ライフサイエンスコーパス: pancreatic beta cell

1 ge (e.g., the liver, vasculature, heart, and pancreatic beta-cells).

2 ent in the insulin secretory granules of the pancreatic beta cell.

3 ulation in the insulin secretory granules of pancreatic beta cells.

4 coupled to the prostaglandin EP3 receptor in pancreatic beta cells.

5 is caused by immune-mediated destruction of pancreatic beta cells.

6 ose-stimulated insulin secretion (GSIS) from pancreatic beta cells.

7 omyocytes, dorsal root ganglion neurons, and pancreatic beta cells.

8 on and progressive loss of insulin-producing pancreatic beta cells.

9 aracterized by the autoimmune destruction of pancreatic beta cells.

10 tory subunit is expressed in human and mouse pancreatic beta cells.

11 ding to the destruction of insulin producing pancreatic beta cells.

12 utoimmune disease that causes severe loss of pancreatic beta cells.

13 functioning of cells, such as adipocytes and pancreatic beta cells.

14 lded protein response (UPR) and ER stress in pancreatic beta cells.

15 and contribute to autoimmune destruction of pancreatic beta cells.

16 ults in part from a deficiency of functional pancreatic beta cells.

17 signaling network in response to glucose in pancreatic beta cells.

18 ning the terminally differentiated status of pancreatic beta cells.

19 tal factors, resulting in the destruction of pancreatic beta cells.

20 insulin secretion, which is the function of pancreatic beta cells.

21 es cell cycle entry of quiescent adult human pancreatic beta cells.

22 insulin storage in the secretory granules of pancreatic beta cells.

23 ich display important characteristics of the pancreatic beta cells.

24 disease characterized by progressive loss of pancreatic beta cells.

25 litus results from autoimmune destruction of pancreatic beta cells.

26 effects of AKT1 on the adaptive response of pancreatic beta cells.

27 at SPARC promoted GSIS by inhibiting RGS4 in pancreatic beta cells.

28 shown to be a component of ER-PM contacts in pancreatic beta-cells.

29 catechol estrogens, on insulin secretion in pancreatic beta-cells.

30 in the insulin-secretory granules (ISGs) of pancreatic beta-cells.

31 P2Y14 was expressed in both human and rodent pancreatic beta-cells.

32 al and pathological conditions, including in pancreatic beta-cells.

33 leading to deleterious downstream effects in pancreatic beta-cells.

34 developing novel approaches to regenerating pancreatic beta-cells.

35 ate progression to autoimmune destruction of pancreatic beta-cells.

36 ce glucose-stimulated insulin secretion from pancreatic beta-cells.

37 secretion in C2C12 myotubes and INS-1 832/13 pancreatic beta-cells.

38 d fibrils as well as the loss of neuronal or pancreatic beta-cells.

39 ein, plays key roles in insulin secretion in pancreatic beta-cells.

40 xpressed in type II taste receptor cells and pancreatic beta-cells.

41 ocytes and glucose-dependent ATP increase in pancreatic beta-cells.

42 GLP-1R potentiation of insulin secretion in pancreatic beta-cells.

43 or self-antigen found in insulin granules of pancreatic beta-cells.

44 Diabetes is linked to loss of pancreatic beta-cells.

45 on insulin secretion is mediated by GHS-R in pancreatic beta-cells.

46 ator of glucose-induced insulin secretion by pancreatic beta-cells.

47 ing in the failure of insulin secretion from pancreatic beta-cells.

48 ng from the destruction of insulin-producing pancreatic beta-cells.

49 ndrome, to the production and maintenance of pancreatic beta-cells.

50 s but relatively silenced, or disallowed, in pancreatic beta-cells.

51 ults from insufficient numbers of functional pancreatic beta-cells.

52 levels of glucose to insulin secretion from pancreatic beta-cells.

53 ted insulin secretion is the hallmark of the pancreatic beta-cell, a critical player in the regulatio

54 DM patients with hypomagnesemia have reduced pancreatic beta-cell activity and are more insulin resis

55 Success or failure of pancreatic beta cell adaptation to ER stress is a determ

56 a better understanding of how to protect the pancreatic beta cells against autoimmune or metabolic as

57 nd we found that deglycosylation in cultured pancreatic beta cells altered insulin secretion.

58 Induced Sbp2 deficiency in pancreatic beta-cells altered expression of only 3 selen

59 Specifically, pancreatic beta cells and adipocytes both rely heavily o

60 it critically affects viability of neurons, pancreatic beta cells and cardiomyocytes.

61 exocytosis of insulin-containing granules in pancreatic beta cells and is required for the postprandi

62 Finally, db/db-PI3Kgamma(-/-) mice have more pancreatic beta cells and larger islets than db/db mice,

63 We find that human pancreatic beta cells and liver organoids are highly per

64 ution in Zn homeostasis in insulin producing pancreatic beta cells and the development of type 2 diab

65 notype and conditional deletion of Gprc6a in pancreatic beta-cell and skeletal muscle respectively im

66 onobese diabetic (NOD) mice express CCL21 in pancreatic beta-cells and do not develop autoimmune diab

67 insulin secretion and insulin sensitivity in pancreatic beta-cells and hepatocytes.

68 ism of the prostaglandin I2 (IP) receptor in pancreatic beta-cells and in glomerular podocytes.

69 ects a range of different tissues, including pancreatic beta-cells and liver.

70 previously reported that ARC is abundant in pancreatic beta-cells and modulates survival of these ce

71 A therapy capable of immunoisolating pancreatic beta-cells and providing normoglycaemia is an

72 s alone was able to drive the destruction of pancreatic beta-cells and the onset of diabetes, T-cell-

73 ynthesis, storage, release, and signaling in pancreatic beta-cells and their functional relevance in

74 ng degree of transcriptional similarity with pancreatic beta cells, and expression of beta cell repro

75 and interferon (IFN)-gamma in rat and human pancreatic beta cells, and it is also up-regulated in be

76 presence of both tau and Abeta inclusions in pancreatic beta cells, and of amylin deposits in the bra

77 GLP1R is highly expressed on pancreatic beta-cells, and activation by endogenous incr

78 s (T1D) in which human GAD65 is expressed in pancreatic beta-cells, and human MHC-II is expressed on

79 abetes is associated with loss of functional pancreatic beta-cells, and restoration of beta-cells is

80 Pancreatic beta-cell apoptosis and proliferation were al

81 but improves insulin sensitivity and reduces pancreatic beta-cell apoptosis.

82 s (T1D) manifests when the insulin-producing pancreatic beta cells are destroyed as a consequence of

83 Pancreatic beta cells are functionally programmed to rel

84 Pancreatic beta cells are responsible for maintaining gl

85 ich glucose regulates insulin secretion from pancreatic beta-cells are now well described, the way gl

86 results in impaired trafficking of Glut2 in pancreatic beta-cells as a consequence of an intracellul

87 Insulin is first produced in pancreatic beta-cells as the precursor prohormone proins

88 suppress the DDR appears to be selective for pancreatic beta cells, as nitric oxide fails to inhibit

89 atty acid-induced apoptosis in human and rat pancreatic beta-cells, as well as in human and murine pa

90 Autoimmunity against pancreatic beta-cell autoantigens is a characteristic of

91 ental autoimmune encephalomyelitis (EAE) and pancreatic beta cell autoreactivity.

92 Pancreatic beta-cells become irreversibly damaged by lon

93 Pancreatic beta cells (beta-cells) differentiate during

94 Cre driver lines are critical for exploring pancreatic beta cell biology with the Cre/LoxP approach.

95 NAs and proapoptotic Bcl-2 proteins in human pancreatic beta-cells, broadening our understanding of c

96 cell swelling stimulate insulin release from pancreatic beta-cells but the mechanisms are poorly unde

97 non-glucose-stimulated insulin secretion of pancreatic beta-cells, but only non-glucose-stimulated i

98 rst-in-class surrogate imaging biomarker for pancreatic beta-cells by targeting the protein GPR44.

99 disease that results from the destruction of pancreatic beta-cells by the immune system that involves

100 The expression and function of NMDARs in pancreatic beta-cells, by contrast, are poorly understoo

101 In pancreatic beta-cells, channels formed by SUR1 and Kir6.

102 Elevated pancreatic beta-cell cholesterol levels impair insulin s

103 Our study establishes that pancreatic beta-cells communicate with vagal sensory neu

104 though most effort has focused on generating pancreatic beta cells, considerable evidence indicates t

105 resses its amyloid self-assembly and related pancreatic beta-cell damage in vitro.

106 trigger that has been suggested to initiate pancreatic beta-cell damage, leading to the development

107 0-like kinase 1 (MST1) is a key regulator of pancreatic beta-cell death and dysfunction; its deficien

108 Islet amyloidosis by IAPP contributes to pancreatic beta-cell death in diabetes, but the nature o

109 reported that the activation of autophagy in pancreatic beta-cells decreases insulin secretion by sel

110 s one of the molecular mechanisms underlying pancreatic beta-cell demise in type 1 diabetes.

111 haracterized by effector T-cell responses to pancreatic beta-cell-derived peptides presented by HLA c

112 ction following CB3 infection may exacerbate pancreatic beta cell destruction in T1D by influencing p

113 tor that may contribute to the initiation of pancreatic beta-cell destruction during the development

114 highlight a role for the microbiota in early pancreatic beta cell development and suggest a possible

115 ent makes it an attractive target to enhance pancreatic beta-cell differentiation and increase beta-c

116 known to stimulate insulin secretion by the pancreatic beta-cells, direct evidence of CCK promoting

117 Pancreatic beta-cell DNA was identified in the circulati

118 pathway may act as a protective mechanism in pancreatic beta cells during a high-calorie diet.

119 lygenic spectrum, implicating loci linked to pancreatic beta cell dysfunction, lipid dysregulation an

120 Oxidative stress is thought to promote pancreatic beta-cell dysfunction and contribute to both

121 e 2 diabetes, a process which contributes to pancreatic beta-cell dysfunction and death.

122 APIs may be predisposed to pancreatic beta-cell dysfunction and have the highest pr

123 nt hyperglycemia is causally associated with pancreatic beta-cell dysfunction and loss of pancreatic

124 a chronic metabolic disease characterized by pancreatic beta-cell dysfunction and peripheral insulin

125 Pancreatic beta-cell dysfunction contributes to onset an

126 NDM-linked activating mutation in STAT3 and pancreatic beta-cell dysfunction.

127 tic glucose metabolism, and both adipose and pancreatic beta-cell dysfunction.

128 /-) mice exhibit glycemic dysregulations and pancreatic beta-cell dysfunctions, we evaluated islet fu

129 sgenic mice that overexpress, selectively in pancreatic beta-cells, either wild-type (WT) or a mutate

130 nsulinemia and abundance of insulin-positive pancreatic beta-cells, even when treatment was administe

131 Pancreatic beta cells exhibit an age-dependent decrease

132 In conclusion, results support that pancreatic beta cells export miR-375-3p to HDL and this

133 Insulin-secreting pancreatic beta-cells express the machinery for DA synth

134 Pancreatic beta cell failure is the central event leadin

135 Progressive pancreatic beta cell failure underlies the transition of

136 aracterized by insulin resistance along with pancreatic beta cell failure.

137 Pancreatic beta-cell failure in type 2 diabetes mellitus

138 into how mitochondrial dysfunction may cause pancreatic beta-cell failure.

139 chronic metabolic stress, may contribute to pancreatic beta-cell failure.

140 esults from a T cell-mediated destruction of pancreatic beta-cells following the infiltration of leuk

141 ke cells.Our incomplete understanding of how pancreatic beta cells form limits the generation of beta

142 Interleukin 6 protects pancreatic beta cells from apoptosis by stimulation of a

143 Generation of pancreatic beta cells from human pluripotent stem cells

144 Our data demonstrate that pancreatic beta-cells from donors with type 1 diabetes e

145 Using mouse pancreatic beta-cells from wild-type and oestrogen recep

146 Inadequate pancreatic beta cell function underlies type 1 and type

147 haracterized by progressive deterioration of pancreatic beta-cell function after hyperglycemia onset.

148 scovery of common pathways that mediate both pancreatic beta-cell function and end-organ function off

149 inked to genes regulating neurotransmission, pancreatic beta-cell function and energy homeostasis.

150 xposure has been shown to be deleterious for pancreatic beta-cell function and insulin release.

151 MicroRNA 199 (miR-199) negatively impacts pancreatic beta-cell function and its expression is high

152 t evidence for the action of sex hormones on pancreatic beta-cell function and the vasculature that a

153 ements in liver function, glucose uptake and pancreatic beta-cell function independent of weight loss

154 tients who are predisposed to the failure of pancreatic beta-cell function is a major concern for the

155 However, its role in regulation of pancreatic beta-cell function is not known.

156 the insulin receptor; however, its impact on pancreatic beta-cell function is unknown.

157 Reduced pancreatic beta-cell function or mass is the critical pr

158 plicated genes are involved in inflammation, pancreatic beta-cell function, and T2DM pathogenesis.

159 play a role in the regulation of metabolism, pancreatic beta-cell function, energy homeostasis, mood

160 e and cell survival are necessary for normal pancreatic beta-cell function, glucose homeostasis, and

161 of volatile organic compounds (VOCs) impairs pancreatic beta-cell function, leading to insulin resist

162 While mitophagy is critical to pancreatic beta-cell function, the posttranslational sig

163 role in controlling glucose homeostasis and pancreatic beta-cell function.

164 ndogenous estrogen metabolites in modulating pancreatic beta-cell function.

165 to a new therapeutic approach for improving pancreatic beta-cell function.

166 sistance, hypoinsulinemia, and deteriorating pancreatic beta-cell function.

167 and insulin secretion, as a manifestation of pancreatic beta-cell function.

168 he mediation in women was driven by improved pancreatic beta-cell function.

169 P2Y14 and UDP-G's role in the regulation of pancreatic beta-cell function.

170 Ca(2+) is an essential signal for pancreatic beta-cell function.

171 tes (T2D) is marked by exhaustive failure of pancreatic beta-cell functional mass to compensate for i

172 e results indicate that WASH participates in pancreatic beta-cell glucose sensing and whole-body gluc

173 onal potential of the GLP-1/GLP-1R system in pancreatic beta cells has led to the development of esta

174 Elevated cholesterol content within pancreatic beta-cells has been shown to reduce beta-cell

175 the development of diabetes, specifically in pancreatic beta-cells, has not been elucidated yet.

176 and interdependence of ATF6alpha and XBP1 in pancreatic beta cells have not been explored.

177 Pancreatic beta cells have one of the highest protein se

178 sfunction in rats expressing human amylin in pancreatic beta-cells (HIP rats).

179 Autophagy is a major regulator of pancreatic beta cell homeostasis.

180 ed in an asymmetric pattern of organ growth, pancreatic beta cell hyperplasia, and elevated plasma in

181 to further examine the functions of WFS1 in pancreatic beta cells in the context of hyperglycemia.

182 omplex to suppress TXNIP, thereby protecting pancreatic beta cells in the diabetic setting by inhibit

183 role of the immune system in homeostasis of pancreatic beta cells in type 2 diabetes mellitus is poo

184 results from the progressive destruction of pancreatic beta-cells in a process mediated primarily by

185 Failure to expand pancreatic beta-cells in response to metabolic stress le

186 d by calcineurin-dependent NFAT signaling in pancreatic beta-cells in response to oxidative or inflam

187 Here we show that the pancreatic beta-cells in zebrafish exhibit different gro

188 Up-regulation of Lnc13 in pancreatic beta-cells increased activation of the proinf

189 Downstream effects on insulin secretion from pancreatic beta cells indicate that these processes are

190 results in part from a deficiency of normal pancreatic beta cells, inducing human beta cells to rege

191 ute to the pathogenesis of T1D by increasing pancreatic beta-cell inflammation.

192 , which is co-secreted with insulin from the pancreatic beta-cells, inhibit the activities of insulin

193 at different glucose concentrations in INS-1 pancreatic beta cells (INS-1), which display important c

194 led receptor (GPCR) previously implicated in pancreatic beta cell insulin transcription and glucose-s

195 Pancreatic beta-cell insulin production is orchestrated

196 nger molecule involved in cell signaling and pancreatic beta-cell insulin secretion.

197 Within the pancreatic beta-cells, insulin secretory granules (SGs)

198 The developing pancreatic beta cell is therefore sensitive to thyroid h

199 The pancreatic beta cell is unique in as much as nutrient se

200 Compromised function of insulin-secreting pancreatic beta cells is central to the development and

201 es have indicated that PI3Kgamma activity in pancreatic beta cells is required for normal insulin sec

202 Insulin production by the pancreatic beta-cell is required for normal glucose home

203 Metabolic deceleration in pancreatic beta-cells is associated with inhibition of g

204 Impaired insulin secretion from the pancreatic beta-cells is central in the pathogenesis of

205 Fine-tuning of insulin release from pancreatic beta-cells is essential to maintain blood glu

206 ellular chloride concentration ([Cl(-)]i) in pancreatic beta-cells is kept above electrochemical equi

207 sceptibility locus, but its specific role in pancreatic beta-cells is largely unknown.

208 ation of islet amyloid polypeptide (IAPP) in pancreatic beta cells-is limited.

209 While this EC subpopulation supports pancreatic beta cells, it declines during ageing concomi

210 In pancreatic beta-cells, it helps counter the endoplasmic

211 that hIAPP fibrils are cytotoxic to cultured pancreatic beta-cells, leading us to determine the struc

212 Loss of VPS41 in pancreatic beta-cells leads to a reduction in insulin SG

213 mutations have not been characterized at the pancreatic beta-cell level.

214 y localizes to the Golgi in Min6-K8 cells, a pancreatic beta-cell-like cell line (mouse insulinoma 6

215 s DNA damage response (DDR) signaling in the pancreatic beta-cell line INS 832/13 and rat islets by i

216 d knockdown of gene expression in the murine pancreatic beta-cell line MIN6.

217 to decreased insulin secretion in the murine pancreatic beta-cell line.

218 In pancreatic beta-cells, liver hepatocytes, and cardiomyoc

219 into fibrils and plaques is associated with pancreatic beta-cell loss in type 2 diabetes (T2D).

220 Pancreatic beta-cell loss through apoptosis is an import

221 fetal sheep is associated with reductions in pancreatic beta cell mass and circulating insulin concen

222 by insulin resistance and a gradual loss of pancreatic beta cell mass and function(1,2).

223 nd caused asymmetric organ growth, increased pancreatic beta cell mass and proliferation, and was ass

224 ABSTRACT: Development of pancreatic beta cell mass before birth is essential for

225 The regulation of pancreatic beta cell mass is a critical factor to help m

226 e mediated by insulin and the development of pancreatic beta cell mass is unknown.

227 Type 2 diabetes (T2D) is caused by loss of pancreatic beta-cell mass and failure of the remaining b

228 tance of MANF for the postnatal expansion of pancreatic beta-cell mass and for adult beta-cell mainte

229 Pancreatic beta-cell mass is a critical determinant of t

230 Insulin receptor antagonism increased pancreatic beta-cell mass threefold.

231 ation ( ad libitum) to mice indeed increased pancreatic beta-cell mass, which led to a modest enhance

232 e in target cells followed by a reduction of pancreatic beta-cell mass.

233 ved single-cell RNA-sequencing of T-cell and pancreatic beta cell maturation, we characterize prolife

234 abolite gamma-hydroxybutyric acid (GHB) from pancreatic beta-cells might mediate glucose suppression

235 Constitutive overexpression of ST8Sia6 in pancreatic beta cells mitigated hyperglycemia in the mul

236 In pancreatic beta-cells, mitochondrial bioenergetics contr

237 Pancreatic beta-cells modulate insulin secretion through

238 ells play a major role in the destruction of pancreatic beta cells, molecular underpinnings promoting

239 In pancreatic beta cells, muscarinic cholinergic receptor M

240 is caused by single gene mutations reducing pancreatic beta cell number or impairing beta cell funct

241 onogenic forms of diabetes caused by reduced pancreatic beta-cell number (due to destruction or defec

242 e zebrafish ortholog results in reduction in pancreatic beta-cell number which we demonstrate to be d

243 and Abeta protein deposits were detected in pancreatic beta cells of subjects with AD as well as in

244 ibe the impact of induced Sbp2 deficiency in pancreatic beta-cells on selenoprotein transcript profil

245 Isolated CD1 mouse islets, INS-1 pancreatic beta-cells, or C2C12 mouse myotubes were incu

246 of glucose uptake by skeletal muscle, and of pancreatic beta-cell phenotype in mice.

247 lcholine (ACh) receptors (M3Rs) expressed by pancreatic beta cells play key roles in stimulating insu

248 Pancreatic beta-cells play a pivotal role in maintaining

249 Thus, electrical activity of pancreatic beta cells plays a central role in GSIS.

250 Collectively, TFG in pancreatic beta-cells plays a vital role in maintaining

251 discovered that the normal expansion of the pancreatic beta cell population during early larval deve

252 nsulin-resistant conditions such as obesity, pancreatic beta-cells proliferate to prevent blood gluco

253 Cholic acid feeding resulted in reduced pancreatic beta-cell proliferation and increased apoptos

254 entified DISC1 as a major player controlling pancreatic beta-cell proliferation and insulin secretion

255 uniquely unmethylated in insulin-expressing pancreatic beta-cells, providing a classic example of th

256 Pancreatic beta-cell regeneration, the therapeutic expan

257 program underlying infrequent replication of pancreatic beta-cells remains largely inaccessible.

258 Pancreatic beta-cell replacement by islet transplantatio

259 t induction of Myc is required for increased pancreatic beta-cell replication and expansion during me

260 ilure of proinsulin-to-insulin processing in pancreatic beta-cells, resulting in hyperproinsulinemia.

261 e showed that DUT silencing in human and rat pancreatic beta-cells results in apoptosis via the intri

262 intracellular domain of DLL1 in adult murine pancreatic beta-cells results in impaired glucose tolera

263 s study explored the role of irisin as a new pancreatic beta-cell secretagogue and survival factor an

264 rated that mice lacking Barr2 selectively in pancreatic beta-cells showed pronounced metabolic impair

265 found that CREB stimulates the expression of pancreatic beta cell-specific genes by targeting CBP/p30

266 Pancreatic beta cells store insulin within secretory gra

267 f CDK1 directly reduces its transcription in pancreatic beta-cells, supporting the idea that DNA meth

268 fficking of K(ATP) and Kv2.1 channels to the pancreatic beta-cell surface, resulting in membrane hype

269 The pathways regulating pancreatic beta cell survival in diabetes are poorly und

270 ber of the transcriptional network governing pancreatic beta-cell survival during stress.

271 g regulators of peptidergic secretion within pancreatic beta cells that are perturbed in Clock (-/-)

272 s the activation of this proapoptotic UPR in pancreatic beta-cells that has been implicated in the on

273 R fetus produce developmental adaptations in pancreatic beta-cells that impair fetal insulin secretio

274 ferentiation of human stem cells can produce pancreatic beta-cells; the loss of this insulin-secretin

275 mpensated by increased insulin production of pancreatic beta-cells, thereby maintaining normoglycemia

276 -associated locus involved in maintenance of pancreatic beta cells through a fine-tuned regulation of

277 atopoietic stem cells, and insulin-releasing pancreatic beta cells through a signaling pathway involv

278 Replacement of pancreatic beta-cells through deceased donor islet trans

279 is regulated by calcium (Ca(2+) ) entry into pancreatic beta-cells through voltage-dependent Ca(2+) (

280 s process in fine-tuning GLP-1R responses in pancreatic beta cells to control insulin secretion.

281 Chronic exposure of pancreatic beta cells to high concentrations of free fat

282 is secreted in conjunction with insulin from pancreatic beta cells to regulate glucose metabolism.

283 elivery of insulin mimicking the function of pancreatic beta-cells to achieve meticulous control of b

284 T-1 cells to mimic the long-term exposure of pancreatic beta-cells to kisspeptin during type 2 diabet

285 eptor 1 (SUR1) regulate insulin secretion in pancreatic beta-cells to maintain glucose homeostasis.

286 a global disease caused by the inability of pancreatic beta-cells to secrete adequate insulin.

287 problem caused primarily by the inability of pancreatic beta-cells to secrete adequate levels of insu

288 Although treatment with the pancreatic beta-cell toxin streptozotocin induced hyperg

289 The pancreatic beta-cell transcriptome is highly sensitive t

290 he communication between skeletal muscle and pancreatic beta-cells under lipotoxic conditions.

291 and dopamine, in insulin storage granules in pancreatic beta-cells, we probed by molecular dynamics (

292 Alterations in miR-216a expression within pancreatic beta cells were also examined using in situ h

293 at the BDNF receptor TrkB.T1 is expressed by pancreatic beta-cells where it regulates insulin release

294 T1D results from autoimmune destruction of pancreatic beta cells, whereas beta cell failure in T2D

295 inase 7 receptor expressed on adipocytes and pancreatic beta-cells), which independently associated w

296 onditions trigger adverse responses from the pancreatic beta cell, which is responsible for producing

297 ssential regulator of insulin secretion from pancreatic beta cells, which is central to blood-sugar h

298 endotoxemia upregulates miR-155-5p in murine pancreatic beta-cells, which improved glucose metabolism

299 overexpression promotes insulin secretion in pancreatic beta cells, while C193S-hSCGN inhibits it.

300 played robust Cre expression and activity in pancreatic beta cells without significant alterations in