ライフサイエンスコーパス: UCP2

1 encoding mitochondrial uncoupling protein 2 (UCP2).

2 ncreased expression of uncoupling protein 2 (UCP2).

3 that are dependent on uncoupling protein 2 (UCP2).

4 ia upregulation of the uncoupling protein 2 (UCP2).

5 ion of oxidative/thermogenic genes (CPT1 and UCP2).

6 ) under the control of uncoupling protein 2 (UCP2).

7 els of the mitochondrial uncoupling protein (UCP2).

8 ation of mitochondrial uncoupling protein 2 (UCP2).

9 MR method for structural characterization of UCP2.

10 ) and human leukemic LAD2 mast cells express UCP2.

11 CPT1 and free radicals that are scavenged by UCP2.

12 nd ER stress by regulating the expression of UCP2.

13 al superoxide production or gene knockout of UCP2.

14 act cell phenotype via dynamic regulation of UCP2.

15 ), 10 muM) amplified GSIS and also activated UCP2.

16 The novel uncoupling proteins (UCP2-5) are implicated in the mitochondrial control of o

17 genetic variants tested, TRPV1 Val585Ile and UCP2 -866 G/A correlated significantly with change in ab

18 The impact of the UCP2 -866G>A and UCP3 -55C>T variants on prospective ris

19 tocytes highly express uncoupling protein-2 (UCP2), a mitochondrial carrier that competes with adenos

20 release, ROS activates uncoupling protein-2 (UCP2), a mitochondrial inner membrane protein that negat

21 POMC neurons involves uncoupling protein 2 (UCP2), a mitochondrial protein that impairs glucose-stim

22 cells to be linked to uncoupling protein-2 (UCP2), a mitochondrial suppressor of reactive oxygen spe

23 a-myosin heavy chain), uncoupling protein 2 (UCP2), a protein involved in the control of mitochondria

24 ss in fatty liver and limiting the impact of UCP2 ablation.

25 In conclusion, whereas UCP2 abundance in fatty hepatocytes exacerbates Fas-medi

26 It has been suggested that UCP2 also plays a role in beta cell apoptosis, but these

27 eration is affected by uncoupling protein-2 (UCP2), an inner mitochondrial membrane carrier that sens

28 ndocrine regulation of uncoupling protein-2 (UCP2), an inner mitochondrial protein, in fetal adipose

29 UCP2, an inner membrane mitochondrial protein, has been

30 However, the physiological contributions of UCP2 and ERBB2 at the low expression levels that are typ

31 UCP2 and FHL1 are important candidate genes that correla

32 1AR, beta2AR, or protein kinase A, increased UCP2 and FHL1 expression was also observed at the onset

33 y and suppressed the increased expression of UCP2 and FHL1 in mice overexpressing Gsalpha.

34 t restriction has long-term consequences for UCP2 and GR mRNA abundance in the lung irrespective of i

35 UCP2 and GR mRNA abundance were significantly lower in A

36 In contrast, knockdown of UCP2 and LETM1 exclusively reduced mitochondrial Ca(2+)

37 non-overexpressed ERBB2 transiently removes UCP2 and paradoxically reduces the mitochondrial membran

38 the FABP inhibitor HTS01037 also upregulated UCP2 and reduced expression of BiP, CHOP, and XBP-1s.

39 y, which mediates STC1-induced expression of UCP2 and sirtuin 3 and protection from I/R.

40 vation of AMPK, diminished the expression of UCP2 and sirtuin 3, and aggravated kidney injury but did

41 tivated AMPK and increased the expression of UCP2 and sirtuin 3, and concomitant treatment with compo

42 ondria through the uncoupling proteins UCP1, UCP2 and UCP3 and the adenine nucleotide translocase (AN

43 Functional promoter variants UCP2 and UCP3 increase the prospective risk of diabetes.

44 s were associated with increased PGC-1alpha, UCP2 and UCP3 mRNA and decreased reactive oxygen species

45 Apoptosis rates in UCP2(+/+) and UCP2(- /-) liver remnants were similar, wh

46 d oxidation (Cpt1alpha, Pparalpha, Acox, and Ucp2) and incorporation into lipids (Gpat and CD36).

47 inhibition were 50 microm (UCP1), 70 microm (UCP2), and 120 microm (UCP3) at pH 7.2.

48 a(2+) uniporter (MCU), uncoupling protein 2 (UCP2), and leucine zipper EF-hand-containing transmembra

49 ed AMPK activity and the expression of STC1, UCP2, and sirtuin 3.

50 ADRB3, FTO, GNB3, INSIG2, LEPR, PPARG, TNF, UCP2, and UCP3) that had been previously reported to be

51 UCP2-deficient ob/ob mice (ob/ob:ucp2-/-) and UCP2-competent littermates (ob/ob:ucp2+/+)

52 te that mitochondrial membrane potential and Ucp2 are key molecular determinants of apoptotic cell cl

53 tf3) and mitochondrial uncoupling protein-2 (Ucp2) are highly induced in Tsc2-deficient neurons, as w

54 These results identify UCP2 as a potential therapeutic target in inflammatory d

55 O, LEP, PPARG, PPARGC1A, SLC2A2, TCF7L2, and UCP2) associated with type 2 diabetes or obesity.

56 Thus, overexpression of UCP2 attenuates ROS generation and prevents mitochondria

57 gical and pathological functions ascribed to UCP2 based on its purported uncoupling properties.

58 cture of isoform 2 of an uncoupling protein (UCP2) binding an inhibitor recently obtained in dodecylp

59 Ucp2(-/-) BMMCs also had elevated histamine content and

60 Furthermore, Ucp2(-/-) BMMCs also had greater production of both IL-6

61 to better understand the role of myocardial UCP2 by examining the effects of UCP2 on bioenergetics,

62 Uncoupling protein 2 (UCP2), by virtue of its mitochondrial proton leak activi

63 Our results suggest that UCP2 can regulate mast cell activation.

64 UCP2 can regulate oxidative stress and/or energetic meta

65 ed ERBB2 signals constitutively and elevated UCP2 can uncouple mitochondria and alleviate oxidative s

66 Adenoviral-mediated expression of UCP2 caused a mild depression of DeltaPsi(m) and increas

67 00 nM) stimulated apoptosis in 3T3-L1 and L1-UCP2 cells (P<0.05).

68 10 nM) restored mitochondrial Deltapsi in LI-UCP2 cells and protected against UCP2 overexpression-ind

69 Ca2+ dose-dependently in both 3T3-L1 and L1-UCP2 cells.

70 itochrondrially derived reactive oxygen from Ucp2-/- cells constitutively activates NF-kappa B, resul

71 Isolated mitochondria from Ucp2-/- cells produced more superoxide/hydrogen peroxide

72 UCP2 closely resembles the bovine ADP/ATP carrier (the o

73 CP2-deficient ob/ob mice (ob/ob:ucp2-/-) and UCP2-competent littermates (ob/ob:ucp2+/+) received a si

74 ndicate that the glutathionylation status of UCP2 contributes to the regulation of GSIS, and differen

75 Together, these data demonstrate that UCP2 controls pancreas development through the ROS-AKT s

76 We hypothesized that UCP2 could also regulate mast cell activation.

77 Therefore, superoxide-mediated activation of UCP2 could play an important role in the pathogenesis of

78 Overexpression of UCP2 decreased reactive oxygen species (ROS) production,

79 pro-oxidant Paraquat reversed the effect of UCP2 deficiency on cell proliferation in in vitro differ

80 We hypothesized that UCP2 deficiency reduces Ca(2)(+)m in pulmonary artery sm

81 iver both in vitro and in vivo revealed that UCP2 deficiency results in a significant decrease in cel

82 In macrophages, UCP2 deficiency suppressed NLRP3-mediated caspase-1 acti

83 lthough heme synthesis was not influenced by UCP2 deficiency, mice lacking UCP2 had a delayed recover

84 groups, but the increase was not affected by UCP2 deficiency.

85 In UCP2-deficient macrophages, inhibition of lipid synthesi

86 Consistently, UCP2-deficient mice displayed impaired lipid synthesis a

87 UCP2-deficient mice displayed improved survival in a mou

88 were impaired in phagocytosis in vitro, and Ucp2-deficient mice showed profound in vivo defects in c

89 Macrophages from Ucp2-deficient mice were impaired in phagocytosis in vit

90 nto heme was unaltered in reticulocytes from UCP2-deficient mice.

91 UCP2-deficient ob/ob mice (ob/ob:ucp2-/-) and UCP2-compe

92 UCP2-deleted alpha-cells have higher levels of intracell

93 Therefore, alpha-cell UCP2 deletion perturbs the fasting/hypoglycemic glucagon

94 The effects of UCP2 deletion were mimicked by the UCP2 inhibitor genipi

95 ndrial redox state via uncoupling protein 2 (UCP2)-dependent alterations in mitochondrial respiration

96 The UCP2-dependent action of ghrelin on NPY/AgRP neurons is

97 igrostriatal dopamine function by activating UCP2-dependent mitochondrial mechanisms.

98 ased mitochondrial protein carbonylation and UCP2-dependent reduction in intracellular reactive oxyge

99 evidence about UCP2 function, we found that UCP2 did not function in this setting as a membrane pote

100 enetic manipulation of uncoupling protein-2 (UCP2) directly affects substantia nigra dopamine cell fu

101 t fatty hepatocytes may benefit from lack of UCP2 during Jo2 challenge.

102 Although the mechanism of the UCP2 effect is likely to be caused by increased expressi

103 In the absence of UCP2, endothelial growth stimulation provoked mitochondr

104 y the superoxide anion, whereas mice lacking UCP2 exhibited increased ROS relative to wild-type contr

105 Thus, modulation of UCP2 expression and function by dietary fat protects neo

106 UCP2 expression and function were basally increased in n

107 However, evidence for a link between UCP2 expression and susceptibility of liver to acute inj

108 This finding prompted us to determine UCP2 expression in Kupffer cells, a major source of intr

109 tly performed a case-control study to assess UCP2 expression in pancreas from BD donors (cases) and s

110 These results reveal that UCP2 expression is a critical factor, which sensitizes s

111 Analysis in silico indicated increased UCP2 expression is common in highly proliferative cell t

112 ich is supported by our current finding that UCP2 expression is increased in nutrient-deprived murine

113 hibitor genipin largely reversed the effects UCP2 expression on mitochondrial Ca(2+) handling, bioene

114 Ectopic UCP2 expression perturbs this metabolic transition and i

115 Increases in UCP2 expression that lower DeltaPsi(m) and contribute to

116 UCP2 expression was found diminished in Kupffer cells of

117 Although UCP2 expression was higher in fa/fa rats regardless of t

118 Moreover, UCP2 expression was increased in human sepsis.

119 HL60 cells fail to increase UCP2 expression, are not uncoupled after coculture, and

120 atum of the CA1 region and were dependent on UCP2 expression, because in UCP2 knock-out mice such cha

121 +-dependent mechanism and inhibits adipocyte UCP2 expression, indicating that the anti-obesity effect

122 ant R126Q) into FABP4/aP2 null cells reduced UCP2 expression, suggesting that the FABP-FFA equilibriu

123 sting that the FABP-FFA equilibrium controls UCP2 expression.

124 g and inflammasome activation via control of UCP2 expression.

125 e found an increased size of the pancreas in Ucp2(-/-) fetuses at embryonic day 16.5, associated with

126 bolism and offer a novel therapeutic target, UCP2, for the prevention/treatment of Parkinson's diseas

127 results suggest that absent or insufficient UCP2 function in the regenerating liver results in incre

128 al that a mitochondrial mechanism related to UCP2 function is essential for appropriate bioenergetic

129 ythropoiesis and suggests that inhibition of UCP2 function may contribute to the development of anemi

130 In support of recent new evidence about UCP2 function, we found that UCP2 did not function in th

131 UCP2 gene expression was higher in pancreas from BD dono

132 glutathione redox capacity was decreased and UCP2 gene expression was increased in both ASD and Sib c

133 llular glutathione and uncoupling protein 2 (UCP2) gene expressions were quantified.

134 itional programming of uncoupling protein-2 (UCP2), glucocorticoid receptor (GR) and 11beta-hydroxyst

135 ronine (T3) influenced the mRNA abundance of UCP2, glucocorticoid receptor (GR) and 11beta-hydroxyste

136 had no effect on lung weight, but increased UCP2, GR and 11betaHSD1 mRNA abundance at every sampling

137 ncentrations were positively correlated with UCP2, GR and 11betaHSD2 mRNA abundance, but negatively c

138 influenced by UCP2 deficiency, mice lacking UCP2 had a delayed recovery from chemically induced hemo

139 apparent conflict with its uncoupling role, UCP2 has also been proposed to be essential for mitochon

140 These data suggest that UCP2 has an apoptotic effect in beta cells via regulatio

141 Uncoupling protein 2 (UCP2) has been shown to conduct calcium from the ER to m

142 upling protein 2 in hypocretin neurons (Hcrt-UCP2) have elevated hypothalamic temperature.

143 Overexpressing UCP2 in 3T3-L1 cells induced marked reductions in mitoch

144 erosclerosis, this newly discovered role for Ucp2 in apoptotic cell clearance has implications for th

145 the mitochondrial membrane transport protein UCP2 in cancer cells is sufficient to restore a balance

146 We next investigated the role of Ucp2 in cytokine-induced apoptosis of rat insulin-produc

147 ard a non-transporter role for low levels of UCP2 in establishing dynamic response capability.

148 Overexpression of UCP2 in HCT116 human colon cancer cells inhibits ROS acc

149 y compromising ATP stores, downregulation of UCP2 in Kupffer cells may account for persistent oxidati

150 histamine release, whereas overexpression of UCP2 in LAD2 cells reduced histamine release after both

151 nt results expose the critical importance of UCP2 in normal nigral dopamine cell metabolism and offer

152 mall interfering RNA-mediated suppression of UCP2 in OCI-AML3 cells reversed mitochondrial uncoupling

153 This first description of the role of UCP2 in oxygen sensing and in pulmonary hypertension vas

154 etion of mitochondrial uncoupling protein 2 (UCP2(-/-)) in mice impaired glucagon secretion from isol

155 ial uncoupling protein uncoupling protein 2 (UCP2) in Foxa1-deficient islets, resulting in partially

156 ncreased expression of uncoupling protein-2 (UCP2) in pancreas from rats with BD as compared with con

157 Lack of UCP2 increased the sensitivity of dopamine neurons to 1-

158 Overexpression of UCP2 increases mitochondrial uncoupling, whereas deletio

159 Protection against hepatotoxicity by UCP2-induction through activation of PPARalpha is associ

160 ffects of UCP2 deletion were mimicked by the UCP2 inhibitor genipin on both murine and human islets a

161 tin immunoprecipitation assays indicate that UCP2 is a direct transcriptional target of Foxa1 in vivo

162 Here we show that UCP2 is a metabolite transporter that regulates substrat

163 Together, these results indicate that UCP2 is a regulator of erythropoiesis and suggests that

164 UCP2 is expressed in various human and rodent tissues, i

165 were recently found in erythroid cells where UCP2 is hypothesized to function as a facilitator of hem

166 In rodents, UCP2 is involved in the control of alpha- and beta-cell

167 As Ucp2 is linked to metabolic diseases and atherosclerosis

168 UCP2 is located in the mitochondrial inner membrane and

169 ypoglycemic glucagon response and shows that UCP2 is necessary for normal alpha-cell glucose sensing

170 UCP2 is present in drug-resistant lines of various cance

171 Despite its name, it is now accepted that UCP2 is rather a metabolite transporter than a UCP.

172 tion slows, energy metabolism decreases, and UCP2 is repressed, resulting in decreased glycolysis and

173 Instead, UCP2 is required to establish mitochondria that are capa

174 y rescued in FABP4/aP2-null macrophages when UCP2 is silenced.

175 UCP2 is thought to protect cardiomyocytes against oxidat

176 Uncoupling protein 2 (UCP2) is a mitochondrial protein that inhibits insulin s

177 Mitochondrial uncoupling protein 2 (UCP2) is an integral membrane protein in the mitochondri

178 Mitochondrial uncoupling protein-2 (UCP2) is highly expressed in steatotic livers and may be

179 Uncoupling protein 2 (UCP2) is involved in various physiological and pathologi

180 The uncoupling protein 2, UCP2, is a member of a family of inner mitochondrial mem

181 disruption of the uncoupling protein-2 gene (Ucp2-/-) is greater macrophage phagocytic activity and f

182 mice have a similar initial phenotype, ob/ob UCP2 knock-out animal survival was 83% when compared wit

183 Liver ATP levels were increased in the ob/ob UCP2 knock-out animals after reperfusion when compared w

184 Although ob/ob UCP2 knock-out mice and ob/ob mice have a similar initia

185 n lean and steatotic (ob/ob), wild-type, and UCP2 knock-out mice subjected to total warm hepatic isch

186 ere dependent on UCP2 expression, because in UCP2 knock-out mice such changes were not observed.

187 n of in situ mitochondrial ROS production in UCP2 knock-out mice was inversely correlated with mitoch

188 ellular necrosis were decreased in the ob/ob UCP2 knock-out mice when compared with ob/ob mice subjec

189 Ucp2 knockdown (80% at the protein and messenger RNA lev

190 UCP2 knockdown impairs proliferation at high glucose but

191 apoptotic protein Bcl-2 were increased after Ucp2 knockdown in INS-1E cells.

192 activated) caspases 9 and 3, suggesting that Ucp2 knockdown interferes with cytokine triggering of th

193 Ucp2 knockout (KO)-PASMCs had lower mitochondrial calciu

194 ther to this, we created alpha-cell-specific UCP2 knockout (UCP2AKO) mice, which we used to demonstra

195 Thus, we used Ucp2 knockout mice.

196 was found to deglutathionylate and activate UCP2 leak and impede GSIS.

197 activity nor down-regulation of already low UCP2 levels drive this reduction in mitochondrial activi

198 We now show that ERBB2 directly controls UCP2 levels, both at low physiological levels and oncoge

199 At low levels of receptor and UCP2, ligand stimulation creates a distinct temporal res

200 exporting C4 compounds out of mitochondria, UCP2 limits the oxidation of acetyl-CoA-producing substr

201 Apoptosis rates in UCP2(+/+) and UCP2(- /-) liver remnants were similar, while parameters

202 eration and oxidant stress, were elevated in UCP2(- /-) livers at every examined time point.

203 hepatotoxicity and suggest that induction of UCP2 may also be a general mechanism for protection of m

204 Targeting UCP2 may be considered a novel treatment strategy for ca

205 Therefore, UCP2 may contribute to the regulation of hypoglycemia-in

206 We conclude that obesity-induced, UCP2-mediated loss of glucose sensing in glucose-excited

207 ological studies indicated a direct role for Ucp2-mediated mitochondrial function in phagocytosis.

208 on of glutathionylation not only deactivates UCP2-mediated proton leak but also enhances GSIS.

209 With our recent discovery that the UCP2-mediated proton leak is modulated by reversible glu

210 produced mitochondrial superoxide activates UCP2-mediated proton leak, thus lowering ATP levels and

211 groups have shown previously that UCP1- and UCP2-mediated proton transport is inhibited by purine nu

212 Liver remnants of UCP2(+ /+) mice 48 hours post-hepatectomy showed a fourf

213 iferation indicated a diminished response in UCP2(- /-) mice with corresponding changes in the expres

214 and was found to be significantly delayed in UCP2(-/-) mice after partial hepatectomy.

215 BMMCs from Ucp2(-/-) mice exhibited greater histamine release, wher

216 greater vascular permeability in the skin of Ucp2(-/-) mice in vivo.

217 minished in Kupffer cells of untreated ob/ob:ucp2+/+ mice, conceivably contributing to increased oxid

218 de challenge compared with similarly treated Ucp2+/+ mice.

219 n either plasma or isolated macrophages from Ucp2-/- mice are significantly elevated in response to b

220 vity of I kappa B kinase in macrophages from Ucp2-/- mice can be blocked by cell-permeable inhibitors

221 hase and inflammatory cytokines is higher in Ucp2-/- mice in vivo and in vitro.

222 ally) proved uniformly fatal; however, ob/ob:ucp2-/- mice survived longer with less depletion of live

223 a B subunits, are all remarkably enhanced in Ucp2-/- mice, most notably even under basal conditions.

224 elevation and lower apoptosis rates in ob/ob:ucp2-/- mice.

225 al potential, we have evaluated the roles of UCP2, mitochondrial uncoupling, and 1alpha, 25-(OH)2-D3

226 both required for the late gestation rise in UCP2 mRNA and differentially regulate glucocorticoid act

227 uggest the insulin stimulates translation of ucp2 mRNA in a process that involves K protein.

228 Silencing of UCP2 mRNA in FABP4/aP2-deficient macrophages negated the

229 s suggest that the developmental ontogeny of UCP2 mRNA in the ovine lung is under local glucocorticoi

230 were maximal at 140 days gestation, whereas UCP2 mRNA peaked at 1 day of age and then declined with

231 ee-hybrid screen revealed K protein bound to ucp2 mRNA through sites located in the 3'-untranslated r

232 High levels of UCP2 mRNA were recently found in erythroid cells where U

233 ucp2 mRNA-K protein complexes were associated with polys

234 t accompanied by a corresponding increase in ucp2 mRNA.

235 ntary exercise induces uncoupling protein 2 (UCP2) mRNA expression and mitochondrial oxygen consumpti

236 UCP2 negatively regulates glucose sensing in POMC neuron

237 Analysis of ROS in UCP2 null erythroid cells revealed altered distribution

238 Ucp2-null mice, however, were sensitive to APAP-induced

239 aim was to determine whether the effects of UCP2 observed on beta-cell mass have an embryonic origin

240 and the mitochondrial inner membrane protein UCP2 occurs frequently in aggressive cancers with dysfun

241 myocardial UCP2 by examining the effects of UCP2 on bioenergetics, Ca(2+) homeostasis, and excitatio

242 h necessary and sufficient for the impact of UCP2 on endothelial cell phenotype.

243 t mice alleviated the effect of knocking out UCP2 on pancreas development.

244 ine content was reduced by overexpression of UCP2 or treatment with the mitochondrial-targeted supero

245 Tumor xenografts of UCP2-overexpressing HCT116 cells retain growth in nude m

246 present study, we tested the hypothesis that UCP2 overexpression could protect cardiomyocytes from ox

247 l-1,2,5,6 tetrahydropyridine (MPTP), whereas UCP2 overexpression decreased MPTP-induced nigral dopami

248 of Ucp2 reduced phagocytic capacity, whereas Ucp2 overexpression enhanced engulfment.

249 Notably, UCP2 overexpression increased signaling from the master

250 UCP2 overexpression markedly inhibited mitochondrial Ca(

251 UCP2 overexpression significantly prolonged the decay ph

252 tapsi in LI-UCP2 cells and protected against UCP2 overexpression-induced apoptosis (P<0.01), whereas

253 ential loss, were dramatically attenuated by UCP2 overexpression.

254 uncoupling proteins (UCP) increased (isoform UCP2, p<0.0001; isoform UCP3, p=0.0036) and those of glu

255 KT, an ROS target, was also activated in the Ucp2(-/-) pancreata.

256 Uncoupling protein 2 (UCP2) plays a regulating role in hPSC energy metabolism

257 on of the antioxidant N-acetyl-l-cysteine to Ucp2(-/-) pregnant mice alleviated the effect of knockin

258 We found that genetic deletion of Ucp2 prevents obesity-induced loss of glucose sensing, a

259 Forced overexpression of UCP2 protected wildtype mice against APAP-induced hepato

260 dies indicate that the PPARalpha target gene UCP2 protects against elevated reactive oxygen species g

261 We asked whether absence of UCP2 protects ob/ob mice from Fas-mediated acute liver d

262 suppression of the exceptionally short lived UCP2 protein and a time delayed transcriptional up-regul

263 We examined UCP2 protein expression and role in mice erythropoiesis

264 UCP2 protein is encoded by nuclear genome, but the prote

265 wed a fourfold increase in the expression of UCP2 protein primarily detected in hepatocytes.

266 d the insulin-induced mitochondrial level of UCP2 protein that was not accompanied by a corresponding

267 p2-/-) and UCP2-competent littermates (ob/ob:ucp2+/+) received a single dose of agonistic anti-Fas an

268 UCP2 reconstituted in lipid vesicles catalyzed the excha

269 Loss of Ucp2 reduced phagocytic capacity, whereas Ucp2 overexpre

270 However, because UCP2 reduces mitochondrial potential, we have evaluated

271 itochondrial uncoupling, whereas deletion of UCP2 reduces uncoupling in the substantia nigra-ventral

272 In conclusion, our results suggest that UCP2 regulates the NLRP3 inflammasome by inducing the li

273 that the mitochondrial uncoupling protein-2 (UCP2) regulates NLRP3-mediated caspase-1 activation thro

274 ne whether glutathionylation is required for UCP2 regulation of GSIS.

275 Although UCP2 reportedly controls mitochondrial oxidant productio

276 PSCs contain active mitochondria and require UCP2 repression for full differentiation potential.

277 The proton transport activity of UCP1 and UCP2 requires activation by fatty acids.

278 ilk, and substituting a low-fat diet reduced UCP2, restored mitochondrial coupling, and permitted sei

279 and that acute pharmacological inhibition of UCP2 reverses loss of glucose sensing.

280 RR = 1.31, 95% CI: 1.08, 1.60) and offspring UCP2 rs660339 (RR = 1.32, 95% CI: 1.06, 1.64) were assoc

281 Compared with wild-type, UCP2-silenced human hepatocellular carcinoma (HepG2) cel

282 tation enabled by the mitochondrial protein, UCP2, Sirt1-induced cellular and behavioral responses we

283 , and independently of uncoupling protein-2 (UCP2), sirtuin-2 (SIRT2), the G protein-coupled receptor

284 Pretreatment with the UCP2-specific inhibitor genipin largely reversed the eff

285 expressed ERBB2, resulting in high levels of UCP2 that contribute mitochondrial uncoupling.

286 Fed ad libitum, Hcrt-UCP2 transgenic mice had the same caloric intake as thei

287 These findings suggest a role of UCP2-UCP3 gene cluster haplotypes in diabetes; in partic

288 nucleotide polymorphisms (SNPs) at the 70-kb UCP2-UCP3 gene cluster in relation to type 2 diabetes ri

289 Genetic variants in the UCP2-UCP3 gene cluster, located on chromosome 11q13, may

290 8-rs668514- rs647126-rs1800006, spanning the UCP2-UCP3 intergenic and UCP3 regions) as significantly

291 0.05) or borderline significant increases in UCP2, UCP4, and UCP5 protein levels, and increased immun

292 main UCP isoforms expressed in the brain are UCP2, UCP4, and UCP5.

293 ponectin-stimulated AMPK phosphorylation and UCP2 upregulation.

294 Upregulation of UCP2 was critical for controlling mitochondrial membrane

295 UCP2 was mainly expressed at early stages of erythroid m

296 The mitochondrial membrane protein Ucp2, which acts to lower the mitochondrial membrane pot

297 alpha, PPAR-delta, PPAR-gamma, cd36/Fat, and Ucp2, which coincided with reduced postprandial plasma l

298 -PASMCs had lower mitochondrial calcium than Ucp2 wildtype (WT)-PASMCs at baseline and during histami

299 These findings link UCP2 with molecular mechanisms of chemoresistance.

300 elevated expression of uncoupling protein 2 (UCP2) without concomitant increases in UCP1 or UCP3.