ライフサイエンスコーパス: HMG

1 HMG Co-A reductase negatively regulates eNOS, and the PL

2 HMG domain transcription factor, Sox2, is a critical gen

3 HMG-17 is developmentally regulated and its unique role

4 HMG-CoA lyase (HMGCL) is crucial to ketogenesis, and inh

5 HMG-CoA reductase (HMGR) catalyzes a rate-limiting step

6 HMG-CoA reductase catalyzes the four-electron reduction

7 HMG-CoA reductase inhibitors or statins are associated w

8 HMG-CoA reductase inhibitors such as statins are cholest

9 HMG-coA reductase inhibitors, commonly known as statins,

10 HMG-CoA reductase levels are regulated in response to st

11 HMG-CoAR is the central enzyme of the mevalonate pathway

12 HMG-CoAR regulates the oncogenic Hippo transducers TAZ/Y

13 HMG-CoAR was positively associated with the expression o

14 HMG-D and ZmHMGB1 differ from HMGB1 in having phosphoryl

15 ested that the transcription factor Sox11, a HMG-domain containing protein that is highly expressed i

16 cells increased expression of KLF2 through a HMG-CoA/prenylation-dependent pathway.

17 from 3-hydroxy-3-methylglutaryl-coenzyme A (HMG Co-A) reductase inhibition.

18 olog of 3-hydroxy-methylglutaryl coenzyme A (HMG CoA) lyase (HCL1).

19 beta-hydroxy-beta-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors (statins) within 60 days a

20 ) and 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase (HMGR)) has been linked to cholestero

21 le of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase and alphaPix.

22 f the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase and subsequently the isoprenylation o

23 f the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase enzyme (statins) are cholesterol-lowe

24 ntly, 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) have been the ma

25 RBs), 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins), and selective s

26 the 3-hydroxyl-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors known as statins have anti

27 Hydroxy-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitors or statins are well tolera

28 ether 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors, described as inhibitors o

29 s, or 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, have anti-inflammatory ef

30 le or 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase.

31 ds to 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) synthase and irreversibly inhibits HMG-CoA synt

32 levels of hydroxymethylglutaryl-coenzyme A (HMG-CoA) synthase, squalene epoxidase, and acyl-CoA:chol

33 Antibodies against HMG-CoA reductase apparently provoke SINAM.

34 An autoantibody directed against HMG-CoA reductase (HMGCR), the pharmacologic target of s

35 Treatment with small interfering RNA against HMG-CoA synthase led to a substantial reduction in HCV r

36 Although HMG Co-A reductase inhibitors ("statins") may prevent ca

37 llele contains a single gene that encodes an HMG-domain protein, implicating the HMG-domain proteins

38 Amphoterin is an HMG protein (HMGB1) that has been shown to have extranuc

39 SOX9 is an HMG-box transcription factor that plays an essential rol

40 Simvastatin, an HMG-coA reductase inhibitor, is known to attenuate infla

41 SOX2, an HMG box transcription factor, plays an essential role in

42 f cholesterol biosynthesis using statins (an HMG-CoA reductase inhibitor) significantly increased the

43 plementary activity between these agents and HMG-CoA reductase inhibitors (statins) based on their ab

44 nd Tip60 interact directly via the ATXN1 and HMG-box protein 1 (AXH) domain of ATXN1.

45 Sp100 isoforms contain SAND, PHD, Bromo, and HMG domains and are highly sumoylated, all characteristi

46 and spliced into four isoforms (A, B, C, and HMG), which differentially regulate transcription.

47 oteins 1c and 2, acetyl-CoA carboxylase, and HMG-CoA reductase mRNAs/proteins and inactive non-phosph

48 ylglycerol, diacylglycerol, malonyl-CoA, and HMG-CoA.

49 edback response, which upregulates HMGCR and HMG-CoA synthase 1 (HMGCS1) following statin treatment.

50 rol synthesis, HMG CoA synthase (HMGCS1) and HMG CoA reductase (HMGCR), were also reduced in PGC1alph

51 ensin-converting enzyme (ACE) inhibitors and HMG CoA reductase inhibitors (statins) have more than do

52 ered N-terminal region consisting of PHD and HMG domains and receptor-binding motifs.

53 hepatic low-density lipoprotein receptor and HMG-CoA reductase expression in ApoE-p50-DKO but not in

54 SREBP cleavage-activating protein (SCAP) and HMG-CoA reductase (HMGR) both possess SSDs required for

55 red for the feedback inhibition of SREBP and HMG-CoA reductase (HMGR).

56 e rescued by cholesterol supplementation and HMG Co-A reductase inhibition.

57 Anti-HMG-CoA reductase-positive patients can be further subdi

58 -associated myopathy, statin-associated anti-HMG-CoA reductase-positive autoimmune myopathy, and stat

59 e autoimmune myopathy, and statin-naive anti-HMG-CoA reductase-positive myopathy.

60 ingle ER-resident membrane proteins, such as HMG-CoA reductase (HMGR), can induce a dramatic restruct

61 rast, the effects of hymeglusin on bacterial HMG-CoA synthase, mvaS, have been minimally characterize

62 larly to the DNA-binding faces of both basic HMG boxes.

63 ist in dynamic assemblies in which the basic HMG boxes and linkers associate with their intrinsically

64 A positive relationship emerged between HMG-CoAR, hormone receptors and TAZ/YAP, suggesting a co

65 erol uptake (LDL receptor) and biosynthesis (HMG-CoA reductase).

66 Statins block HMG-CoA reductase (HMGCR), the rate-limiting enzyme of t

67 nce assignments from the NMR spectra of both HMG-boxes of TFAM.

68 In yeast, the membrane-bound HMG-CoA reductase degradation (HRD) ubiquitin-ligase com

69 a nucleus-encoded, high-mobility-group-box (HMG-box) protein that regulates transcription of the mit

70 insights into the binding mechanisms used by HMG boxes to recognize varied DNA structures and sequenc

71 was characterized and demonstrated to cleave HMG-CoA to acetoacetate and acetyl-CoA with catalytic an

72 th elevated 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase activity and mRNA levels.

73 hat inhibit 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase, the rate-limiting enzyme in the synt

74 ident enzyme 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase catalyzes the rate-limiting step in s

75 homologues, 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) synthase and the fatty acid biosynthesis enzyme

76 3-Hydroxy-3-methylglutaryl-CoA (HMG-CoA) synthase catalyzes the first physiologically ir

77 erivatives, such as acetyl-CoA, butyryl-CoA, HMG-CoA, and malonyl-CoA, as well as NADPH but not NADP(

78 CSA13 inhibited colonic HMG-CoA reductase activity in an FPRL1-dependent manner.

79 omatic residue (position 15 of the consensus HMG box) that is invariant among SRY-related HMG box tra

80 l dominant mutations in the highly conserved HMG box of the transcription factor Sox4.

81 e we describe a role of the highly conserved HMG-box transcription factor SOX-2 in postmitotic specif

82 a disprove the hypothesis that the conserved HMG box domain is the only functional domain of Sry, and

83 roteins are composed of one or two conserved HMG box domains, each forming three alpha-helices that f

84 mphoid enhancer factor (LEF) factors contain HMG domains and bind to related consensus sites.

85 finger domains (ZF1-3) and the corresponding HMG DNA-binding domain of TCF3/4 factors.

86 edded ubiquitin ligases, in yeast Hrd1/Der3 (HMG-CoA reductase degradation/degradation of the ER) and

87 experiments show that the drug can displace HMG box-containing proteins essential for kDNA function

88 We found that two out of eight HMG samples showed trisomy of chromosome 1q, which encom

89 sumoylation state of Caenorhabditis elegans HMG-CoA synthase (HMGS-1).

90 treatment and variants in the gene encoding HMG-CoA reductase are associated with reductions in both

91 this step was Sox17, encoding an endodermal HMG-box transcription factor.

92 BIAD1 to the cholesterol biosynthetic enzyme HMG CoA reductase, which is subject to sterol-accelerate

93 ERAD of the cholesterol biosynthetic enzyme HMG-CoA reductase.

94 pathway, including the rate-limiting enzyme HMG-CoA reductase.

95 re better in patients whose tumors expressed HMG-CoAR (p = 0.044 and p = 0.043).

96 y of TFAM is mainly contributed by its first HMG-box, while the second HMG-box has low-DNA-binding ca

97 ible wavelength spectrophotometric assay for HMG-CoA synthase has been developed.

98 225 MBC samples were immunostained for HMG-CoAR and 124 were considered eligible for exploring

99 ough HMGA1 (high-mobility group A1; formerly HMG-I/Y) is an oncogene that is widely overexpressed in

100 NA levels of the cholesterol synthesis genes HMG CoA reductase, squalene synthase, and FPP synthase b

101 le and multiple 3-hydroxy-3-methyl-glutaryl (HMG) substitutions.

102 d expression of 3-hydroxy-3-methyl-glutaryl (HMG)-CoA reductase (Hmg1) under iron starvation, reduced

103 an inhibitor of 3-hydroxy-3-methyl-glutaryl (HMG)-CoA reductase and the N-bisphosphonate zoledronic a

104 y prepared from isolated human milk glycans (HMGs), and our studies on their recognition by viruses,

105 support for the role of the N-terminal gp59 HMG motif in fork binding and the interaction of the C-t

106 group C of Sry-related high-mobility group (HMG) box (Sox) transcription factors has three members i

107 Y comprises a conserved high-mobility group (HMG) box DNA-binding domain and poorly conserved regions

108 a DNA sequence-specific high-mobility group (HMG) box that binds Wnt response elements (WREs).

109 sisting of a quartet of high-mobility group (HMG) box transcription factors, SOX4, SOX13, TCF1, and L

110 e Y chromosome)-related high mobility group (HMG) box) proteins require the calcium-binding protein c

111 ions cluster in the SRY high mobility group (HMG) box, a conserved motif of specific DNA binding and

112 inding is mediated by a high mobility group (HMG) box.

113 DNA sequences through a high mobility group (HMG) domain.

114 on factor A (TFAM) is a high-mobility group (HMG) protein at the nexus of mitochondrial DNA (mtDNA) r

115 chondria (TFAM), a dual high-mobility group (HMG) protein involved in maintenance and compaction of t

116 High mobility group (HMG) proteins concentrate in the nucleus, interacting wi

117 tural homology with the high mobility group (HMG) proteins from eukaryotic organisms.

118 x17) is a member of the high mobility group (HMG) transcription factor superfamily, which plays criti

119 High mobility group (HMG) transcription factors of the T-cell-specific transc

120 Here we show that the high-mobility group (HMG) transcription factors Tcf1 and Lef1 are essential f

121 reproduction in which a high mobility group (HMG) transcription-factor gene is flanked by triose-phos

122 tion of the SRY-related high mobility group (HMG)-box 4 (Sox4) gene in insulin secretion was tested u

123 eodomain, alpha-box, or high mobility group (HMG)-domain transcription factors.

124 proteins belong to the high-mobility-group (HMG) domain-containing transcription factors, and functi

125 e linker histone H1 and high-mobility-group (HMG) proteins with nucleosomes leads to changes in chrom

126 ng WDHD1 (WD repeat and high mobility group [HMG]-box DNA-binding protein), one of the genes that was

127 Hemimegalencephaly (HMG) is a developmental brain disorder characterized by

128 undant vertebrate chromosomal protein HMGB1 (HMG-D and ZmHMGB1, respectively) differ from HMGB1 in ha

129 The HRD (HMG-CoA reductase degradation) pathway is a conserved ro

130 amino acids are normally conserved in human HMG proteins and 27 are conserved in the human Sox sub-f

131 ollection as a previously unidentified human HMG-CoA lyase (HMGCL).

132 Hydroxmethylglutaryl (HMG)-coenzyme A (CoA) reductase inhibitors (statins) low

133 n vitro results with 24S-hydroxycholesterol, HMG CoA reductase and squalene synthase mRNA levels were

134 diminution of sterol synthesis, identifying HMG-CoA synthase as a potential drug target and suggesti

135 A total of 33 amino acids in HMG proteins are known to have natural variants in disea

136 lso causes a 65% protein content decrease in HMG-CoA reductase (HMGR) and a 28% decrease in sterol sy

137 addition, both fungi and humans deficient in HMG CoA lyase accumulate acidic intermediates as a conse

138 ovascular risk parameters via a reduction in HMG-CoA reductase activity, along with an increase in ar

139 ly, deletion of SET1 leads to a reduction in HMG-CoA reductase protein and total cellular ergosterol.

140 Numerous natural variants in HMG proteins are associated with disease phenotypes.

141 of antiviral and proviral agents, including HMG-CoA reductase inhibitors (antiviral) and corticoster

142 hen administered at a high dosage (including HMG-CoA reductase inhibitors >75 mg/day/adult).

143 ore rapidly after mTOR inhibition, including HMG-CoA synthase, whose enhanced degradation probably li

144 15(S)-HETE by inducing HMG-CoA reductase expression caused increased farnesylat

145 Statins inhibit HMG-CoA reductase, a key enzyme in cholesterol synthesis

146 Statins lower cholesterol by inhibiting HMG-CoA reductase, the rate-limiting enzyme of the metab

147 (HMG-CoA) synthase and irreversibly inhibits HMG-CoA synthase in a dose-dependent manner.

148 DNA looping assays in vivo that an isolated HMG box A domain derived from human HMGB2 folds poorly a

149 trate that TFAM is phosphorylated within its HMG box 1 (HMG1) by cAMP-dependent protein kinase in mit

150 The E3 ubiquitin ligase HMG-coA reductase degradation 1 homolog (Hrd1) and, cons

151 requirement for mitochondrial OPA3 to limit HMG-CoA-derived MGC and protect the electron transport c

152 Duplication of the mating type matA(HMG) gene in this haploid organism triggers Mat-induced

153 s as a specific feature associated with matA(HMG) regulation during sexual development.

154 m (ER)-localized 3-hydroxy-3-methylglutaryl (HMG) CoA reductase.

155 Mammalian 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase (HMGR) undergoes sterol-dependent, en

156 3-Hydroxy-3-methylglutaryl (HMG)-CoA reductase (HMGR), the rate-limiting enzymes of

157 eptor-binding motifs, SET methyltransferase, HMG and PHD domains.

158 pa3 mutants derives from extra-mitochondrial HMG-CoA through a non-canonical pathway.

159 d protein analysis identified, mitochondrial HMG-CoA synthase, aldehyde dehydrogenase, and catalase a

160 articularly high levels of the mitochondrial HMG-CoA synthase 2 (Hmgcs2) compared with all other tiss

161 Moreover, HMG-CoAR expression may be a favorable prognostic indica

162 ion, revealed the features of a noncanonical HMG box.

163 te myocardin function, we identified a novel HMG box-containing protein HMG2L1 (high mobility group 2

164 were similar to each other and to other NSS HMG-box proteins.

165 tive selection caused by loss of the nuclear HMG box protein TOX.

166 haromyces pombe, where the nucleocytoplasmic HMG protein Oxs1 acts cooperatively with Pap1 to regulat

167 W-FO) on serum and liver lipids, activity of HMG-CoA reductase in liver microsomes and EPA+DHA incorp

168 The activity of HMG-CoA reductase was reduced (p<0.05) in the FVW-FO fed

169 anti-HCV effects are reversed by addition of HMG-CoA, mevalonic acid, or geranylgeraniol.

170 hich may influence the binding affinities of HMG-domain proteins for Pt-GG adducts, and that these co

171 Statins, a class of HMG-CoA reductase inhibitors, display pleiotropic immuno

172 cated in the sterol-regulated degradation of HMG-CoA reductase and Insig-1 through ER-associated degr

173 the robust sterol-accelerated degradation of HMG-CoA reductase.

174 ole in the sterol-accelerated degradation of HMG-CoA reductase.

175 The DNA binding domain of HMG proteins is known to be important in many diseases,

176 ate, an inhibitor of an enzyme downstream of HMG-CoA reductase, and to gliotoxin, an inhibitor acting

177 de of geranyl lipid production downstream of HMG-CoA reductase.

178 ive study designed to evaluate the effect of HMG-CoA reductase inhibitors on atherosclerosis.

179 asma cholesterol levels, liver expression of HMG-CoA reductase was found to be approximately 2-fold l

180 ngly, renal as well as hepatic expression of HMG-CoA synthase 2 increased with prolonged starvation.

181 in many diseases, with the Sox sub-family of HMG proteins of particular significance.

182 The statin family of HMG-coenzyme A reductase inhibitors have potent anti-inf

183 genetic variant known to mimic inhibition of HMG-CoA reductase (the intended drug target) with the sa

184 maging sensor, we confirm that inhibition of HMG-CoA reductase blocks MYC phosphorylation in vivo.

185 Here, we show that inhibition of HMG-CoA reductase by atorvastatin (AT) blocks both MYC p

186 3 silencing or pharmacological inhibition of HMG-CoA reductase in these cells decreases protein isopr

187 The inhibition of HMG-CoA reductase may be a useful target for the treatme

188 Finally, we show that inhibition of HMG-CoA reductase suppresses MYC phosphorylation through

189 rs blocks their sensitivity to inhibition of HMG-CoA reductase.

190 s its anti-HCV effects through inhibition of HMG-CoA synthase.

191 Simvastatin, a potent inhibitor of HMG-CoA reductase, suppressed 15(S)-HETE-induced Rac1 ac

192 The interaction of HMG proteins with chromatin is dynamic.

193 nsmembrane span ER-resident Hmg2p isozyme of HMG-CoA reductase fused to GFP, which undergoes regulate

194 revealed by the early embryonic lethality of HMG-17 homozygous mice.

195 l fibrosis via FPRL1-dependent modulation of HMG-CoA reductase pathway.

196 pplementation with the enzymatic products of HMG-CoA reductase functionally rescued lymphangiogenic s

197 ase catalyzes the four-electron reduction of HMG-CoA to mevalonate and is an enzyme of considerable b

198 er increase in SREBP2 and down-regulation of HMG-CoA reductase protein.

199 tDNA transcription; second, that a subset of HMG-CoA reductase inhibitors, combined with propranolol,

200 ar free cholesterol, causing upregulation of HMG Co-A reductase, the rate-limiting enzyme in choleste

201 reased capture of ZOL and by upregulation of HMG-CoA synthase and reductase transcription.

202 sights into diverse recognition functions of HMGs and show the utility of the SGM approach and MAGS a

203 Further identification of serine ADPr on HMG proteins and hundreds of other targets indicates tha

204 Statins, or HMG CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductas

205 In other organisms, HMG CoA lyase catalyzes the last step in the leucine cat

206 of the rate-limiting enzyme in the pathway, HMG-CoA reductase (HMGCR).

207 olesterol metabolism proteins such as PCSK9, HMG-CoA reductase, ATP citrate lyase, and NPC1L1.

208 l components of red mold fermented products, HMG-CoA reductase inhibitors, did not exacerbate pre-exi

209 hypolipidemic property of FVW-FO and reduced HMG-CoA reductase activity which is proportional to the

210 droxy-3-methylglutaryl-coenzyme A reductase (HMG-CoA reductase) by statins has shown potential effica

211 droxy-3-methylglutaryl-coenzime A reductase (HMG-CoA) reductase.

212 ors during acute kidney injury that regulate HMG CoA reductase (HMGCR) activity, the rate-limiting st

213 actor sex-determining region Y (SRY)-related HMG box 2 (SOX2) in regulating the epigenetic landscape

214 iments indicated that the LSC is SRY-related HMG box transcription factor 9 positive (Sox9(+) ) and c

215 HMG box) that is invariant among SRY-related HMG box transcription factors (the SOX family) and conse

216 Sox genes code for SRY-related HMG domain-bearing transcription factors involved in var

217 The SRY-related HMG-box 5 (SOX5) gene encodes a member of the SOX family

218 The SRY-related HMG-box family of transcription factors member SOX2 regu

219 ciated transcription factor, and SRY-related HMG-box gene 10).

220 , including sex-determining region Y-related HMG box 2 (Sox2), a well established regulator of stem c

221 a and Sox9 (sex determining region Y-related HMG box transcription factor 9).

222 We studied resected HMG tissue to test whether the condition might reflect s

223 buted by its first HMG-box, while the second HMG-box has low-DNA-binding capability.

224 t stem cells specifically recognized several HMGs that were then further structurally defined as nove

225 of Mice also specifically recognized several HMGs.

226 The total neutral and sialylated HMGs were derivatized with a bifunctional fluorescent ta

227 egion Y) encode proteins containing a single HMG (high-mobility group) domain.

228 a protein that bent DNA similar to a single HMG box and only at higher protein concentrations.

229 tively) differ from HMGB1 in having a single HMG box, as well as basic and acidic flanking regions th

230 Wnt signaling repression domain in the SOX17 HMG box.

231 argeting activities of Oct4 (POU DBD), Sox2 (HMG box DBD), Klf4 (zinc finger DBD), and c-Myc (bHLH DB

232 r that is a fungal ortholog of the hSRY/SOX9 HMG box proteins.

233 Basal protein levels of SREBP2, HMG-CoA reductase, and steroidogenic acute regulatory pr

234 We found that Sry HMG box protein 9-positive (Sox9(+)) epithelial cell adh

235 nt, and hybrid MatA protein carrying the SRY HMG box is fully capable of driving both early and late

236 Statins (HMG-CoA reductase inhibitors) are the most prescribed cl

237 y deficient HMGCL R41M mutant with substrate HMG-CoA have been determined to 2.4 and 2.2 A, respectiv

238 -limiting enzymes for cholesterol synthesis, HMG CoA synthase (HMGCS1) and HMG CoA reductase (HMGCR),

239 binding protein HMGB1 consists of two tandem HMG-box domains joined by a basic linker to a C-terminal

240 in-induced upregulation of the statin target HMG-CoA reductase.

241 ns are cholesterol-lowering drugs, targeting HMG-CoA reductase, thereby reducing the risk of coronary

242 sive and cooperative binding of the two TFAM HMG-box domains and the linker between them.

243 asal branch within the fungi, indicates that HMG-domain proteins were present as ancestral sex determ

244 vere growth defect in BMDMs, indicating that HMG CoA lyase gene function is critical for macrophage c

245 There is experimental evidence to show that HMG-CoA reductase inhibitors (statins) may inhibit proli

246 analyses for 10-year survival suggested that HMG-CoAR expression is a protective factor (HR 0.50, 95%

247 findings demonstrate for the first time that HMG-CoA reductase plays a determinant role in 12/15-Lox-

248 The HMG box has structural conservation between the first tw

249 The HMG box transcription factor SOX4 involved in neuronal d

250 The HMG domain within HMGB2 is crucial for interaction with

251 The HMG-box transcription factor LEF1 controls many developm

252 The HMG-Box transcription factor SOX2 is expressed in neural

253 The HMG-COA reductase degradation 1 (HRD1) and degradation o

254 The HMG-CoA reductase inhibitors (statins) are widely prescr

255 The HMG-I/Y protein, proposed as orchestrating enhanceosome

256 /LSP complexes are dynamic entities, and the HMG boxes induce the U-turn against the tendency of the

257 ch are presumably displaced from DNA and the HMG boxes, respectively, in the HMGB1-nucleosome complex

258 es the PWWP domain of LEDGF proteins and the HMG domain of SSRP1.

259 We also show that BCL11A and the HMG-box-containing transcription factor SOX6 interact ph

260 Calcium/CaM directly binds the HMG domain of the BAF57 subunit within the BAF complex.

261 gh a bipartite mechanism, involving both the HMG domain and the C-clamp, which enables TCF to locate

262 Minor-groove DNA binding by the HMG box results in substantial DNA bending toward the ma

263 adult pituitary progenitors that express the HMG box transcription factors SOX2 and SOX9.

264 ondensation with acetoacetyl-CoA to form the HMG-CoA product.

265 codes an HMG-domain protein, implicating the HMG-domain proteins as an earlier form of fungal MAT loc

266 remarkable identity through evolution in the HMG box DNA-binding domain and in the C-terminal 33 resi

267 Proteins in the HMG family are important transcription factors.

268 tion elsewhere in the protein, including the HMG box.

269 Each of the HMG boxes and the C-terminal tail were evaluated for the

270 ulates DNA binding and bending by one of the HMG boxes in the FL protein.

271 f the tail with the DNA-binding faces of the HMG boxes.

272 oteins, including a divergent version of the HMG domain.

273 Individual sub-groups of the HMG family have specificity in the location of the third

274 Helices alpha1 and alpha2 of the HMG-box constitute the main p53-binding region.

275 LDLR SRE was observed in the presence of the HMG-CoA reductase inhibitor, lovastatin, when PP2A activ

276 The up-regulation of the HMG-CoA reductase pathway in the endothelium is the majo

277 nerves during embryogenesis and rely on the HMG domain containing Sox10 transcription factor for spe

278 ain and poorly conserved regions outside the HMG box.

279 arteriovenous angiogenesis by targeting the HMG-CoA reductase (HMGCR) pathway.

280 Here, we show that the HMG-box protein Capicua (Cic) restricts cell growth in D

281 Here we show that the HMG-box transcription factor, Sox9, is expressed in mult

282 et al., in this issue, demonstrates that the HMG-CoA reductase inhibitor lovastatin can normalize pro

283 ructure with fork DNA has suggested that the HMG-like domain could bind to the duplex DNA ahead of th

284 Depleting endogenous cholesterol with the HMG CoA reductase inhibitor lovastatin leads to a 2-fold

285 iposomes ([S]-LIP), that are loaded with the HMG-CoA reductase inhibitor simvastatin [S], were evalua

286 hyl-beta-cyclodextrin, 2) treatment with the HMG-CoA reductase inhibitor simvastatin, and 3) shRNA-me

287 were partially rescued by treatment with the HMG-CoA reductase inhibitor simvastatin.

288 ts of AT are blocked by cotreatment with the HMG-CoA reductase product mevalonate.

289 Therefore, HMG-CoA reductase is a critical regulator of MYC phospho

290 ay inhibitors targeting downstream enzyme to HMG-CoA reductase (upstream enzyme) and farnesyl-pyropho

291 HMGB1 contains two HMG boxes that bind and bend DNA (the A box and the B bo

292 Understanding HMG-CoA reductase regulation has tremendous implications

293 ction in HCV replication, further validating HMG-CoA synthase as an enzyme essential for HCV replicat

294 We show that despite these variations, HMG-D and ZmHMGB1 exist in dynamic assemblies in which t

295 evalonate, implying a dependence on vascular HMG-CoA reductase inhibition.

296 of low-density lipoprotein cholesterol with HMG-CoA reductase inhibitors (statins).

297 In comparison with HMG-CoA (CoA) synthase, the homologous enzyme from prima

298 idemia in mild to moderate CKD patients with HMG-CoA reductase inhibitors.

299 Overall survival was longer in patients with HMG-CoAR-positive tumors compared with their negative co

300 The yeast HMG-CoA reductase isozyme Hmg2, like its mammalian count