontaneously arising insulinomas (RIP-Tag2-HA mice), a high proportion of clo
280 racted RNA from nine laser-captured surgical insulinoma samples and from isolated islets of nine dono
285 e genomic and epigenetic landscapes of human insulinomas to gain insight into possible pathways for t
286 or beta cell expansion, we surveyed 38 human insulinomas to obtain insights into therapeutic pathways
288 ta and pHLXB9 can serve as novel targets for insulinoma treatment and have implications for understan
289 ransiently transfected islet-derived hamster insulinoma tumor and betaTC-3 cells revealed that the pr
291 ess T Ag from the RIP and develop pancreatic insulinomas, we demonstrate that epitope IV- but not epi
292 t is involved in insulin production by human insulinomas, we extracted RNA from nine laser-captured s
295 ents histologic diagnosis confirmed a benign insulinoma, whereas one patient refused surgery despite
297 preclinical research specifically focused on insulinomas, with potential translational implications.