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 is also found outside classical brown adipose tissu

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

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

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

9 UCP1-deficient BAT mitochondria exhibit reduced mitochon

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

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

12 imals showed increased uncoupling protein 1 (UCP1) and TGR5 expression levels in brown adipose tissue

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

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

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

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

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

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

19 show higher levels of uncoupling protein 1 (UCP1) expression in WAT, which correlates with smoking s

20 -1alpha protein level, uncoupling protein 1 (UCP1) expression, and oxygen consumption, while the oppo

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

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

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

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

25 ecreased expression of uncoupling protein 1 (UCP1) in brown adipose tissue.

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

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

28 observed expression of uncoupling protein 1 (UCP1) in SAT exposed to PDAC exosomes, SAT from mice wit

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

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

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

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

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

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

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

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

37 roton gradient through uncoupling protein 1 (UCP1) to generate heat, but the evolutionary events unde

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

39 e ectopic formation of uncoupling protein 1 (UCP1)(+pos) adipose tissue with long-term engraftment (>

40 tonomous expression of uncoupling protein 1 (UCP1), a biomarker of beige and brown adipogenesis, rema

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

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

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

46 ogenic markers such as uncoupling protein 1 (UCP1), PR domain containing 16, and early B cell factor

47 mediated primarily by uncoupling protein 1 (UCP1), the development of the UCP1 knockout mouse has en

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

49 xidation, 2) stimulate uncoupling protein 1 (UCP1)-independent respiration in subcutaneous white fat,

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

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

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

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

54 express mitochondrial uncoupling protein 1 (UCP1).

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

56 xpenditure mediated by uncoupling protein 1 (UCP1).

57 sically low because of uncoupling protein 1 (UCP1).

58 ine at position 253 in uncoupling protein 1 (UCP1).

59 ation of mitochondrial uncoupling protein 1 (UCP1).

60 requires mitochondrial uncoupling protein 1 (UCP1).

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

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

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

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

65 In mammals, uncoupling protein-1 (UCP1) in brown and beige adipocytes uncouples fatty acid

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

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

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

69 Uncoupling protein-1 (UCP1) plays a central role in energy dissipation in brow

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

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

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

73 rgy expenditure, but whether it can activate UCP1 is unknown.

74 2 weeks in Wistar and Lou/C rats to activate UCP1 and delineate its metabolic impact.

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

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

77 t a unified model in which beige adipocytes (UCP1(+) multilocular cells) in rodents initially arise p

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

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

80 Although UCP1 expression declined in long-term BAT grafts, this d

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

100 egulates the key thermogenic protein in BAT, UCP1.

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

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

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

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

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

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

107 g and this effect is manifested through both UCP1- and creatine-mediated mechanisms.

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

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

110 f mitochondrial respiratory chain complexes, UCP1, and PGC1alpha were attenuated in iWAT from Gcgr(-/

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

112 e targets of specific amino acids to control UCP1-dependent and -independent thermogenesis, thereby c

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

114 g to attenuated thermogenesis via decreasing UCP1 expression.

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

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

117 n paucilocular adipocytes lacking detectable UCP1.

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

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

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

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

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

123 out to identify small molecules that enhance UCP1 levels and activity using a high-throughput screen

124 of beige adipocyte precursors, and expanded UCP1-expressing cell clusters in inguinal white adipose

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

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

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

128 formation of brownlike adipocytes expressing UCP1 (uncoupling-protein-1) in subcutaneous white adipos

129 htheria toxin expression in cells expressing UCP1 (Ucp1(Cre+/DTA+)).

130 for adipocyte FAO in a background of extant UCP1.

131 fluorescently labeled nucleotide analog, for UCP1.

132 acting-protein-1 as a regulatory complex for UCP1 transcription.

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

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

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

136 adipose cells with expression of functional UCP1.

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

138 dance with upregulation of thermogenic genes UCP1 and DIO2.

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

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

141 nge correlated positively with the change in UCP1 in SC WAT, leading to the hypothesis that mast cell

142 atty acids induce a conformational change in UCP1.

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

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

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

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

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

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

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

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

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

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

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

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

155 Mutation of the two succinylated lysines in UCP1 to acyl-mimetic glutamine and glutamic acid signifi

156 ted levels of thermogenic markers, including UCP1, increased numbers of beige adipocyte precursors, a

157 evels of brown-selective proteins, including UCP1.

158 Finally, the BAT of IIA+ mice had increased UCP1 and other proteins indicative of mitochondrial unco

159 exposed to caffeine (1 mM) showed increased UCP1 protein abundance and cell metabolism with enhanced

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

161 In vivo administration of FGF9 increases UCP1 expression and thermogenic capacity.

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

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

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

165 tion elevated facultative incorporation into UCP1, elevated energy expenditure through thermogenic ad

166 Isolated UCP1 KO brown adipocytes exhibited defective induction o

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

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

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

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

171 tion of thermogenic and beige/brown markers (UCP1, PRDM16, ZIC-1 and TBX1) and increased mitochondria

172 and no other mitochondrial proteins matched UCP1.

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

174 Diet can modulate UCP1 function but the capacity of individual nutrients t

175 is demonstrates that BMAT adipocytes are not UCP1-expressing beige/brown adipocytes.

176 enesis requires skeletal muscle UCP3 but not UCP1.

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

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

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

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

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

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

183 nts to promote the abundance and activity of UCP1 is not well established.

184 xylate carrier and decreased the activity of UCP1, UCP3, and complex III of the respiratory chain alo

185 leotides compete to regulate the activity of UCP1.

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

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

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

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

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

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

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

193 non, we produce the first direct evidence of UCP1-independent BAT thermogenesis in knockout mice.

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

195 4 in mice resulted in elevated expression of UCP1 and beige adipogenesis of subcutaneous AT in obesit

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

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

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

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

200 levels of FASN without current expression of UCP1.

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

202 The reduced function of UCP1 and other proteins in Sirt5KO BAT results in impair

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 (FGF), FGF6 and FGF9, as potent inducers of UCP1 expression in adipocytes and preadipocytes.

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

208 on against body weight gain and induction of UCP1 in adipose tissues associated with dietary protein

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

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

211 ed by guanosine 5'-diphosphate inhibition of UCP1.

212 CHKB-CPT1B synteny, and the insufficiency of UCP1 to account for eutherian BAT, these data support a

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

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

215 Although significantly higher levels of UCP1 protein were observed in interscapular brown adipos

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

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

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

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

220 d blockers, and site-directed mutagenesis of UCP1, we propose a mechanism of genipin's action on UCPs

221 Overexpression of UCP1 in SAT might be a biomarker of early-stage PDAC, bu

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

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

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

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

226 lerated the rate of enzymatic proteolysis of UCP1.

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

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

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

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

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

232 f redox signaling and mechanistic studies of UCP1 function.

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

234 Thus, succinylation of UCP1 and other mitochondrial proteins plays an important

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

236 and inguinal WAT through the upregulation of UCP1 and other thermogenic genes.

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

238 mplex I-derived OAA in a manner dependent on UCP1.

239 Overexpressed UCP1 in bacterial membranes was extracted using mild det

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

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

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

243 y white but contains some cells that possess UCP1.

244 seems to suggest the existence of a possible UCP1-independent thermogenic mechanism responsible for t

245 kout mouse has enabled the study of possible UCP1-independent non-shivering thermogenic mechanisms, w

246 lipid uptake and lipolysis, and potentiates UCP1 expression.

247 pression data to identify genes that predict UCP1.

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

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

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

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

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

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

254 sion of the mitochondrial uncoupling protein UCP1.

255 eat via the mitochondrial uncoupling protein UCP1.

256 ipocytes that express the uncoupling protein UCP1.

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

258 Reconstituted UCP1 in phospholipid vesicles also exhibited highly heli

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

260 F6 and FGF9 are adipokines that can regulate UCP1 through a transcriptional network that is dissociat

261 noradrenaline-induced hyperthermia requires UCP1 but not UCP3.

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

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

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

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

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

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

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

269 Cardiolipin stabilizes UCP1, as demonstrated by reconstitution experiments and

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

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

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

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

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

275 the hit compound increased body temperature, UCP1 protein levels, and thermogenic gene expression.

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

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

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

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

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

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

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

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

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

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

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

287 ing protein 1 (UCP1), the development of the UCP1 knockout mouse has enabled the study of possible UC

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

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

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

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

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

293 lly active tissue that dissipates energy via UCP1 as heat, and BAT mass is correlated negatively with

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

295 pound effects on mitochondrial function were UCP1- or AKAP1-independent, suggesting compound effects

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

297 an neck fat is significantly associated with UCP1 expression.

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

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

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