ライフサイエンスコーパス: UCP2

1 ation of mitochondrial uncoupling protein 2 (UCP2).

2 encoding mitochondrial uncoupling protein 2 (UCP2).

3 ncreased expression of uncoupling protein 2 (UCP2).

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

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

6 n factor A (MafA), and uncoupling protein 2 (Ucp2).

7 iated by mitochondrial uncoupling protein 2 (UCP2).

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

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

10 act cell phenotype via dynamic regulation of UCP2.

11 ), 10 muM) amplified GSIS and also activated UCP2.

12 MR method for structural characterization of UCP2.

13 on are the uncoupling proteins, particularly UCP2.

14 ) and human leukemic LAD2 mast cells express UCP2.

15 CPT1 and free radicals that are scavenged by UCP2.

16 pounds do exist that can selectively inhibit UCP2.

17 nd ER stress by regulating the expression of UCP2.

18 ssociated with metabolism and mood: Trhr and Ucp2.

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

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

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

22 Uncoupling protein 2 (UCP2), a mitochondrial anion carrier, is thought to sepa

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

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

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

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

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

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

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

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

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

32 UCP2, an inner membrane mitochondrial protein, has been

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

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 in inflammation, whereas the mRNA levels of UCP2 and PPARD were decreased in peripheral blood mononu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

60 UCP2 can regulate oxidative stress and/or energetic meta

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

62 atio and the renal expressions of PRR, NOX4, UCP2, caspase3, phos-FOXO3a, phos-NF-kappaB, collagen, a

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

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

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

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

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

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

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

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

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

72 d the reverse, and deletion of mitochondrial Ucp2 decreased oxidative protein modification and reduce

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

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

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

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

77 out of UCP2 (Ucp2(DeltaLysM)), we found that UCP2 deficiency significantly increases glycolysis and o

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

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

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

81 In UCP2-deficient macrophages, inhibition of lipid synthesi

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

83 UCP2-deficient mice displayed improved survival in a mou

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

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

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

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

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

89 hondrial function explains the resistance of Ucp2-deleted retinas to glaucoma and may provide a thera

90 This paradox was resolved after finding that Ucp2 deletion also increased levels of mitophagy in cell

91 Our data suggest that Ucp2 deletion facilitates increased mitochondrial functi

92 To test the relevance of macrophage-specific Ucp2 deletion in vivo, Ucp2(DeltaLysM) and Ucp2(fl/fl) m

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 f macrophage-specific Ucp2 deletion in vivo, Ucp2(DeltaLysM) and Ucp2(fl/fl) mice were rendered obese

96 abolished the metabolic differences between Ucp2(DeltaLysM) macrophages and their floxed controls.

97 Furthermore, Ucp2(DeltaLysM) macrophages show attenuated pro-inflamma

98 macrophages isolated from diet-induced obese Ucp2(DeltaLysM) mice showed decreased TNFalpha secretion

99 Using a myeloid-specific knockout of UCP2 (Ucp2(DeltaLysM)), we found that UCP2 deficiency signific

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

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

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

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

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

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

106 this manuscript, we show that, while loss of Ucp2 does increase mitochondrial membrane potential and

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

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

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

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

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

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

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

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

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

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

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

118 Ectopic UCP2 expression perturbs this metabolic transition and i

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

120 UCP2 expression was found diminished in Kupffer cells of

121 Moreover, UCP2 expression was increased in human sepsis.

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

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

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

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

126 ity of SOD2 and ATP production and increased UCP2 expression.

127 g and inflammasome activation via control of UCP2 expression.

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

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

130 lysaccharide stimulation compared with their Ucp2(fl/fl) littermates.

131 c Ucp2 deletion in vivo, Ucp2(DeltaLysM) and Ucp2(fl/fl) mice were rendered obese and insulin resista

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

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

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

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

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

137 UCP2 gene expression was higher in pancreas from BD dono

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

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

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

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

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

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

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

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

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

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

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

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

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

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

152 We hypothesized that deletion of Ucp2 in either RGCs or retinal glia would increase retin

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

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

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

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

157 Here, we investigate the role of UCP2 in macrophage activation in the context of obesity-

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

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

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

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

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

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

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

165 Overexpression of UCP2 increases mitochondrial uncoupling, whereas deletio

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

167 III of the respiratory chain alongside with UCP2 inhibition.

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

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

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

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

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

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

174 As Ucp2 is linked to metabolic diseases and atherosclerosis

175 UCP2 is located in the mitochondrial inner membrane and

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

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

178 However, its specificity for UCP2 is questionable, and the underlying mechanism behin

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

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

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

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

183 UCP2 is thought to protect cardiomyocytes against oxidat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

198 UCP2 knockdown impairs proliferation at high glucose but

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

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

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

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

203 Thus, we used Ucp2 knockout mice.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

236 t accompanied by a corresponding increase in ucp2 mRNA.

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

238 UCP2 negatively regulates glucose sensing in POMC neuron

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

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

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

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

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

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

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

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

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

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

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

250 Notably, UCP2 overexpression increased signaling from the master

251 UCP2 overexpression markedly inhibited mitochondrial Ca(

252 UCP2 overexpression significantly prolonged the decay ph

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

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

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

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

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

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

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

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

261 We examined UCP2 protein expression and role in mice erythropoiesis

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

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

264 stically, ROS promoted uncoupling protein 2 (UCP2) protein expression and phosphorylation of AMPK, up

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

266 UCP2 reconstituted in lipid vesicles catalyzed the excha

267 Loss of Ucp2 reduced phagocytic capacity, whereas Ucp2 overexpre

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

269 her, these results demonstrate that although UCP2 regulates both metabolism and the inflammatory resp

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

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

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

273 The mitochondrial uncoupling protein 2 (UCP2) relieves oxidative and neuronal damage in a variet

274 Although UCP2 reportedly controls mitochondrial oxidant productio

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

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

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

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

279 es by upregulation of mitochondria NOX4/SOD2/UCP2 signaling pathway.

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

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

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

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

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

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

286 Using a myeloid-specific knockout of UCP2 (Ucp2(DeltaLysM)), we found that UCP2 deficiency si

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.