ライフサイエンスコーパス: beta cell

1 he liver, vasculature, heart, and pancreatic beta-cells).

2 ulate insulin secretion from the neighboring beta-cell.

3 omoted GSIS by inhibiting RGS4 in pancreatic beta cells.

4 the prostaglandin EP3 receptor in pancreatic beta cells.

5 the insulin secretory granules of pancreatic beta cells.

6 es that antagonize IFNalpha effects on human beta cells.

7 destruction of insulin producing pancreatic beta cells.

8 roducing cells following genetic ablation of beta cells.

9 in dysfunctional type 2 diabetic (T2D) human beta cells.

10 through which YIPF5 loss of function affects beta cells.

11 network in response to glucose in pancreatic beta cells.

12 function of granule age in pancreatic islet beta cells.

13 p2 loss causes functional iron deficiency in beta cells.

14 important characteristics of the pancreatic beta cells.

15 racterized by progressive loss of pancreatic beta cells.

16 9 human insulinomas, and five sets of normal beta cells.

17 SMAD7 was either absent or overexpressed in beta cells.

18 ced L-type Ca(V) currents in mouse and human beta-cells.

19 xpressed in both human and rodent pancreatic beta-cells.

20 ological conditions, including in pancreatic beta-cells.

21 d therapeutic strategy augmenting functional beta-cells.

22 ells mistakenly destroy healthy ('innocent') beta-cells.

23 abetogenicity of tacrolimus in primary human beta-cells.

24 baboon amylin fibers, are toxic to cultured beta-cells.

25 this finding has not been verified in human beta-cells.

26 g that ATGL is the principal lipase in human beta-cells.

27 ll pancreatic lineages, including functional beta-cells.

28 that Slit functions as a repellent signal to beta-cells.

29 ized insulin is preferentially secreted from beta-cells.

30 is able to proliferate both rodent and human beta-cells.

31 ascular permeability and glucose delivery to beta-cells.

32 e enhanced by increasing serotonin levels in beta-cells.

33 mouse beta-cells, LDs are prominent in human beta-cells.

34 s an autoimmune disease of insulin-producing beta-cells.

35 indicate that GLP-1R is widely expressed in beta-cells, absent in alpha-cells, and expressed at the

36 is suggests that 1,5-(PP)(2)-InsP(4) impacts beta-cell activity by regulating granule localization an

37 lure acting as a growth factor necessary for beta-cell adaptation to higher metabolic load.

38 We show that nitric oxide protects beta-cells against virally mediated lysis by limiting EM

39 hibitor nanodrug suppressed proliferation of beta cells and increased the expression of PTEN, a miR-2

40 ibition enhances IGF-1 and HGF signalling in beta cells and increases expression of the growth factor

41 Kindlin-2 loss reduces the percentage of beta-cells and concomitantly increases that of alpha-cel

42 portant for determining the ultimate fate of beta-cells and hence progression of type 1 diabetes (T1D

43 beta-cells point to a direct effect of AG on beta-cells and not, as earlier suggested, to an exclusiv

44 The antigenic peptides processed by beta-cells and presented through surface HLA class I mol

45 ma that the rodent islet has a mantle of non-beta-cells and that the islet is completely separated fr

46 9-hydroxystearic acids were able to suppress beta-cell apoptosis induced by proinflammatory cytokines

47 ucose-stimulated insulin secretion (GSIS) in beta cells are the proximity of insulin granules to the

48 d GLP-1R antibody indicated that >90% of the beta-cells are GLP-1R positive, contradicting the findin

49 By their nature and function, beta-cells are prone to biosynthetic stress with limited

50 ing mechanism enriches the inactive cargo in beta-cells as compared to other pancreatic cells; import

51 Insulin is first produced in pancreatic beta-cells as the precursor prohormone proinsulin.

52 Autoimmunity against pancreatic beta-cell autoantigens is a characteristic of childhood

53 a suggest the critical function of TBK1 as a beta-cell autonomous replication barrier and present PIA

54 ha(z)-null mice from HFD-induced diabetes is beta-cell autonomous, as beta cell-specific Galpha(z)-nu

55 as associated with increased accumulation of beta-cell autoreactive T cells in the spleen and pancrea

56 Notably, disrupting YIPF5 in beta cell-based models induced ER stress signaling and r

57 Pancreatic beta-cells become irreversibly damaged by long-term expo

58 lls cultured >=96 hours did not contain more beta cells but a higher endocrine purity (49% versus 36%

59 ly activate the immune system and can damage beta cells by either directly infecting them or stimulat

60 es from the destruction of insulin-producing beta-cells by islet-specific autoreactive T cells.

61 ic hyperglycemia, highly selectively killing beta-cells by receptor-targeted photodynamic therapy (rt

62 Therefore, beta-cell Ca(2+) handling is tightly controlled.

63 In beta cells, Ca(2+), cyclic adenosine monophosphate (cAMP

64 Studies show that beta-cell circadian clocks are important regulators of G

65 s produced from human embryonic cell-derived beta-cell clusters.

66 The molecular mechanisms of beta-cell compensation to metabolic stress are poorly un

67 effort has focused on generating pancreatic beta cells, considerable evidence indicates that glucago

68 <15 um diameter were identified in 5%-12% of beta cell containing aggregates, 3-76 months posttranspl

69 ssed the roles of the DA precursor L-DOPA in beta-cell DA synthesis and release in conjunction with t

70 effects of metabolic stress predominate and beta cell death or dysfunction occurs.

71 ycemia, diabetes incidence, hypoinsulinemia, beta-cell death, and loss of beta-cell mass observed in

72 (IAPP) is linked to pancreatic inflammation, beta-cell degeneration, and the pathogenesis of type 2 d

73 However, the role of beta-cell-derived exosomes in metabolic homeostasis is p

74 edict type 1 diabetes (T1D) but do not cause beta cell destruction.

75 y contribute to the initiation of pancreatic beta-cell destruction during the development of autoimmu

76 opes implicated in CD8 T cell (CTL)-mediated beta-cell destruction in type 1 diabetes (T1D).

77 Autoimmune beta-cell destruction leads to type 1 diabetes, but the

78 pha/miR-17 pathway as a central component in beta-cell destruction processes and as a potential targe

79 ice with a deletion of VPS41 specifically in beta-cells develop diabetes due to severe depletion of i

80 gies, we dissect the contribution of MAFB to beta-cell development and function specifically in human

81 ent human models that are used to study both beta-cell development and function, including EndoC-beta

82 SC-beta cells differentiated from four hPSC lines exhibited

83 timulate insulin secretion by the pancreatic beta-cells, direct evidence of CCK promoting insulin rel

84 hat mice lacking both DLL1 and DLL4 in adult beta-cells display improved glucose tolerance, increased

85 e preparations in order to reach the desired beta-cell dose and therefore result in a better metaboli

86 F levels were upregulated in mouse and human beta cells during metabolic stress-induced compensation

87 ied free fatty acids, the major fuel used by beta-cells during fasting.

88 es the range of evidence implicating HIFs in beta cell dysfunction, diabetes pathogenesis, and diabet

89 s, a process which contributes to pancreatic beta-cell dysfunction and death.

90 These mechanisms differentially affect early beta-cell dysfunction and eventual fate.

91 beta-Cell dysfunction and reduction in beta-cell mass ar

92 control Ca(2+) handling and how they impact beta-cell dysfunction in type 2 diabetes.

93 cts human beta-cells from tacrolimus-induced beta-cell dysfunction in vitro.

94 beta-Cell dysfunction is a common contributor to the pat

95 in beta-cells will confer protection against beta-cell dysfunction under diabetogenic conditions.

96 th subsequent adiposity, insulin resistance, beta-cell dysfunction, and metabolic syndrome, leading t

97 e to the nutrient surplus ensues, leading to beta-cell dysfunction, dedifferentiation, and apoptosis.

98 onic lipid exposure is associated with islet beta-cell dysfunction, we investigated LD accumulation i

99 ication in beta-cells lacking Furin, causing beta-cell dysfunction.

100 w that SG population age is modulated by the beta-cell environment in vivo in the db/db mouse islets

101 ranule aging is affected by variation in the beta-cell environment, such as hyperglycemia.

102 on, vesicular trafficking, and regulation of beta-cell epigenetic and transcriptional program.

103 EC-specific ablation of Gja1 restores beta-cell expansion in the aged pancreas.

104 Further, angiogenesis and beta-cell expansion in the pancreas are coupled by a dis

105 Here we show that beta-cells express abundant Kindlin-2 and deleting its e

106 Insulin-secreting pancreatic beta-cells express the machinery for DA synthesis and ca

107 Consequently, tau knockdown in mouse islet beta-cells facilitates microtubule turnover, causing inc

108 ic targets to be exploited in the context of beta cell failure in diabetes in the near future.

109 omotes beta-cell function in mouse models of beta-cell failure acting as a growth factor necessary fo

110 nd a combination of these processes leads to beta-cell failure and severe hyperglycemia.

111 iculum stress signalling that contributes to beta-cell failure in T1DM (mostly IRE1 driven) and T2DM

112 Understanding the mechanisms behind beta-cell failure is critical to prevent or revert disea

113 induces loss of human beta-cell maturity and beta-cell failure through activation of the BMP/SMAD sig

114 tabolic stress, may contribute to pancreatic beta-cell failure.

115 In persistently depolarized beta cells from KATP channel knockout (KO) mice, the res

116 (NOD) mice, protecting the insulin-producing beta-cells from destruction.

117 ow-molecular-weight compounds that protected beta-cells from GLT, we identified compound A that selec

118 advances have been made in producing mature beta-cells from human pluripotent stem cells that respon

119 l inhibition of BMP signaling protects human beta-cells from tacrolimus-induced beta-cell dysfunction

120 improved insulin sensitivity (P = 0.03) and beta cell function (P = 0.01).

121 ing pancreatic beta cell number or impairing beta cell function.

122 signaling targets involved in the control of beta cell function.

123 therapies for the long-term preservation of beta cell function.

124 to measure BCM, routine clinical measures of beta-cell function (e.g., C-peptide release) may not ref

125 on, individually and together, impaired both beta-cell function and identity by reducing expression o

126 199 (miR-199) negatively impacts pancreatic beta-cell function and its expression is highly increase

127 n beta-cells may preserve beta-cell mass and beta-cell function and protect against diabetes.

128 We analyzed beta-cell function in adult islets when SMAD7 was either

129 s improves metabolic parameters and promotes beta-cell function in mouse models of beta-cell failure

130 receptor; however, its impact on pancreatic beta-cell function is unknown.

131 eases absolute insulin secretion but impairs beta-cell function, 2) causes insulin resistance, and 3)

132 asting glucose, insulin, insulin resistance, beta-cell function, and adiponectin at age 11.5 years.

133 in the regulation of metabolism, pancreatic beta-cell function, energy homeostasis, mood and behavio

134 gical biomarkers, anthropometry, measures of beta-cell function, insulin sensitivity, and lifestyle)

135 he joint association of 25(OH)D and PTH with beta-cell function, systemic inflammation, and kidney fu

136 ch is also produced in the pancreas, affects beta-cell function, with particular attention to the rol

137 ed similar levels of insulin sensitivity and beta-cell function.

138 nal factor eIF4G1 on glucose homeostasis and beta-cell function.

139 disease duration, in parallel with declining beta-cell function.

140 lycemia associated with continued decline in beta-cell function.

141 ypoinsulinemia, and deteriorating pancreatic beta-cell function.

142 nit (Galpha(z)) is an important modulator of beta-cell function.

143 ulation of key transcription factors ensures beta-cell function.

144 with type 1 and type 2 diabetes with reduced beta-cell function.

145 ondrial genetic variation is associated with beta-cell functions and incident DM in non-Hispanic, Bla

146 nclude studies of islet morphology and human beta-cell gene expression in T1DM and T2DM, the identifi

147 through desensitization or downregulation of beta-cell GIP receptors (GIP-R).

148 ine alpha to beta-cell signaling through the beta-cell GLP-1 receptor.

149 rous female mice had significantly decreased beta-cell Glp1r expression, but no reduction in GLP-1R p

150 -type Ca(V) channels is a key determinant of beta-cell glucose-stimulated Ca(2+) entry and thus the s

151 Furthermore, Rab7a inhibition promotes beta cell growth and islet survival, and protects agains

152 egenerative medicine approaches to enhancing beta cell growth and survival represent potential treatm

153 ctors such as insulin, IGF-1 and HGF support beta cell growth and survival, but in people with type 2

154 ial of the GLP-1/GLP-1R system in pancreatic beta cells has led to the development of established GLP

155 ment of diabetes, specifically in pancreatic beta-cells, has not been elucidated yet.

156 ctional fat, transgenic mice display massive beta-cell hyperplasia, reflecting a beneficial mitochond

157 Active maintenance of beta-cell identity through fine-tuned regulation of key

158 her found selective loss of islet-associated beta cells in dogs with sDM and sDMPanc, suggesting that

159 P (cAMP) levels and reduced proliferation of beta-cells in a manner dependent on the activity of cAMP

160 ra- or peri-nuclearly localized primarily in beta-cells in experimental mice and also in human post-m

161 ion is restricted to embryonic and neo-natal beta-cells in mice.

162 lt from destruction of the insulin-producing beta-cells in pancreatic islets that is mediated by auto

163 tigate if SKAP2 has a functional role in the beta-cells in relation to T1D.

164 portunities to use therapies that revitalize beta-cells, in combination with immune intervention stra

165 rrent research on the GLP-1/GLP-1R system in beta cells, including the regulation of signaling by end

166 ng proteins control an array of processes in beta-cells, including the synthesis and secretion of ins

167 Loss of SMAD7 in beta cells inhibited proliferation, and SMAD7 overexpres

168 t glucose concentrations in INS-1 pancreatic beta cells (INS-1), which display important characterist

169 novel function of the Delta/Notch pathway in beta-cell insulin secretion.

170 Within the pancreatic beta-cells, insulin secretory granules (SGs) exist in fu

171 E4(x12)-Cy7 and optoacoustically visualized beta-cell insulinoma xenografts in vivo for the first ti

172 s of Langerhans, depleting insulin-secreting beta-cells (insulitis).

173 rate that primary cilia not only orchestrate beta-cell-intrinsic activity but also mediate cross talk

174 In this review, we focus on the beta-cell ion channels that control Ca(2+) handling and

175 We propose an alternative view in which the beta-cell is the key contributor to the disease.

176 slet-specific autoreactive T cells to rescue beta-cells is a promising approach to treat new-onset T1

177 ne-tuning of insulin release from pancreatic beta-cells is essential to maintain blood glucose homeos

178 y locus, but its specific role in pancreatic beta-cells is largely unknown.

179 ude that whereas electrical coupling between beta-cells is sufficient for the propagation of excitati

180 The loss of insulin-producing beta-cells is the central pathological event in type 1 a

181 strongly suggest that TSPAN-7 modulation of beta-cell L-type Ca(V) channels is a key determinant of

182 tion and impaired lysosomal acidification in beta-cells lacking Furin, causing beta-cell dysfunction.

183 Distinct from mouse beta-cells, LDs are prominent in human beta-cells.

184 role of T1DM and T2DM candidate genes at the beta-cell level and the endoplasmic reticulum stress sig

185 platform, we successfully engineer INS-1E, a beta-cell line, to repurpose the insulin secretion machi

186 ll development and function, including EndoC-beta cell lines and human induced pluripotent stem cell-

187 ecent years the emergence of authentic human beta-cell lines, and advances in genome-editing technolo

188 are perturbed in Clock (-/-) and Bmal1 (-/-) beta-cell lines.

189 xidative metabolism attenuates EMCV-mediated beta-cell lysis by inhibiting viral replication.

190 ors may be a useful strategy to expand adult beta cell mass.

191 has proven to be a powerful tool to quantify beta-cell mass (BCM) in vivo.

192 n characterized by a complete destruction of beta-cell mass (BCM); however, there is growing evidence

193 n-induced diabetes and presented a preserved beta-cell mass and a reduction in islet inflammation.

194 tained VDR levels in beta-cells may preserve beta-cell mass and beta-cell function and protect agains

195 Reduction of beta-cell mass and function is central to the pathogenes

196 beta-Cell dysfunction and reduction in beta-cell mass are hallmark events of diabetes mellitus.

197 rial function, adipose tissue integrity, and beta-cell mass during obesity is a major challenge.

198 mitochondrial dysfunction has on increasing beta-cell mass during obesity-related insulin resistance

199 Human islet isolates with insufficient beta-cell mass for implantation within 72 hours can be c

200 se, a beta-cell mitogen and key regulator of beta-cell mass in response to increased insulin demand.

201 er in extending our knowledge on the role of beta-cell mass in the pathophysiology of type 1 and type

202 Loss of functional beta-cell mass is the key mechanism leading to the two m

203 ypoinsulinemia, beta-cell death, and loss of beta-cell mass observed in Ak littermates.

204 lts from combinatorial defects in functional beta-cell mass plus peripheral glucose uptake.

205 beta-cell mass was normal under steady state and under m

206 beta-Cell mass was normal under steady state and under m

207 utoimmune-mediated destruction of functional beta-cell mass, whereas T2D results from combinatorial d

208 ts on novel strategies to protect functional beta-cell mass.

209 tification of tracer uptake as a measure for beta-cell mass.

210 e show that tacrolimus induces loss of human beta-cell maturity and beta-cell failure through activat

211 results suggest that sustained VDR levels in beta-cells may preserve beta-cell mass and beta-cell fun

212 asis of this disorder highlights fundamental beta-cell mechanisms.

213 ta-cell proliferative response to glucose, a beta-cell mitogen and key regulator of beta-cell mass in

214 We used 3 human beta cell models (YIPF5 silencing in EndoC-betaH1 cells,

215 The cause of this selective loss of beta cells needs to be further elucidated but overall, o

216 equipped "hub" or "leader" cells within the beta-cell network drive islet oscillations and that elec

217 by single gene mutations reducing pancreatic beta cell number or impairing beta cell function.

218 ansgenic expression of placental lactogen in beta-cells of Ak mice drastically reduces the severe hyp

219 eases in both proliferation and apoptosis in beta-cells of betaeIF4G1KO.

220 increases in proliferation and apoptosis in beta-cells of betaeIF4G1KO.

221 act of induced Sbp2 deficiency in pancreatic beta-cells on selenoprotein transcript profiles in the p

222 ings, focusing on studies performed on human beta-cells or on samples obtained from patients with dia

223 lective release of small-molecule cargoes in beta-cells over other islet cells ex vivo or other cell-

224 ice presented the same metabolic profile and beta-cell phenotype as the control mice with an intact A

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

226 The experiments with SUR1-KO beta-cells point to a direct effect of AG on beta-cells

227 litus, the path toward endogenous renewal of beta-cell populations has remained elusive.

228 ption Factor B (MAFB) to be present in human beta-cells postnatally, while its expression is restrict

229 The case here is the pancreatic islet beta-cell presented with excessive levels of nutrients s

230 ugh there is substantial evidence that mouse beta-cells process proinsulin using prohormone convertas

231 ducible nitric oxide synthase expression and beta-cell production of nitric oxide.

232 ified one candidate (miR-216a) implicated in beta cell proliferation for subsequent validation by RT-

233 with downregulation of PTEN and increase in beta cell proliferation in that group.

234 critical regulators of insulin secretion and beta cell proliferation.

235 showed excellent DYRK1A inhibition and human beta-cell proliferation capability.

236 re, knockdown of HB-EGF in rat islets blocks beta-cell proliferation in response to glucose ex vivo a

237 to efforts to identify molecules to promote beta-cell proliferation, protection, and imaging.

238 ecreasing food intake and promoting adaptive beta-cell proliferation.

239 a crucial role in pregnancy-induced maternal beta-cell proliferation.

240 nding EGF-like growth factor (HB-EGF) in the beta-cell proliferative response to glucose, a beta-cell

241 ar mechanisms underlying stress responses in beta-cells promises to reveal new therapeutic opportunit

242 cium influx in islet cells, and all measured beta-cell-protective effects correlated with this activi

243 or "roadmap" for pathways that control human beta cell regeneration.

244 epsilon (IKKepsilon) have shown to stimulate beta-cell regeneration in multiple species.

245 thusiasm for Myc as a therapeutic target for beta-cell regeneration.

246 of Myc could have therapeutic potential for beta-cell regeneration.

247 y reveals the role of Wisp1 as an inducer of beta cell replication, supporting the idea that the use

248 We previously reported that beta-cell replication is strongly increased in a subgrou

249 gentle" induction of Myc expression enhances beta-cell replication without induction of cell death or

250 mine whether nitric oxide contributes to the beta-cell response to viral infection.

251 Sex had an impact on all beta-cell responses, with male animals exhibiting greate

252 ndicate that in adults with type 1 diabetes, beta cell responsiveness to hyperglycemia and alpha cell

253 Genetic activation of beta-catenin in beta-cells restores the diabetes-like phenotypes induced

254 key components of the secretory machinery of beta-cells, resulting in impaired glucose- or KCl-induce

255 duction of mature glucagon from proglucagon, beta-cells retained the ability to produce mature insuli

256 In a beta-cell selective manner, these findings indicate that

257 ical and immunological methods, we show that beta cells selectively respond to intracellular dsRNA by

258 ion, our results suggest that SKAP2 controls beta-cell sensitivity to cytokines possibly by affecting

259 Metabolic stress reduces beta-cell sensitivity to GLP-1, yet the underlying mecha

260 tes whether this interaction is relevant for beta cell signaling and plays a role for negative effect

261 uman islets, suggesting a paracrine alpha to beta-cell signaling through the beta-cell GLP-1 receptor

262 GPRC6A's unique regulation of beta-cell, skeletal muscle and hepatic function may repr

263 The pool of beta cell-specific CD8(+) T cells in type 1 diabetes (T1

264 induced diabetes is beta-cell autonomous, as beta cell-specific Galpha(z)-null mice phenocopy the ful

265 IS phase was absent from PIs from NOX4-null, beta-cell-specific knockout mice (NOX4betaKO) (though no

266 beta-Cell stress provokes an immune attack that has cons

267 7a inhibition may provide a means to promote beta cell survival in the context of metabolic stress an

268 tor trafficking can be used to promote islet beta cell survival.

269 um overload in pancreatic islets can improve beta-cell survival and function under GLT stress and thu

270 s of peptidergic secretion within pancreatic beta cells that are perturbed in Clock (-/-) and Bmal1 (

271 Here, we show in human beta-cells that ER stress regulates ERAP1 gene expressio

272 d by calcium (Ca(2+) ) entry into pancreatic beta-cells through voltage-dependent Ca(2+) (Ca(V) ) cha

273 division and (trans-)differentiation of non-beta cells to produce insulin.

274 HC class I, may expand antigens presented by beta cells to the immune system.

275 lasmic reticulum (ER) stress and potentiated beta cells to undergo apoptosis.

276 tory from their generation and exocytosis in beta cells to uptake and presentation in islets and peri

277 Excitotoxicity caused beta-cells to be more susceptible to HFD-induced impairm

278 Generating beta-cells to mitigate the aberrant glucose homeostasis

279 lecular mechanisms underlying the failure of beta-cells to respond to glucose in T2D remains unknown.

280 isease caused by the inability of pancreatic beta-cells to secrete adequate insulin.

281 TBK1 overexpression decreased sensitivity of beta-cells to the elevation of cyclic AMP (cAMP) levels

282 of ER stress in the increased visibility of beta-cells to the immune system and position the IRE1alp

283 ssociated with reduced expression of the key beta-cell transcription factor MAFA and abolished insuli

284 Encapsulated beta cell transplantation offers a potential cure for a

285 Beta cells treated with TM also exhibited concomitant al

286 ted mouse and human islets and find that the beta cell trophic effect of Wisp1 is dependent on Akt si

287 ign, slowly proliferating, insulin-producing beta cell tumors that provide a molecular "recipe" or "r

288 ion to mouse and human pancreatic alpha- and beta-cells using 3-D confocal and immunofluorescence mic

289 focuses on the current status of generating beta-cells via these diverse routes, highlighting the un

290 us description of the HLA-A2/A3 peptidome of beta-cells, we analyzed the HLA-A3-restricted peptides t

291 hemogenetic and pharmacologic stimulation of beta-cells were blocked by a 5-HT(3)R antagonist and wer

292 Glucose-responsive INS-1 beta-cells were incubated with increasing concentrations

293 ition, transgenic mice overexpressing VDR in beta-cells were protected against streptozotocin-induced

294 DLL1 and DLL4 are specifically expressed in beta-cells, whereas JAGGED1 is expressed in alpha-cells.

295 ng studies have highlighted discrepancies in beta-cells which exist between mice and men.

296 s differ from the activities of cytokines on beta cells, which are mediated by inducible nitric oxide

297 hether enhancement of the circadian clock in beta-cells will confer protection against beta-cell dysf

298 neral" coregulators Sin3a and Sin3b in islet beta-cells, with Sin3a being dispensable for differentia

299 mmune disease in which the insulin-producing beta cells within the pancreas are destroyed.

300 The coordinated electrical activity of beta-cells within the pancreatic islet drives oscillator