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1 ent in the insulin secretory granules of the pancreatic beta cell.
2 ning the terminally differentiated status of pancreatic beta cells.
3 tal factors, resulting in the destruction of pancreatic beta cells.
4 insulin secretion, which is the function of pancreatic beta cells.
5 es cell cycle entry of quiescent adult human pancreatic beta cells.
6 aracterized by the autoimmune destruction of pancreatic beta cells.
7 insulin storage in the secretory granules of pancreatic beta cells.
8 CKD is caused by a direct effect of urea on pancreatic beta cells.
9 stimulus-secretion coupling in primary mouse pancreatic beta cells.
10 types of cells, including cardiomyocytes and pancreatic beta cells.
11 ical regulator of autophagosome formation in pancreatic beta cells.
12 tory subunit is expressed in human and mouse pancreatic beta cells.
13 acting/modulator protein in rodent and human pancreatic beta cells.
14 mice displayed lower ATG5 and LC3 levels in pancreatic beta cells.
15 utoimmune disease that causes severe loss of pancreatic beta cells.
16 functioning of cells, such as adipocytes and pancreatic beta cells.
17 lded protein response (UPR) and ER stress in pancreatic beta cells.
18 and contribute to autoimmune destruction of pancreatic beta cells.
19 ults in part from a deficiency of functional pancreatic beta cells.
20 leading to deleterious downstream effects in pancreatic beta-cells.
21 Diabetes is linked to loss of pancreatic beta-cells.
22 on insulin secretion is mediated by GHS-R in pancreatic beta-cells.
23 ator of glucose-induced insulin secretion by pancreatic beta-cells.
24 ing in the failure of insulin secretion from pancreatic beta-cells.
25 ng from the destruction of insulin-producing pancreatic beta-cells.
26 ndrome, to the production and maintenance of pancreatic beta-cells.
27 s but relatively silenced, or disallowed, in pancreatic beta-cells.
28 een SCHAD and glutamate dehydrogenase in the pancreatic beta-cells.
29 ucose-stimulated insulin secretion (GSIS) in pancreatic beta-cells.
30 ctions including the release of insulin from pancreatic beta-cells.
31 rs, and the postnatal growth and function of pancreatic beta-cells.
32 s to Ca(2+) homeostasis in insulin-secreting pancreatic beta-cells.
33 emopoietic stem cells, and insulin-releasing pancreatic beta-cells.
34 gnaling pathways coupled to proliferation in pancreatic beta-cells.
35 e found that the Klotho gene is expressed in pancreatic beta-cells.
36 iabetes of the young, regulates mitophagy in pancreatic beta-cells.
37 ce glucose-stimulated insulin secretion from pancreatic beta-cells.
38 ) channel located in both cardiomyocytes and pancreatic beta-cells.
39 lf-reactive T cells attack insulin-secreting pancreatic beta-cells.
40 secretion in C2C12 myotubes and INS-1 832/13 pancreatic beta-cells.
41 developing novel approaches to regenerating pancreatic beta-cells.
42 d fibrils as well as the loss of neuronal or pancreatic beta-cells.
43 ein, plays key roles in insulin secretion in pancreatic beta-cells.
44 xpressed in type II taste receptor cells and pancreatic beta-cells.
45 ocytes and glucose-dependent ATP increase in pancreatic beta-cells.
46 GLP-1R potentiation of insulin secretion in pancreatic beta-cells.
47 ate progression to autoimmune destruction of pancreatic beta-cells.
48 or self-antigen found in insulin granules of pancreatic beta-cells.
49 DM patients with hypomagnesemia have reduced pancreatic beta-cell activity and are more insulin resis
50 hat Glu-OCN-controlled production of DLK1 by pancreatic beta-cells acts as a negative feedback mechan
51 juvant for modulating the T-cell response to pancreatic beta-cell-Ag and reversing early-stage hyperg
53 In response to fasting or hyperglycemia, the pancreatic beta-cell alters its output of secreted insul
55 t the proliferation of the insulin-producing pancreatic beta cells and especially their expansion dur
56 ound that the predominant P4 ATPases in pure pancreatic beta cells and human and rat pancreatic islet
57 exocytosis of insulin-containing granules in pancreatic beta cells and is required for the postprandi
58 Finally, db/db-PI3Kgamma(-/-) mice have more pancreatic beta cells and larger islets than db/db mice,
59 ution in Zn homeostasis in insulin producing pancreatic beta cells and the development of type 2 diab
60 (VA) is required both for the maintenance of pancreatic beta-cell and alpha-cell mass and for glucose
61 ved from prediabetes BB rats with destructed pancreatic beta-cells and controls than pancreas derived
65 previously reported that ARC is abundant in pancreatic beta-cells and modulates survival of these ce
67 an unrealized dynamic adaptive plasticity of pancreatic beta-cells and underscore the rationale for t
68 ng degree of transcriptional similarity with pancreatic beta cells, and expression of beta cell repro
69 in glucose metabolism through actions beyond pancreatic beta cells, and further points to functionall
70 and interferon (IFN)-gamma in rat and human pancreatic beta cells, and it is also up-regulated in be
71 ) controls the rate of glucose metabolism in pancreatic beta cells, and its activity is rate-limiting
72 -GPCRs acutely regulate insulin release from pancreatic beta cells, and variants in genes encoding se
74 abetes is associated with loss of functional pancreatic beta-cells, and restoration of beta-cells is
75 tor is found on gut enteroendocrine L-cells, pancreatic beta-cells, and sympathetic neurons, and is i
77 Pro-inflammatory cytokines contribute to pancreatic beta cell apoptosis in type 1 diabetes at lea
78 ion destroys the BiP binding site and causes pancreatic beta-cell apoptosis and diabetes in mice.
79 evaluated whether TYK2 plays a role in human pancreatic beta-cell apoptosis and production of proinfl
81 mall-molecule BRD0476, a novel suppressor of pancreatic beta-cell apoptosis, inhibits interferon-gamm
82 duced by inflammatory stress, but it induced pancreatic beta-cell apoptosis, reduced pancreatic beta-
85 s (T1D) manifests when the insulin-producing pancreatic beta cells are destroyed as a consequence of
92 ugh we induced VAD in the entire animal, the pancreatic beta-cells are exquisitely sensitive to VAD-a
93 ich glucose regulates insulin secretion from pancreatic beta-cells are now well described, the way gl
97 suppress the DDR appears to be selective for pancreatic beta cells, as nitric oxide fails to inhibit
98 atty acid-induced apoptosis in human and rat pancreatic beta-cells, as well as in human and murine pa
99 for Hnf1alpha are hyperglycemic, with their pancreatic beta-cells being defective in glucose-sensing
100 Cre driver lines are critical for exploring pancreatic beta cell biology with the Cre/LoxP approach.
102 NAs and proapoptotic Bcl-2 proteins in human pancreatic beta-cells, broadening our understanding of c
103 e not only increased in palmitate-stimulated pancreatic beta-cells but also regulate beta-cell homeos
105 1 diabetes (T1D) results from destruction of pancreatic beta cells by autoreactive effector T cells.
106 previously showed that activation of TGR5 in pancreatic beta cells by bile acids induces insulin secr
107 rst-in-class surrogate imaging biomarker for pancreatic beta-cells by targeting the protein GPR44.
108 disease that results from the destruction of pancreatic beta-cells by the immune system that involves
109 The expression and function of NMDARs in pancreatic beta-cells, by contrast, are poorly understoo
110 cose-signal amplifier and calcein-AM-stained pancreatic beta-cell capsules, is developed by Z. Gu and
113 diabetes, and have reduced immunity against pancreatic beta cells compared with control NOD mice.
115 Islet amyloidosis by IAPP contributes to pancreatic beta-cell death in diabetes, but the nature o
118 erstanding the functional roles of TCF7L2 in pancreatic beta cells, despite evidence of TCF7L2 expres
119 ction following CB3 infection may exacerbate pancreatic beta cell destruction in T1D by influencing p
120 highlight a role for the microbiota in early pancreatic beta cell development and suggest a possible
121 a haploinsufficient requirement for PDX1 in pancreatic beta cell differentiation, and a potentially
123 e elevated O-GlcNAc-modified proteins within pancreatic beta cells due to chronic hyperglycemia-induc
127 nescence effector p16(Ink4a) is expressed in pancreatic beta cells during aging and limits their prol
128 exocytosis and endocytosis are paramount to pancreatic beta cell dysfunction in diabetes mellitus.
129 and is implicated in insulin resistance and pancreatic beta cell dysfunction in the metabolic syndro
131 tified as a key player in the progression of pancreatic beta-cell dysfunction contributing to insulin
133 /-) mice exhibit glycemic dysregulations and pancreatic beta-cell dysfunctions, we evaluated islet fu
134 sgenic mice that overexpress, selectively in pancreatic beta-cells, either wild-type (WT) or a mutate
141 However, the presence of FFA2 and FFA3 on pancreatic beta-cells, FFA3 on neurons, and FFA2 on leuk
142 esults from a T cell-mediated destruction of pancreatic beta-cells following the infiltration of leuk
143 ke cells.Our incomplete understanding of how pancreatic beta cells form limits the generation of beta
145 uppresses blood glucose levels by protecting pancreatic beta cells from oxidative stress and improvin
148 ctivates signaling pathways known to support pancreatic beta cell function and survival by modulating
150 plays an essential role in the regulation of pancreatic beta cell function, affecting important proce
151 y the impact of the cell-autonomous clock on pancreatic beta cell function, we examined pancreatic is
154 : during the biological evening by decreased pancreatic beta-cell function (27% lower early-phase ins
155 el proteins concerned with the modulation of pancreatic beta-cell function (adipsin p=0.0056) and hae
156 hat highlights (a) the importance of iron in pancreatic beta-cell function and dysfunction in diabete
157 scovery of common pathways that mediate both pancreatic beta-cell function and end-organ function off
158 inked to genes regulating neurotransmission, pancreatic beta-cell function and energy homeostasis.
159 uced pancreatic beta-cell apoptosis, reduced pancreatic beta-cell function and enhanced hepatic gluco
161 t evidence for the action of sex hormones on pancreatic beta-cell function and the vasculature that a
163 ements in liver function, glucose uptake and pancreatic beta-cell function independent of weight loss
164 tients who are predisposed to the failure of pancreatic beta-cell function is a major concern for the
167 e and cell survival are necessary for normal pancreatic beta-cell function, glucose homeostasis, and
168 abetes pathogenesis through direct impact on pancreatic beta-cell function, senescence-associated sec
171 wn to regulate cytokine-induced apoptosis in pancreatic beta cells (genes from the apoptotic machiner
172 ucose-stimulated insulin secretion (GSIS) in pancreatic beta cells has been extensively explored.
178 ed in an asymmetric pattern of organ growth, pancreatic beta cell hyperplasia, and elevated plasma in
179 the production of vast amounts of insulin by pancreatic beta cells in response to glucose stimulation
181 omplex to suppress TXNIP, thereby protecting pancreatic beta cells in the diabetic setting by inhibit
182 ed that expression of the chemokine CCL22 in pancreatic beta cells in the NOD mouse prevents autoimmu
184 e 2 diabetes have revealed the importance of pancreatic beta-cells in genetic susceptibility to diabe
185 d by calcineurin-dependent NFAT signaling in pancreatic beta-cells in response to oxidative or inflam
189 gnificantly altered cytosolic zinc influx in pancreatic beta cells, indicating an important role for
190 results in part from a deficiency of normal pancreatic beta cells, inducing human beta cells to rege
191 , which is co-secreted with insulin from the pancreatic beta-cells, inhibit the activities of insulin
192 ung AnkbR1788W/R1788W mice displayed primary pancreatic beta cell insufficiency that was characterize
193 n a metabolic syndrome that combines primary pancreatic beta cell insufficiency with peripheral insul
197 undercarboxylated osteocalcin (Glu-OCN) and pancreatic beta-cell insulin; in turn, insulin favors os
198 Glucose stimulation of insulin secretion in pancreatic beta cells involves cell depolarization and s
200 g by the integrated stress response (ISR) in pancreatic beta cells is coupled to metabolic alternatio
201 es have indicated that PI3Kgamma activity in pancreatic beta cells is required for normal insulin sec
202 rotein secretion system of insulin-producing pancreatic beta cells is stressed, leading to increased
206 ellular chloride concentration ([Cl(-)]i) in pancreatic beta-cells is kept above electrochemical equi
208 active T-cells that attack insulin-secreting pancreatic beta-cells, it has been suggested that diseas
210 dy, we demonstrate that inhibition of CK2 in pancreatic beta-cells, knockdown of CK2alpha expression,
211 that hIAPP fibrils are cytotoxic to cultured pancreatic beta-cells, leading us to determine the struc
215 hase arrest in COS-1 and CHO cells, and in a pancreatic beta cell line that express endogenous Kv2.1.
217 e previously developed and described 2 human pancreatic beta cell lines (EndoC-betaH1 and EndoC-betaH
221 fetal sheep is associated with reductions in pancreatic beta cell mass and circulating insulin concen
222 nd caused asymmetric organ growth, increased pancreatic beta cell mass and proliferation, and was ass
226 ceptors are important biomarkers for imaging pancreatic beta-cell mass and detection of benign insuli
227 d for the preservation and/or restoration of pancreatic beta-cell mass and function in individuals wi
231 d, but then eventually surpassed, the normal pancreatic beta-cell mass, leading to islet hyperplasia
239 pite lacking identifiable stem cells, murine pancreatic beta cell number expands in response to an in
246 discovered that the normal expansion of the pancreatic beta cell population during early larval deve
247 KATP channels, and L-type Ca(2+) channels in pancreatic beta-cells, preceding insulin secretion.
248 nsulin-resistant conditions such as obesity, pancreatic beta-cells proliferate to prevent blood gluco
251 entified DISC1 as a major player controlling pancreatic beta-cell proliferation and insulin secretion
252 uniquely unmethylated in insulin-expressing pancreatic beta-cells, providing a classic example of th
253 program underlying infrequent replication of pancreatic beta-cells remains largely inaccessible.
254 at increased the number of insulin-producing pancreatic beta cells represent potential new therapeuti
255 e showed that DUT silencing in human and rat pancreatic beta-cells results in apoptosis via the intri
256 s study explored the role of irisin as a new pancreatic beta-cell secretagogue and survival factor an
258 in neurons, is also the major Syt in rodent pancreatic beta-cells shown to mediate glucose-stimulate
264 s the activation of this proapoptotic UPR in pancreatic beta-cells that has been implicated in the on
265 R fetus produce developmental adaptations in pancreatic beta-cells that impair fetal insulin secretio
266 nsulin secretion is an essential function of pancreatic beta-cells that is partially lost in individu
267 on and inflammatory hyperalgesia, whereas in pancreatic beta-cells the channel has been linked to glu
268 mpensated by increased insulin production of pancreatic beta-cells, thereby maintaining normoglycemia
269 nstrated a potential in molecular imaging of pancreatic beta-cells; this may be useful in early detec
270 -associated locus involved in maintenance of pancreatic beta cells through a fine-tuned regulation of
271 atopoietic stem cells, and insulin-releasing pancreatic beta cells through a signaling pathway involv
273 7-amino acid residue peptide, is produced in pancreatic beta-cells through proteolytic cleavage of it
274 of signals finely tune insulin secretion by pancreatic beta cells to prevent both hyper-and hypoglyc
275 is secreted in conjunction with insulin from pancreatic beta cells to regulate glucose metabolism.
276 elivery of insulin mimicking the function of pancreatic beta-cells to achieve meticulous control of b
282 ) is an autoimmune disease caused by loss of pancreatic beta cells via apoptosis while neighboring al
284 es apoptotic and proinflammatory pathways in pancreatic beta-cells via modulation of IFNalpha signali
285 in live neuroendocrine chromaffin cells and pancreatic beta-cells, visualized using confocal and sup
287 ppression of the autoimmune reaction against pancreatic beta cells was evidenced by a reduction in th
288 erties of cAMP and metabolic oscillations in pancreatic beta cells, we propose here that in addition
289 Because DLK1 is colocalized with insulin in pancreatic beta-cells, we examined the role of DLK1 in i
290 and dopamine, in insulin storage granules in pancreatic beta-cells, we probed by molecular dynamics (
292 immune assault against the insulin-producing pancreatic beta-cells, where chronic local inflammation
293 T1D results from autoimmune destruction of pancreatic beta cells, whereas beta cell failure in T2D
294 ate the cytoprotective mechanisms in CD31(-) pancreatic beta cells, which become resistant to immune-
295 endotoxemia upregulates miR-155-5p in murine pancreatic beta-cells, which improved glucose metabolism
296 overexpression promotes insulin secretion in pancreatic beta cells, while C193S-hSCGN inhibits it.
297 Glucose-stimulated insulin secretion from pancreatic beta-cells within islets of Langerhans plays
298 lipid composition of ISG and mitochondria in pancreatic beta cells without and with glucose stimulati
299 played robust Cre expression and activity in pancreatic beta cells without significant alterations in
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