ライフサイエンスコーパス: UCP1

1 UCP1 and UCP3 in brown adipose tissue mediate early and

2 UCP1 catalyzes proton leak across the mitochondrial inne

3 UCP1 Cys253 is sulfenylated during thermogenesis, while

4 UCP1 dissipates the mitochondrial proton motive force (D

5 UCP1 expression also increases superoxide production and

6 UCP1 is also found outside classical brown adipose tissu

7 UCP1 knockout (KO) and wild-type (WT) mice housed at the

8 UCP1 was folded in octyl glucoside, as indicated by its

9 UCP1, PGC1alpha, and other markers of browning and therm

10 UCP1-deficient BAT mitochondria exhibit reduced mitochon

11 UCP1-deficient mice that can adapt to the cold have incr

12 d higher expression of uncoupling protein 1 (UCP1) and a higher degree of uncoupling in vitro in mito

13 wn-fat-defining marker uncoupling protein 1 (UCP1) and adipogenic transcription factors PPARgamma and

14 zed cells that express uncoupling protein 1 (UCP1) and dissipate chemical energy as heat.

15 d-induced activator of uncoupling protein 1 (UCP1) and oxidative capacity in BAT.

16 Both uncoupling protein 1 (UCP1) and UCP3 are important for mammalian thermoregulat

17 ncreased expression of uncoupling protein 1 (UCP1) and UCP3 in brown adipose tissue.

18 Uncoupling protein 1 (UCP1) catalyzes fatty acid-activated, purine nucleotide-

19 HFD feeding increased uncoupling protein 1 (UCP1) expression (fold increase: 3.5) in brown adipose t

20 tissue and increasing uncoupling protein 1 (UCP1) expression in both white and brown adipose tissue.

21 A 90% reduction in uncoupling protein 1 (UCP1) expression in interscapular BAT was accompanied by

22 -1alpha protein level, uncoupling protein 1 (UCP1) expression, and oxygen consumption, while the oppo

23 ysfunction and reduces uncoupling protein 1 (UCP1) expression.

24 ease expression of the uncoupling protein 1 (UCP1) gene.

25 brown adipocyte marker uncoupling protein 1 (UCP1) in both adipose tissue depots, although these effe

26 ased the expression of uncoupling protein 1 (UCP1) in brown adipose tissue (BAT) and subcutaneous WAT

27 ffects are mediated by uncoupling protein 1 (UCP1) in brown adipose tissue (BAT).

28 lished by induction of uncoupling protein 1 (UCP1) in brown and beige adipocytes, the principal sites

29 rmogenesis mediated by uncoupling protein 1 (UCP1) in mammals.

30 duced up-regulation of uncoupling protein 1 (UCP1) in primary human adipocytes, which was reversed by

31 Uncoupling protein 1 (UCP1) is highly expressed in brown adipose tissue, where

32 Uncoupling protein 1 (UCP1) is nearly absent in brown adipose tissue lacking H

33 Mitochondrial uncoupling protein 1 (UCP1) is responsible for nonshivering thermogenesis in b

34 Uncoupling protein 1 (UCP1) is the established mediator of brown adipose tissu

35 tivation of the unique uncoupling protein 1 (UCP1) located within the inner mitochondrial membrane.

36 Uncoupling protein 1 (UCP1) mediates nonshivering thermogenesis and, upon cold

37 Uncoupling protein 1 (UCP1) plays a central role in nonshivering thermogenesis

38 We combined an uncoupling protein 1 (UCP1) reporter system and expression profiling to define

39 vity and expression of uncoupling protein 1 (UCP1) through the three beta-adrenergic receptor subtype

40 ed with recruitment of uncoupling protein 1 (UCP1)(+) beige adipocytes in WAT, a process known as bei

41 xtensive expression of uncoupling protein 1 (UCP1), a definitive marker of brown adipocytes, within H

42 lpha, PDK4, PPARalpha, uncoupling protein 1 (UCP1), and neuron-derived orphan receptor-1 (NOR-1), and

43 d by the expression of uncoupling protein 1 (UCP1), but brown adipose tissue has been considered to h

44 is were independent of uncoupling protein 1 (UCP1), but required expression of liver-derived fibrobla

45 creases adipose tissue uncoupling protein 1 (UCP1), energy expenditure and food intake, and these eff

46 zed by the presence of uncoupling protein 1 (UCP1), has been described as metabolically active in hum

47 erexpression of either uncoupling protein 1 (UCP1), superoxide dismutase 2 (SOD2), or glyoxalase 1 (G

48 ose tissue (BAT) (i.e. uncoupling protein 1 (UCP1)-based) and skeletal muscle (i.e. sarcolipin (SLN)-

49 in fuel oxidation and uncoupling protein 1 (UCP1)-mediated thermogenesis.

50 d that a population of uncoupling protein 1 (UCP1)-positive human adipocytes possessed molecular sign

51 pearance of pockets of uncoupling protein 1 (UCP1)-positive, multilocular adipocytes and serves to in

52 t chain components and uncoupling protein 1 (UCP1).

53 express mitochondrial uncoupling protein 1 (UCP1).

54 using tissue-specific uncoupling protein 1 (UCP1).

55 xpenditure mediated by uncoupling protein 1 (UCP1).

56 ctor of thermogenesis: uncoupling protein 1 (UCP1).

57 ired for activation of uncoupling protein 1 (UCP1).

58 ration, which requires uncoupling protein 1 (UCP1).

59 requires mitochondrial uncoupling protein 1 (UCP1).

60 ved the stimulation of uncoupling protein 1 (UCP1; P<0.01), peroxisome proliferator-activated recepto

61 energy as heat via the uncoupling protein-1 (UCP1) and BAT activity correlates with leanness in human

62 serve as repressors of uncoupling protein-1 (UCP1) in classic brown adipose tissue in female mice, we

63 nducible expression of uncoupling protein-1 (UCP1) in the artery wall.

64 Uncoupling protein-1 (UCP1) is abundantly expressed in the mitochondrial inner

65 y increased lipolysis, uncoupling protein-1 (UCP1) mRNA, and glucose uptake, are regulated by the adr

66 own adipose tissue and uncoupling protein-1 (UCP1), which mediate adaptive non-shivering thermogenesi

67 ession of the uncoupling protein PGC-1alpha, UCP1, and a series of mitochondria-related genes.

68 e adrenergic independent p38 MAPK-PGC-1alpha-UCP1 pathway.

69 Toward this goal, we generated a UCP1;SLN double knock-out (DKO) mouse model and challeng

70 stem cells (ADMSCs) into lipid-accumulating, UCP1-expressing beige adipose tissue.

71 2 weeks in Wistar and Lou/C rats to activate UCP1 and delineate its metabolic impact.

72 elease by mast cells and inhibited adipocyte UCP1 mRNA induction by conditioned medium (CM).

73 hlorpheniramine potently inhibited adipocyte UCP1 mRNA induction by mast cell CM.

74 Ps expressed the molecular identity of adult-UCP1 expressing cells (PAX3, CIDEA, DIO2) with both brow

75 These cells likely possess alternative UCP1-independent thermogenic mechanisms.

76 t10b mice lacks expression of PGC-1alpha and UCP1, the presence of unilocular lipid droplets and expr

77 PARgamma coactivator-1alpha (PGC-1alpha) and UCP1 expression, induced mitochondriogenesis, and increa

78 file in both diet-induced obese C57BL/6J and UCP1-DTA mice and resulted in a significantly improved g

79 esistance in diet-induced obese C57BL/6J and UCP1-DTA mice to alter food intake, body weight, body co

80 ssion of brown adipose tissue PGC1-alpha and UCP1.

81 athetic activation leads to angiogenesis and UCP1-dependent thermogenesis in mouse brown and white ad

82 alpha, DIO2, NRF1, CYTC, COX2, ATP5beta, and UCP1.

83 wn adipose tissue markers PRDM16, CIDEa, and UCP1, consistent with a resistance to HFD-induced obesit

84 induces proliferation, differentiation, and UCP1 expression in pre-adipocytes and mature brown adipo

85 we show that Lkb1 controls BAT expansion and UCP1 expression in mice.

86 F21 was not elevated in serum, and FGF21 and UCP1 mRNAs were not induced in liver or brown adipose ti

87 e significant induction of the Ucp1 gene and UCP1 protein expression in inguinal white adipose tissue

88 at derived from a myf-5 cellular lineage and UCP1-positive cells that emerge in white fat from a non-

89 as evidenced by the increased PGC1alpha and UCP1 expressions, mitochondrial biogenesis, and oxygen c

90 The expression of PGC1alpha and UCP1 were 2- to 3-fold up-regulated in Id1(-/-) BAT, sug

91 induction of PGC1alpha, PDK4, PPARalpha, and UCP1 but not NOR-1.

92 established by their hydrophobic tails, and UCP1 effectively operates as an H(+) carrier activated b

93 n of recognition patterns obtained with anti-UCP1 antibody and ATP led to the conclusion that the ATP

94 lipin stabilized the structure of associated UCP1 and enhanced the proton transport activity of the p

95 sacrificed 4h after BDNF injection, and BAT UCP1 gene expression was measured with quantitative real

96 did not induce a significant increase in BAT UCP1 expression.

97 In BAT, UCP1 expression increased similarly in response to the t

98 e to adenylate cyclase activation from being UCP1 negative to being UCP1 positive, which is a definin

99 activation from being UCP1 negative to being UCP1 positive, which is a defining feature of the beige/

100 C and the quantitative relationship between UCP1 and selected subunits of mitochondrial respiratory

101 We further establish that mice lacking both UCP1 and 3 (UCPDK) fail to show methamphetamine-induced

102 Loss of both UCP1 and UCP3 accelerate the loss of body temperature co

103 etary protein restriction, and requires both UCP1 and FGF21 but is independent of changes in food int

104 nalysis reveals that this cascade induced by UCP1 deletion is associated with a dramatic reduction in

105 By comparison, UCP1 knockout (UCP1KO) mice exhibit blunted methamphetam

106 Congenic UCP1-deficient mice on a C57BL/6J genetic background sho

107 raging investigation of factors that control UCP1-dependent respiration in vivo.

108 wn adipose tissue temperature, and decreased UCP1 expression suggesting an impairment of thermogenesi

109 n the skeletal muscle of mice with defective UCP1/brown adipose tissue thermogenesis, has been evalua

110 Fatty acid activators destabilize UCP1 in a similar way, which can also be prevented by ca

111 n paucilocular adipocytes lacking detectable UCP1.

112 ting NAP1L5 and a 2.1-Mb deletion disrupting UCP1 and IL15.

113 ls resulted in the establishment of distinct UCP1-expressing implants that successfully attracted hos

114 RNAs encoding traditional BAT markers (i.e., UCP1, expressed in 100% of BAs Adrb3, expressed in <50%

115 ype littermates, these mice exhibit elevated UCP1 expression in BAT and subcutaneous white adipose ti

116 d versus severe cold adaptation by employing UCP1(-/-) and SLN(-/-) mice.

117 usly demonstrated that Lou/C animals express UCP1 in beige adipocytes in inguinal white adipose tissu

118 ties and regulation of bacterially expressed UCP1, -2, and -3 reconstituted in liposomes.

119 in multilocular adipocytes that co-expressed UCP1+, whereas high FASN expression occurred in pauciloc

120 ction method, we have successfully expressed UCP1 in Escherichia coli membranes in high yield.

121 s, appeared in yeast mitochondria expressing UCP1 and was absent in skeletal muscle mitochondria from

122 fluorescently labeled nucleotide analog, for UCP1.

123 Immunostaining for UCP1 was performed on biopsy specimens from the neck and

124 ed that in iBAT, the expression patterns for UCP1 and other mitochondrial proteins resembled each oth

125 Apart from UCP1-based nonshivering thermogenesis in brown adipocyte

126 ever, the LCFA anions cannot dissociate from UCP1 due to hydrophobic interactions established by thei

127 s in pigs, a species that lacks a functional UCP1 protein.

128 adipose cells with expression of functional UCP1.

129 expression of brown adipocyte-related genes UCP1, UCP3, PGC1alpha and PRDM16, as well as COX8B and A

130 dance with upregulation of thermogenic genes UCP1 and DIO2.

131 Tissue from this region had UCP1-immunopositive, multilocular adipocytes indicating

132 respond to cyclic AMP stimulation with high UCP1 expression and respiration rates.

133 Inhibition of SERCA2b impairs UCP1-independent beige fat thermogenesis in humans and m

134 atty acids induce a conformational change in UCP1.

135 s that enable mice, genetically deficient in UCP1 and sensitive to acute exposure to the cold at 4 de

136 on, and BAT thermogenesis were diminished in UCP1 KO mice, but BAT (18)F-FDG uptake was fully retaine

137 n containing 1 (PM20D1), that is enriched in UCP1(+) versus UCP1(-) adipocytes.

138 lecular markers that were highly enriched in UCP1-positive human adipocytes, a set that included pota

139 onally, comparisons of energy expenditure in UCP1-deficient and wild type mice fed an obesogenic diet

140 there is up-regulation of SLN expression in UCP1-KO mice, and loss of SLN is compensated by increase

141 able; however, body temperature is higher in UCP1-deficient mice by 0.1-0.3 degrees C, and respirator

142 However, the FGF21-dependent increase in UCP1 and energy expenditure by LP has no effect on the a

143 ha antagonist indicates that the increase in UCP1 expression and oxygen consumption is PPARalpha-depe

144 However, no HFD-induced increase in UCP1 expression was observed in the AdCXCR4ko mice, whic

145 n iWAT, associated with a marked increase in UCP1 expression, in Lou/C rats only.

146 tes as revealed by a significant increase in UCP1 mRNA (p = 0.03) and lipolysis-related ATGL mRNA (p

147 Consistent with the increase in UCP1, exercise training increases the presence of brown-

148 in 2 (UCP2) without concomitant increases in UCP1 or UCP3.

149 ipocytes in white fat depots, are induced in UCP1-deficient mice by gradual cold adaptation.

150 Conversely, knockout of IRF4 in UCP1(+) cells causes reduced thermogenic gene expression

151 sm of thermogenesis that is probably used in UCP1-deficient mice, whether there are others remains to

152 evels of brown-selective proteins, including UCP1.

153 ability to reduce fat deposition or increase UCP1 expression in adipose tissue.

154 of MCR4 blocked leptin's ability to increase UCP1 mRNA in both brown and white adipose tissue, but no

155 tions (16 degrees C) significantly increased UCP1 expression, suggesting increased reliance on BAT-ba

156 a PDE3 and a PDE4 inhibitor to fully induce UCP1 mRNA and lipolysis in brown adipocytes, whereas nei

157 ins resembled each other, whereas in ingWAT, UCP1 varied approximately 100-fold during the transition

158 its a dominant negative effect by inhibiting UCP1 expression.

159 hypothermia upon cold exposure, and inhibits UCP1-dependent increases in whole-body energy expenditur

160 We show for the first time that ATP inhibits UCP1, -2, and -3 with similar affinities.

161 Isolated UCP1 KO brown adipocytes exhibited defective induction o

162 helical content and binding to ATP, a known UCP1 proton transport inhibitor.

163 ere we find that in mice genetically lacking UCP1, cold-induced activation of metabolism triggers inn

164 ctivation by long-chain fatty acids (LCFAs), UCP1 increases the conductance of the inner mitochondria

165 pecific marker CD137 and the browning marker UCP1 in all types of white fat, including visceral fat,

166 and no other mitochondrial proteins matched UCP1.

167 ue-resident F4/80(hi)CD206(-)PD-L2(-)MHCII(-)UCP1(+) phenotype in the peritoneal cavity of mice and d

168 Ki values for ATP inhibition were 50 microm (UCP1), 70 microm (UCP2), and 120 microm (UCP3) at pH 7.2

169 TP are similar to those obtained with native UCP1 isolated from brown adipose tissue mitochondria (Ki

170 enesis requires skeletal muscle UCP3 but not UCP1.

171 II]) in lean C57BL/6J and obese (DIO, ob/ob, UCP1-DTA) mice.

172 d brown adipose tissue (BAT)-deficient obese UCP1-DTA (uncoupling protein 1-diphtheria toxin A) mice.

173 Consistent with these in vitro observations, UCP1-Wnt10b transgenic mice, which express Wnt10b in int

174 d form of Ucp1 mRNA, resulting in absence of UCP1 protein and impairment in uncoupled respiration and

175 However, absence of UCP1 results in a photosynthetic phenotype.

176 Absence of UCP1 results in localized oxidative stress but does not

177 In the absence of UCP1, beige fat dynamically expends glucose through enha

178 thermogenic activity, despite the absence of UCP1, whereas liver and skeletal muscle showed no change

179 However, in the absence of UCP1-based thermogenesis, induction of Slc25a25 in mice

180 brown fat and an almost complete absence of UCP1.

181 Activation of UCP1 in ectopic tissues, such as beige cells in iWAT, ma

182 ify Zfp516 as a transcriptional activator of UCP1 as well as PGC1alpha, thereby promoting a BAT progr

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

184 leotides compete to regulate the activity of UCP1.

185 novel methods to purify milligram amounts of UCP1 from native sources by using covalent chromatograph

186 The self-assembly of UCP1 into tetramers was unambiguously characterized by c

187 ndings reveal the fundamental composition of UCP1, which is essential for understanding the mechanism

188 that fatty acids change the conformation of UCP1, reconciling the apparent discrepancy between exist

189 ve increased respiration, and that Cys253 of UCP1 is a key target.

190 ions that extend well beyond the deletion of UCP1 itself.

191 ivation of macrophages and downregulation of UCP1 expression dependent on the kinase Erk in adipocyte

192 While expansion of UCP1-expressing adipose depots may be achieved in rodent

193 4 in mice resulted in elevated expression of UCP1 and beige adipogenesis of subcutaneous AT in obesit

194 LN is compensated by increased expression of UCP1 and browning of white adipose tissue.

195 e/paracrine manner to increase expression of UCP1 and other thermogenic genes in fat tissues.

196 were associated with increased expression of UCP1 and Pref-1 in subcutaneous WAT.

197 scular depots with regulatable expression of UCP1 provide a genetically based mechanism of protection

198 on of Wnt signaling suppresses expression of UCP1 through repression of PGC-1alpha.

199 adipose tissue development and expression of UCP1 when expressed from the fatty acid binding protein

200 in having extremely low basal expression of UCP1, but, like classical brown fat, they respond to cyc

201 levels of FASN without current expression of UCP1.

202 Self-associated functional forms of UCP1 in lipid membranes were observed for the first time

203 The structure and function of UCP1 are not fully understood, partially due to the diff

204 nearly half of adipocytes with a history of UCP1 expression expressed high levels of FASN without cu

205 crease BAT (18)F-FDG uptake independently of UCP1 thermogenic function.

206 the full action of ATRA on the induction of UCP1 and PGC-1alpha expression in brown adipocytes and t

207 nhibitor alone could potentiate induction of UCP1 mRNA, whereas a PDE4 inhibitor alone could augment

208 Neither induction of UCP1 nor lipolysis was altered by inhibition of PDE1, PD

209 PR-Cas9 markedly abolished the high level of UCP1 in brown adipocytes differentiated from the preadip

210 differentiation but also increased levels of UCP1 mRNA and protein expression.

211 ncludes studies of developmental lineages of UCP1(+) adipocytes, including the discovery of beige fat

212 s study, we sought to understand how loss of UCP1 or SLN is compensated during cold exposure and whet

213 DG uptake is a reliable surrogate measure of UCP1-mediated heat production.

214 achieved direct patch-clamp measurements of UCP1 currents from the IMM of BAT mitochondria.

215 Indeed, the number of UCP1-positive brown fat cells in intermuscular fat in 12

216 sed by adenovirus-mediated overexpression of UCP1 and UCP3.

217 n, which was normalized by overexpression of UCP1, SOD2, or GLO1.

218 ria, we determined the expression pattern of UCP1 and other mitochondrial proteins as well as analyze

219 These results identify a population of UCP1(+) cells within human tissue undergoing HO that do

220 Our assessment of the properties of UCP1 indicate that it is not unique among mitochondrial

221 y determined by estimating the proportion of UCP1 to respiratory complex components showed no signifi

222 lerated the rate of enzymatic proteolysis of UCP1.

223 ells are subject to further up-regulation of UCP1 after stimulation with a beta3-adrenergic receptor

224 e tissue (AT), with massive up-regulation of UCP1 and PGC1alpha.

225 blocked nesfatin-1-induced up-regulation of UCP1, PGC1alpha, COX8B and ATP5B in differentiated brown

226 In independent assessments of the role of UCP1 as a mediator of MR's effects on EE and insulin sen

227 suggest that the main physiological role of UCP1 in Arabidopsis leaves is related to maintaining the

228 sing this mouse model to examine the role of UCP1 in physiology.

229 tence of the functional oligomeric states of UCP1 in the lipid membranes has important implications f

230 f redox signaling and mechanistic studies of UCP1 function.

231 A subset of UCP1+ adipocytes develops within white adipose tissue in

232 While interscapular tissue of UCP1-Wnt10b mice lacks expression of PGC-1alpha and UCP1

233 ria and function as endogenous uncouplers of UCP1-independent respiration.

234 we investigated the effects of mast cells on UCP1 induction by adipocytes.

235 Overexpressed UCP1 in bacterial membranes was extracted using mild det

236 idea, Pgc1alpha, Pparalpha, and particularly UCP1, are markedly elevated in these cells.

237 ively regulated the expression of PGC1alpha, UCP1, and cellular respiration.

238 Knocking out the positive UCP1 regulators, PREX1 and EDNRB, in brown preadipocytes

239 y white but contains some cells that possess UCP1.

240 pression data to identify genes that predict UCP1.

241 ectedly, the mast cell marker CPA3 predicted UCP1 gene expression.

242 r temperatures, release factors that promote UCP1 expression, and are an important immune cell type i

243 fat, which expresses the thermogenic protein UCP1, provides a defense against cold and obesity.

244 TP carrier AAC2 and ovine uncoupling protein UCP1 allow optimal conditions for stability in detergent

245 aAR-dependent increase of uncoupling protein UCP1 expression and expansion of beige/brite adipocytes

246 eat via the mitochondrial uncoupling protein UCP1, defending against hypothermia and obesity.

247 lacking the mitochondrial uncoupling protein UCP1, has provided an opportunity to analyze the relatio

248 sion of the mitochondrial uncoupling protein UCP1.

249 eat via the mitochondrial uncoupling protein UCP1.

250 ipocytes that express the uncoupling protein UCP1.

251 nhanced expression of the uncoupling protein UCP1.

252 mitochondria through the uncoupling proteins UCP1, UCP2 and UCP3 and the adenine nucleotide transloca

253 ton leak, mitochondrial uncoupling proteins (UCP1-3) increase mitochondrial respiration and may there

254 ton flux in liposomes containing recombinant UCP1, -2, and -3.

255 Reconstituted UCP1 in phospholipid vesicles also exhibited highly heli

256 titutively active Gq protein in mice reduces UCP1 expression in BAT, whole-body energy expenditure an

257 noradrenaline-induced hyperthermia requires UCP1 but not UCP3.

258 enditure during protein restriction requires UCP1, promotes a resistance to cold stress, and is depen

259 Here we report a robust UCP1-independent thermogenic mechanism in beige fat that

260 Despite significant UCP1 up-regulation in iWAT and dramatic weight loss, the

261 Similarly, UCP1(-/-) mice adapted to mild cold up-regulated muscle-

262 ergrown tissue was composed of normal-sized, UCP1-negative unilocular adipocytes, with mitochondrial

263 ily of mitochondrial anion carriers (SLC25), UCP1 is believed to transport H(+) by an unusual mechani

264 nd pharmacologic analyses show that squirrel UCP1 acts as the typical thermogenic protein in vitro.

265 Cardiolipin stabilizes UCP1, as demonstrated by reconstitution experiments and

266 se cells in culture and in vivo to stimulate UCP1 expression and a broad program of brown-fat-like de

267 e, and retinoic acid concurrently stimulated UCP1 and Lcn2 expression in adipocytes.

268 stamine and IL-4, and this medium stimulated UCP1 expression and lipolysis by 3T3-L1 adipocytes.

269 ptors or the SERCA2b-RyR2 pathway stimulates UCP1-independent thermogenesis in beige adipocytes.

270 adipose tissue as a mechanism that supports UCP1-dependent thermogenesis and whole-body energy expen

271 These findings establish that UCP1 is required for the MR-induced increase in EE but n

272 It is well established that UCP1 is activated by fatty acids and inhibited by purine

273 Furthermore, we find that UCP1 is not dimeric but monomeric, as indicated by size

274 e mice fed an obesogenic diet indicates that UCP1-based brown fat-based thermogenesis plays no role i

275 r research groups have shown previously that UCP1- and UCP2-mediated proton transport is inhibited by

276 of purified preparations by TLC reveal that UCP1 retains tightly bound cardiolipin, with a lipid pho

277 Here we show that UCP1 expression in aortic smooth muscle cells causes hyp

278 We show that UCP1 is an LCFA anion/H(+) symporter.

279 We showed that UCP1 turnover is very different in iBAT and inguinal WAT

280 These studies suggest that UCP1 and SLN are required to maintain optimal thermogene

281 Together, our findings suggest that UCP1 contributes to local thermogenesis in the squirrel

282 d, and interacts with PRDM16 to activate the UCP1 promoter.

283 er, CITED1, was selectively expressed in the UCP1-positive beige cells as well as in human BAT.

284 dispensable step in the transcription of the UCP1 gene in mice.

285 ies, p38 MAPK controls the expression of the UCP1 gene through their respective interactions with a c

286 side within a critical enhancer motif of the UCP1 gene.

287 directly binds to the proximal region of the UCP1 promoter, not to the enhancer region where other tr

288 Here, by high-throughput screening using the UCP1 promoter, we identify Zfp516 as a transcriptional a

289 cytes observed during HO in the mouse, these UCP1(+) cells also expressed the peroxisome proliferator

290 ical examination, however, reveals that this UCP1 is in mitochondria of brown adipocytes interspersed

291 insulin, and increased brown adipose tissue UCP1 expression.

292 lucose tolerance tests in CNTF(Ax15)-treated UCP1-DTA compared with pair-fed mice of similar body wei

293 er show that PDGF-CC stimulation upregulates UCP1 expression and acquisition of a beige phenotype in

294 (PM20D1), that is enriched in UCP1(+) versus UCP1(-) adipocytes.

295 e of an atomic force microscope to visualize UCP1 reconstituted into lipid bilayers and to analyze th

296 e metabolism are compensatorily induced when UCP1-dependent thermogenesis is ablated, and creatine re

297 WAT suggest significant 'browning', but with UCP1 expression in WAT of Opa3(L122P) mice only 62% of t

298 of Gq in human WAT inversely correlates with UCP1 expression.

299 Genetic tracing with UCP1-cre, however, indicated nearly half of adipocytes w

300 Reciprocal expression of Wnt10b with UCP1 and PGC-1alpha in interscapular tissue from cold-ch