ライフサイエンスコーパス: UCP

1 UCP are submicron-sized, inorganic crystals that are exc

2 UCP-2, UCP-3, and PPARalpha expression were reduced when

3 UCP-3 mRNA expression in gastrocnemius muscle from diabe

4 UCP-3tg fibres were as strong as the wild-type and maint

5 UCP-strep particles were immobilized on cellulose paper,

6 UCP-subtype-specific primers were designed for the assay

7 UCPs are believed to mediate the transmembrane transfer

8 UCPs are therefore potentially important regulators of e

9 UCPs with strong green emission were synthesized and sub

10 BAT uncoupling protein 1 (UCP-1) content was significantly decreased compared with

11 In uncoupling protein 1 (UCP-1) knockout mice, the middle and highest doses of th

12 tudy, we have measured uncoupling protein 1 (UCP-1) mRNA, a specific marker for BAT, in isolated adip

13 Brown adipose tissue uncoupling protein-1 (UCP-1) mRNA levels (collected Day 25) were 80% higher in

14 erexpression of either uncoupling protein-1 (UCP-1) or manganese superoxide dismutase (MnSOD), which

15 de overproduction with uncoupling protein-1 (UCP-1) or manganese superoxide dismutase (MnSOD).

16 and PPARgamma but not uncoupling protein-1 (UCP-1), the CD45 hematopoietic lineage marker, or the CD

17 9; 95% confidence interval [CI], 48.67-126); UCP, 1042 (SE, 1000; 95% CI, 0-3004); and TAMU, 9 oocyst

18 hrough an induction of uncoupling protein 2 (UCP-2) and through regulation of the nuclear respiratory

19 he expression level of uncoupling protein 2 (UCP-2) leads to a rapid and dramatic fall in mitochondri

20 Uncoupling protein 2 (UCP-2) was increased as were other genes barely expresse

21 0 minutes post-PH) and uncoupling protein-2 (UCP-2) (which begins around 30 minutes and peaks from 6-

22 P due to overexpressed uncoupling protein-2 (UCP-2) or (2) induction of growth inhibitor p21 leading

23 ndicated that mRNA for uncoupling protein-2 (UCP-2) was increased in the cPLA(2)-overexpressing MIN6

24 UCP-2, UCP-3, and PPARalpha expression were reduced when cardia

25 of diabetes on muscle uncoupling protein 3 (UCP-3), a potential regulator of muscle energy metabolis

26 of mice overexpressing uncoupling protein 3 (UCP-3tg) were compared with the performance of bundles f

27 Uncoupling protein-3 (UCP-3) is a recently identified member of the mitochondr

28 5% in O vs YA muscles, uncoupling protein-3 (UCP-3) protein level was upregulated with age by 353%.

29 tion suppressed mRNA levels for UCP-2 (49%), UCP-3 (36%), and COX-IV (59%) and eliminated the acute r

30 th the recently published NMR structure of a UCP family member, our data provide a valuable insight i

31 P2 is rather a metabolite transporter than a UCP.

32 stant uncoupling protein-diphtheria toxin A (UCP-DTA) transgenic mice, a murine model of metabolic sy

33 n, yielding breakdown products that activate UCPs.

34 -trans-nonenal act independently to activate UCPs, or if they share a common pathway, perhaps by supe

35 Furthermore, AAPH activated UCPs, and this was blocked by MitoPBN.

36 r cytokine (TNF-alpha) administration affect UCP-2 and UCP-3 expression, and 2) whether peroxisome pr

37 ice reveal increased expression of UCP-1 and UCP-3 in brown adipose tissue and increased UCP-3 and in

38 the level of uncoupling protein (UCP)-1 and UCP-3 in the muscle.

39 Analysis of tissue mass, PGC-1alpha and UCP-1 content, the presence of multilocular adipocytes,

40 ria genesis, up-regulation of PGC-1alpha and UCP-2, and down-regulation of perilipin.

41 (TNF-alpha) administration affect UCP-2 and UCP-3 expression, and 2) whether peroxisome proliferator

42 Pase-2a activity and expression of UCP-2 and UCP-3, and GLUT-1 and GLUT-2 and significantly decreased

43 creased expression of both cardiac UCP-2 and UCP-3.

44 d tissue to reveal patterns of caspase-3 and UCP-2 expression.

45 a decrease in UCP-2 mRNA in WAT (47-52%) and UCP-3 mRNA in SM (33-37%).

46 lipid emulsions, linoleic or oleic acid, and UCP-2 expression was evaluated by Northern blotting and

47 by 80% and inhibits NF kappaB activation and UCP-2 induction by 50% and 80%, respectively.

48 ANT (carboxyatractylate and bongkrekate) and UCP (GDP).

49 ependent upregulation of both UCP-2 mRNA and UCP-2 protein.

50 evels of uncoupling protein (UCP)-2 mRNA and UCP-3 mRNA in white adipose tissue (WAT) and SM.

51 rial membrane, suppression of UCP-2 mRNA and UCP-3 mRNA may in fact lower respiratory demands in WAT

52 ll-known obesity models, including ob/ob and UCP-DTA mice.

53 for iBAT thermogenesis, including PGC1a and UCP-1.

54 ional forms used to model ROS production and UCP regulation yield insight into these mechanisms, as m

55 sertional knockout of one of the Arabidopsis UCP genes (AtUCP1) are presented that resolve this issue

56 eficient in a mitochondrial protein known as UCP-3 (for 'uncoupling protein-3') have a diminished the

57 f the structure of membrane proteins such as UCPs, we confirmed that UCP2 binds nucleotides.

58 d to cold water did possess functional avian UCP, demonstrated by a superoxide-stimulated, GDP-inhibi

59 conductance, indicating no functional avian UCP.

60 increased proton transport activity of avian UCP (dependent on superoxide and inhibited by GDP) and i

61 d with a markedly greater abundance of avian UCP mRNA.

62 cant step for the development of paper-based UCP-LRET nucleic acid hybridization assays, which offer

63 ffects, chronic AGRP treatment decreased BAT UCP-1, suppressed plasma TSH, and increased fat mass and

64 e of transgenic mice with deficiency of BAT (UCP promoter-driven diphtheria toxin A transgenic mice [

65 n caused AMPK-dependent upregulation of both UCP-2 mRNA and UCP-2 protein.

66 41%(n = 14) and 44%(n = 15) were detected by UCP-LFA and Gold-LFA, respectively.

67 %(n = 161) of MB patients were identified by UCP-LFA and 78%(n = 133) by Gold-LFA.

68 d of the series, recovery heat production by UCP-3tg fibres, 1.575 +/- 0.246 relative units, was twic

69 nic fatty acid head group is translocated by UCP, and the proton is transported electroneutrally in t

70 the bilayer and cannot support uncoupling by UCP.

71 ryptosporidium parvum isolates (Iowa [calf], UCP [calf], and TAMU [horse]) of the C genotype was inve

72 lted in decreased expression of both cardiac UCP-2 and UCP-3.

73 In contrast, cardiac UCP-2 expression is regulated in part by a fatty acid-de

74 fasting, and STZ-induced diabetes), cardiac UCP-3 but not UCP-2 expression increased.

75 The level of cardiac UCP-3 but not UCP-2 expression was severely reduced (20-

76 In this work, by using well-characterized UCP-specific CD4 T cell clones, we showed that hTERT pro

77 LRRK2 levels were required for constitutive UCP expression.

78 asing mitochondrial density while decreasing UCP activity may be an effective way to increase glucose

79 UCP-DTA mice but not in PPARalpha-deficient UCP-DTA mice.

80 erleptinemic brown adipose tissue deficient (UCP-DTA) mice in comparison with controls.

81 Six days post-denervation, UCP-1 protein levels and AMPK alpha2 protein and activit

82 a major mechanism underlying MnSOD-dependent UCPs expression that consequently triggers the PI3K/Akt/

83 TRPM8-mediated calcium entry, downregulated UCP-1 expression, and mitigated uncoupled respiration; m

84 In the absence of doxycycline, UCP-1 mRNA and protein were undetectable.

85 In the presence of doxycycline, UCP-1 was expressed and oxygen consumption doubled.

86 RNA transcripts of each UCP generated by in vitro transcription were used to val

87 PARalpha) regulates the expression of either UCP-2 or UCP-3.

88 vely (all values means +/- S.E.M., n = 6 for UCP-3tg and n = 5 for wild-type).

89 Denervation suppressed mRNA levels for UCP-2 (49%), UCP-3 (36%), and COX-IV (59%) and eliminate

90 physiological situations support a role for UCP-3 in energy balance and lipid metabolism.

91 oot ganglion (DRG) neurons were screened for UCP expression by Western blotting and immunocytochemist

92 ells showed clear mitochondrial staining for UCP-1 protein by confocal microscopy.

93 infected with different isolates (MD, GCH1, UCP, and IOWA) of C. parvum, indicating that both Cp900

94 ults suggest that in the adult rodent heart, UCP-3 expression is regulated by PPARalpha.

95 o test whether lipids up-regulate hepatocyte UCP-2, cultures of rat hepatocytes were treated with lip

96 pts in cultured hepatocytes; after 24 hours, UCP-2 messenger RNA levels were increased 4.5-fold, and

97 Moreover, the unresolved mystery is how UCP operates in vivo despite the permanent presence of h

98 Furthermore, an example is given of how UCP can be used for analyte multiplexing using a two-ple

99 quantitative assay for measurement of human UCP mRNA.

100 on of transgenic mice that overexpress human UCP-3 in skeletal muscle.

101 deficient ob/ob mice and the hyperleptinemic UCP-DTA mice.

102 on for 5 h was associated with a decrease in UCP-2 mRNA in WAT (47-52%) and UCP-3 mRNA in SM (33-37%)

103 e in control ZDF rat islets, was improved in UCP-2-overexpressing islets.

104 pling was not associated with an increase in UCP content, but fatty acid oxidation genes and expressi

105 perirenal depot, showed a marked increase in UCP-1 expression in response to thiazolidinediones.

106 ulin secretion and prevented the increase in UCP-2 expression in islets from high-fat-fed GK rats.

107 2 compared to TBI alone and this increase in UCP-2 expression was associated with a decrease in expre

108 The increases in UCP protein expression in two important thermogenic tiss

109 lpha-interacting MED1 subunit of Mediator in UCP-1 induction, as well as the accumulation of TRalpha,

110 arly during lipid metabolism participates in UCP-2 induction, addition of the cell-impermeable antiox

111 very heat represents inefficient recovery in UCP-3tg fibres.

112 e mechanisms underlying leptin resistance in UCP-DTA mice may provide valuable insights into the basi

113 mitochondrial ROS production, also increased UCP-2 messenger RNA levels.

114 evels were increased 4.5-fold, and increased UCP-2 protein was shown by immunocytochemistry.

115 UCP-3 in brown adipose tissue and increased UCP-3 and inhibition of acetyl-CoA carboxylase in skelet

116 In HeLa cells, increased UCP-2 expression leads to a form of cell death that is n

117 t (SD)-treated animals, indicating increased UCP-mediated proton conductance that can reduce reactive

118 Finally, AICAR markedly increased UCP-2 expression and reduced both O(2).(-) and prostacyc

119 eatment with ghrelin significantly increased UCP-2 compared to TBI alone and this increase in UCP-2 e

120 We conclude that AMPK activation increases UCP-2, resulting in the inhibition of both O(2).(-) and

121 her a high-fat ketogenic diet (KD) increases UCP levels and activity in hippocampi of juvenile mice.

122 The abilities of individual UCPs to prevent hyperglycemic PCD were assessed by adeno

123 y livers, suggesting that lipids also induce UCP-2 in hepatocytes.

124 Lipids increase ROS and induce UCP-2 in hepatocytes.

125 ssive supply of lipid substrates by inducing UCP-2 to facilitate substrate disposal while constrainin

126 In normal pancreatic islets, UCP-2 is upregulated by leptin and is low in leptin-resi

127 The main UCP isoforms expressed in the brain are UCP2, UCP4, and

128 ent activation of highly conserved mammalian UCPs may facilitate the Warburg effect in the absence of

129 re-function relationships of other mammalian UCPs in other tissues.

130 d for the uncoupling protein family members (UCP).

131 r-driven diphtheria toxin A transgenic mice [UCP-DTA]) mice.

132 re might result from increased mitochondrial UCPs (ie, less efficient ATP synthesis) and depleted GLU

133 oduction through activation of mitochondrial UCPs.

134 responses, in concert with increased muscle UCP-3 expression, may also contribute to the catabolic e

135 This provides evidence that skeletal muscle UCP-3 has the potential to influence metabolic rate and

136 Here we show that UCP4, a neuronal UCP, influences store-operated Ca(2+) entry, a process i

137 nd accompanied by the modulation of neuronal UCP expression levels, further highlighting a cross-talk

138 STZ-induced diabetes), cardiac UCP-3 but not UCP-2 expression increased.

139 The level of cardiac UCP-3 but not UCP-2 expression was severely reduced (20-fold) in PPARa

140 onclude that coenzyme Q is not a cofactor of UCP-mediated proton transport.

141 ulating insulin or glucose concentrations of UCP-DTA mice.

142 ondrial proton gradients as a consequence of UCP-2 upregulation.

143 We examine short- and long-term effects of UCP activation inhibition and changes in the mitochondri

144 white adipose cells activates expression of UCP-1 and key mitochondrial enzymes of the respiratory c

145 -treated mice reveal increased expression of UCP-1 and UCP-3 in brown adipose tissue and increased UC

146 calcium ATPase-2a activity and expression of UCP-2 and UCP-3, and GLUT-1 and GLUT-2 and significantly

147 Studies on the expression of UCP-3 in animals and humans in different physiological s

148 ight, and insulin and glucose homeostasis of UCP-DTA mice are all extraordinarily resistant to leptin

149 tral lipids, and age-dependent impairment of UCP-1 activation and temperature regulation.

150 d in a dose- and time-dependent induction of UCP-2 transcripts in cultured hepatocytes; after 24 hour

151 GSH did not alter lipid-related induction of UCP-2.

152 m all depots resulted in increased levels of UCP-1 mRNA, compared with those of the vehicle-treated c

153 tional level, thus making the measurement of UCP mRNA beneficial for both diagnosis and research of w

154 The quantitative measurement of UCP mRNA was further demonstrated with cultured cells an

155 However, the mechanism of UCP-mediated proton translocation across the lipid bilay

156 may involve, at least in part, modulation of UCP-2 expression.

157 creation of a dominant interfering mutant of UCP-2 whose expression increases resting mitochondrial m

158 Overexpression of UCP-1 or MnSOD also prevented hyperglycemia-induced DNA

159 Because overexpression of UCP-2 or UCP-3 can depolarize the inner mitochondrial me

160 Furthermore, overexpression of UCP-2 significantly ablated both O(2).(-) and prostacycl

161 this effect is dependent on the presence of UCP-1 protein and sleep responses require the intact sen

162 been described, the physiological purpose of UCP in plants has not been established.

163 The regulation of UCP expression is mainly controlled at the transcription

164 t least in part mediated by up-regulation of UCP-2, thereby stabilizing mitochondria and preventing u

165 Three subtypes of UCP have been identified so far.

166 inner mitochondrial membrane, suppression of UCP-2 mRNA and UCP-3 mRNA may in fact lower respiratory

167 A comprehensive survey of UCP expression from 17 human tissues measured by the new

168 riments confirm that the proton transport of UCP-mediated uncoupling takes place in the lipid bilayer

169 Rodents possess two types of UCP-1 positive brown adipocytes arising from distinct de

170 eta-cells to glucose through upregulation of UCP-2 and uncoupling of mitochondrial metabolism from AT

171 tly suppressed AICAR-induced upregulation of UCP-2, suggesting that AMPK lies upstream of p38 kinase.

172 romide (MitoPBN) prevented the activation of UCPs by superoxide but did not block activation by hydro

173 ty and diabetes is mediated by activation of UCPs independently of changes in expression levels.

174 share a common pathway for the activation of UCPs.

175 nonenal correlated with tissue expression of UCPs, appeared in yeast mitochondria expressing UCP1 and

176 It correlates with the tissue expression of UCPs, appears in mitochondria from yeast expressing UCP1

177 ers the structure as well as the function of UCPs.

178 Knockdown of UCPs and mTOR suppresses lactate production and increase

179 Overexpression of UCPs prevents glucose-induced transient mitochondrial me

180 UCP inhibitor genipin confirmed the role of UCPs in this mechanism.

181 ydroperoxide (TBHP) and glutathione (GSH) on UCP-2 induction were also assessed.

182 des are unique because they express only one UCP ortholog, ceUCP4 (ucp4).

183 CI, 4.46-13.65); TAMU versus Iowa, P=.002 or UCP, P=.019.

184 Because overexpression of UCP-2 or UCP-3 can depolarize the inner mitochondrial membrane, s

185 regulates the expression of either UCP-2 or UCP-3.

186 ck rate between TAMU (86%) and Iowa (52%) or UCP (59%).

187 not be attributed to up-regulation of other UCP mRNAs.

188 ling capabilities equivalent to UCP3L; other UCPs may compensate for a deficiency of bioactive UCP3L;

189 iopsy samples including plasma, cell pellet (UCP) and supernatant (USN) from spun urine, from 17 pati

190 T) and referred as universal cancer peptide (UCP).

191 of a novel reporter, upconverting phosphors (UCP), in this assay format.

192 of micrometer-sized upconversion phosphors (UCPs) and a pH indicator (Neutral Red) that absorbs thei

193 RET) associated with upconverting phosphors (UCPs) can be used to develop a paper-based DNA hybridiza

194 e catalytic function and regulation of plant UCPs have been described, the physiological purpose of U

195 in 35.3%, 47.1% and 52.9% of pre-NAC plasma, UCP and USN samples respectively, and urine samples cont

196 duction of mitochondrial oxidant production, UCP-2 expression, nor hepatocyte DNA synthesis, although

197 ose tissues that express uncoupling protein (UCP) 1 and thus can uncouple mitochondrial respiration f

198 e between the effects of uncoupling protein (UCP) 1 and UCP3L on basal O(2) consumption in whole yeas

199 ell-specific increase in uncoupling protein (UCP) 2 and 4 expression.

200 he mitochondrial carrier uncoupling protein (UCP) 2 belongs to the family of the UCPs.

201 Uncoupling protein (UCP) 2 is a mitochondrial inner-membrane protein that me

202 ease in this leak due to uncoupling protein (UCP) activation by ROS.

203 to enhance mitochondrial uncoupling protein (UCP) activity.

204 The identification of uncoupling protein (UCP) genes has fueled a search for genes involved in ene

205 A role for uncoupling protein (UCP) homologues in mediating the proton leak in mammalia

206 , the sole mitochondrial uncoupling protein (UCP) in nematodes.

207 , activate mitochondrial uncoupling protein (UCP)-1 and oxidize fatty acids to generate heat.

208 rown fat signature genes uncoupling protein (UCP)-1 and peroxisome proliferator-activated receptor ga

209 mice as was the level of uncoupling protein (UCP)-1 and UCP-3 in the muscle.

210 through the activity of uncoupling protein (UCP)-1.

211 -inducible expression of uncoupling protein (UCP)-1.

212 acid beta-oxidation and uncoupling protein (UCP)-2 expression decreased after treatment with VSL#3 o

213 by a twofold increase in uncoupling protein (UCP)-2 levels in GK rat islets.

214 g steady-state levels of uncoupling protein (UCP)-2 mRNA and UCP-3 mRNA in white adipose tissue (WAT)

215 The discovery of uncoupling protein (UCP)-2, a ubiquitously expressed protein homologous to U

216 ression of mitochondrial uncoupling protein (UCP)-2.

217 pates energy as heat via uncoupling protein (UCP)1.

218 Uncoupling protein (UCP)2 is a mitochondrial inner membrane protein that is

219 ved in lipid metabolism (uncoupling protein [UCP]1, UCP3, PPAR gamma coactivator 1alpha [PGC-1alpha],

220 ds induce mitochondrial uncoupling proteins (UCP) 2 and 3 in muscle and fat, providing a mechanism to

221 ression of mitochondria uncoupling proteins (UCP) and glucose transporters (GLUT).

222 Uncoupling proteins (UCP) are inner mitochondrial membrane transporters which

223 , cardiac mitochondrial uncoupling proteins (UCP) increased (isoform UCP2, p<0.0001; isoform UCP3, p=

224 upling by mitochondrial uncoupling proteins (UCP) is still in debate.

225 s and regulation of the uncoupling proteins (UCP).

226 of brain mitochondrial uncoupling proteins (UCP-2, 4, and 5).

227 e physiological role of uncoupling proteins (UCPs) 2 and 3 is uncertain, their activation by superoxi

228 Uncoupling proteins (UCPs) are a family of proteins located in the inner mito

229 Uncoupling proteins (UCPs) are composed of three repeated domains of approxim

230 Mitochondrial uncoupling proteins (UCPs) are involved in body weight regulation and glucose

231 Uncoupling proteins (UCPs) are located in the mitochondrial inner membrane an

232 rning the regulation of uncoupling proteins (UCPs) in the heart.

233 Uncoupling proteins (UCPs) occur in the inner mitochondrial membrane and diss

234 Uncoupling proteins (UCPs) oppose this phenotype by inducing futile mitochond

235 Uncoupling proteins (UCPs) regulate energy expenditure in living cells by ind

236 es a potent ability for uncoupling proteins (UCPs) to prevent this process.

237 mRNA levels of uncoupling proteins (UCPs) were significantly higher in adipose, heart (UCP2)

238 on through induction of uncoupling proteins (UCPs), and transgenic overexpression of STC1 inhibits re

239 was to evaluate whether uncoupling proteins (UCPs), located in the inner membrane of mitochondria, pl

240 increased expresson of uncoupling proteins (UCPs).

241 changes are mediated by uncoupling proteins (UCPs).

242 do not normally express uncoupling proteins, UCP-2 is expressed in hepatocytes of genetically obese m

243 selective antioxidants and then reactivating UCPs with distal cascade components.

244 , activating TRPM8 with menthol up-regulated UCP-1 expression and augmented uncoupled respiration pre

245 ) production may contribute to lipid-related UCP-2 induction, the DNA-binding activity of the ROS-act

246 However, its close relative UCP-1 is expressed exclusively in brown adipose tissue,

247 ays were also increased in insulin-resistant UCP-DTA hearts.

248 Insulin-resistant UCP-DTA mice crossed into a PPARalpha-null background di

249 -1alpha is recruited to the TRalpha-RXRalpha-UCP-1 enhancer complex through interaction of an N-termi

250 ression of the brown adipose tissue-specific UCP-1 and Cidea genes that are involved in respiratory u

251 lpha-activated brown adipose tissue-specific UCP-1 enhancer to investigate mechanistic aspects of PGC

252 ell lung cancer, the presence of spontaneous UCP-specific CD4 T cell responses increases the survival

253 tissue (WAT) via a mechanism that stimulates UCP-1 expression.

254 bsequently functionalized with streptavidin (UCP-strep).

255 cent up-converting phosphor anti-PGL-I test [UCP-LFA].

256 nce that NF kappaB is antiapoptotic and that UCP-2 may decrease mitochondrial oxidant production in s

257 We conclude that UCP-2 has uncoupling function when overexpressed in lept

258 Our findings indicate that UCP-3 is important in MDMA-induced hyperthermia and poin

259 by lipid peroxidation products suggest that UCPs are central to the mitochondrial response to reacti

260 on and increases ATP levels, suggesting that UCPs contribute to increased glycolysis.

261 cellular Ca(2+) homeostasis, suggesting that UCPs may play roles in modulating Ca(2+) signaling in ph

262 n of mitochondrial membrane potential by the UCP inhibitor genipin confirmed the role of UCPs in this

263 Initial heat production was similar for the UCP-3tg and wild-type fibres, decreasing during the seri

264 The increase in the UCP levels along with increased fatty acid oxidation may

265 isms were proposed: direct activation of the UCP proton transport mechanism by superoxide or its prod

266 Alkylsulfonates are useful as probes of the UCP transport mechanism.

267 lpha, PPARgamma, PGC-1alpha, and MED1 on the UCP-1 enhancer in brown adipocytes.

268 These data suggest that the UCP homologue, UCP2, mediates the proton leak in mitocho

269 Therefore, the UCP-LFA platform, which allows multiplexing with differe

270 ets of diabetic ZDF rats, we transferred the UCP-2 gene to the islets of diabetic ZDF rats and lean (

271 fairly higher sensitivity obtained with the UCP-LFA assay.

272 The UCPs generate green and red luminescence upon excitation

273 The UCPs served as donors that were LRET-paired with Cy3-lab

274 proton transport were also similar among the UCPs, ranging from 8 to 20 micromol.min(-1).mg(-1), depe

275 Solely the green light of the UCPs is affected by the pH indicator, while the red emis

276 The emission peaks of the UCPs match the red and green color channels of standard

277 ent proton transport catalyzed by any of the UCPs nor did it affect nucleotide regulation of the UCPs

278 r did it affect nucleotide regulation of the UCPs.

279 protein (UCP) 2 belongs to the family of the UCPs.

280 gonucleotide probes were conjugated onto the UCPs via streptavidin-biotin linkage.

281 Thus, the roles of these UCPs in both metabolic efficiency and the linkage to obe

282 indicating that gene transcription of these UCPs may be coordinately regulated by common mechanisms.

283 estigate domain specific properties of these UCPs.

284 More recently, a third UCP (UCP3) was identified, which is expressed largely in

285 nd increased immunoreactivity to these three UCP isoforms was most prominently seen in the dentate gy

286 ological signal to induce uncoupling through UCPs and ANT and thus decrease mitochondrial ROS product

287 Thus, UCP lateral flow assays can be used for applications tha

288 , and a 60% increase in brown adipose tissue UCP-1 mRNA.

289 cle of hydroperoxyl radical entry coupled to UCP-catalyzed superoxide anion export.

290 ubiquitously expressed protein homologous to UCP-1, has raised the possibility that energy balance of

291 drial biogenesis, was activated in wild-type UCP-DTA mice but not in PPARalpha-deficient UCP-DTA mice

292 +/- 0.052 to 0.661 +/- 0.061 relative units (UCP-3tg), and from 0.806 +/- 0.024 to 0.729 +/- 0.039 re

293 nce the abnormalities in leptin-unresponsive UCP-2-underexpressing islets of diabetic ZDF rats, we tr

294 10-fold lower ATP levels due to upregulated UCP-2 throughout the time course after CCl4 administrati

295 arrhea was seen for the TAMU (94.5 h) versus UCP (81.6 h) and Iowa (64.2 h) isolates.

296 takes place in the lipid bilayer and not via UCP itself.

297 of enhanced energy dissipation as heat when UCP-3tg is overexpressed.

298 To determine whether UCP-2 does, in fact, have uncoupling activity and, if so

299 DF-ND rats as compared to ZL controls, while UCP-1 and mitochondrial concentrations were significantl

300 cate that the interaction of superoxide with UCPs may be a mechanism for decreasing the concentration