ライフサイエンスコーパス: MGP

1 MGP binds calcium ions through gamma-carboxylated glutam

2 MGP carboxylation status was not determined.

3 MGP colocalized intracellularly with BMP2.

4 MGP has also been identified as an inhibitor of bone mor

5 MGP has been shown to be an inhibitor of arterial wall a

6 MGP inhibited BMP-4 activity similarly to that of BMP-2

7 MGP inhibits calcification independent of BMP-2-driven o

8 MGP is a well-established inhibitor of calcification gen

9 MGP is also one of the most abundant genes in the trabec

10 MGP maps to chromosome 12p near D12S363.

11 MGP mRNA was assayed by relative quantitative and real-t

12 MGP overexpression reduced vascular BMP activity, athero

13 MGP promoter activity was also stimulated by BMP-4 in a

14 MGP protein is active and functions as an inhibitor of B

15 MGP requires to be activated by gamma-glutamyl carboxyla

16 MGP was a candidate on the basis of its localization to

17 MGP was also released into the medium and removed by ult

18 MGP/BMP2 colocalization was analyzed by confocal microsc

19 metallointercalator complex 1-Rh(MGP)2phi5+ [MGP = 4-(guanidylmethyl)-1,10-phenanthroline; phi = phen

20 BMP-4, MGP, ALK1, and ALK2 were predominantly expressed on the

21 y the cytomegalovirus (CMV; control, n = 6), MGP (n = 6), or VE-cad (n = 12) promoters.

22 agulation factor carboxylation and abolished MGP carboxylation at the physiological concentration of

23 vus and 20 E. gallinarum isolates) acidified MGP, 41 of 46 (89%) were LM and ARA positive, and 45 of

24 hanism represented by the presence of active MGP appears to be compromised in glaucomatous tissue.

25 Mice deficient in MGP alone (MGP(-/-) OPN(+/+)) showed calcification of their arterie

26 trate, methyl-alpha-D-glucopyranoside (alpha-MGP), stimulated release, whereas the SGLT1 inhibitor ph

27 ed larger GLP-1 responses than luminal alpha-MGP in matched concentrations.

28 zin (luminally) abolished responses to alpha-MGP and glucose.

29 n factor carboxylation but do not ameliorate MGP carboxylation.

30 we discuss how this can be implemented in an MGP framework and illustrate its application to simple m

31 years ago from the duplication of an ancient MGP gene and may exhibit intermediate functional feature

32 CGP and MGP studies identified resilient species with stress tol

33 and molecular mechanisms involved in CGP and MGP.

34 is expressed in endothelial cells (EC), and MGP deficiency results in developmental defects suggesti

35 proteins (a chimeric coagulation factor and MGP) in HEK293 cells.

36 ot in the binding of coagulation factors and MGP.

37 fication inhibitory activities of fetuin and MGP may be related to their ability to form stable compl

38 ain structure to fetuin and, like fetuin and MGP, contains several residues of phosphoserine and accu

39 ions suggest that spp24 may, like fetuin and MGP, play a role in inhibiting calcification.

40 00F carboxylation was poor with both FIX and MGP.

41 Additional studies analyzed FIX- and MGP-derived peptides containing the Gla domain linked to

42 inhibited BMP-dependent neuronal growth and MGP expression increased in sympathetic neurons during t

43 n tumor angiogenesis, and identifies ID4 and MGP as possible therapeutic targets for GBM.

44 mm), phosphate by 1.6-fold (to 5.6 mm), and MGP by 25-fold (to 12 microg/ml).

45 fication and characterization of both OC and MGP from the Adriatic sturgeon, a ray-finned fish charac

46 OC, ON, and MGP were present in the deposits and vascular endothelia

47 showed significant upregulation of THBS2 and MGP genes in CD subserosa compared to the submucosa.

48 Expression of VEGF and MGP was induced by TGF-beta1, but the induction of MGP p

49 dem actions of the extracellular antagonists MGP and CV2.

50 tain MGP, was found to be recognized by anti-MGP antibodies.

51 TDC5 cells with inducible sense or antisense MGP cDNA constructs, we found that overexpression of MGP

52 3/4, AnkG, and MUC1 but not TM markers AQP1, MGP, CHI3L1, or TIMP3.

53 had twice as much arterial calcification as MGP(-/-) OPN(+/+) at 2 wk, and over 3 times as much at 4

54 Because MGP protein has been shown to play a key role in inhibit

55 tion, which modified the association between MGP and albuminuria.

56 To detect binding between MGP and BMP-2, we performed immunoprecipitation using MG

57 linking, and blocked the interaction between MGP and BMP-4.

58 The interaction between MGP and HSP70 was confirmed by coimmunoprecipitation and

59 HSP70 binds MGP and enhances BMP activity, thereby functioning as a

60 Importantly, mice deficient in both MGP and OPN had twice as much arterial calcification as

61 g for negative feedback regulation of BMP by MGP.

62 rrected the craniofacial anomalies caused by MGP deficiency, suggesting a local role for MGP in the d

63 identified by Luminex (for types detected by MGP PCR) or direct sequencing or cloning before sequenci

64 elial-epithelial interactions, maintained by MGP, are essential in pulmonary cell differentiation.

65 n of the calcification mechanism mediated by MGP could be used to regulate resistance and elevated IO

66 Heterozygous 'knock-in' mice expressing C19F MGP recapitulate most of the skeletal anomalies observed

67 mRNAs were not detected in either calcified MGP(-/-) or noncalcified wild-type (MGP(+/+)) vessels.

68 uncarboxylated MGP (ucMGP) and carboxylated MGP (cMGP) than controls.

69 truct, which produced non-gamma-carboxylated MGP and fully gamma-carboxylated MGP.

70 arboxylated MGP and fully gamma-carboxylated MGP.

71 ssociate with reduced levels of carboxylated MGP, and inhibitory effects of quercetin do not involve

72 n, shown by mass spectrometry not to contain MGP, was found to be recognized by anti-MGP antibodies.

73 Conversely, MGP deficiency increased BMP activity, which may explain

74 arboxylase activity and were able to convert MGP to its active conformation.

75 ood vessels of matrix Gla protein deficient (MGP(-/-)) mice.

76 Inactive vitamin K-dependent MGP (desphospho-uncarboxylated [dp-uc] MGP) and prothrom

77 Inactive vitamin K-dependent MGP (dp-ucMGP) and prothrombin (PIVKA-II) were measured,

78 Expression of the gene encoding MGP was reduced in the glaucomatous tissue by -4.4 +/- 1

79 These experiments establish MGP as a novel regulator of BMP function in the nervous

80 in, the differentiating chondrocytes express MGP in a stage-specific biphasic manner as in vivo.

81 This highly specific complex of fetuin, MGP, and mineral prevents the growth, aggregation, and p

82 C1QL3, CBLN2, CNTN4, CYP19A1, ESR1/2, FEZF2, MGP, NECAB2, PCP4, PVALB, SCN3B, SCUBE1, ZBTB20, and oth

83 ybridization demonstrated that the genes for MGP and Ank were expressed locally in vibrissae, whereas

84 MGP or an intracellular carrier protein for MGP.

85 accumulation overlap with those reported for MGP; OC was detected in bone cells and mineralized struc

86 MGP deficiency, suggesting a local role for MGP in the developing nasal septum.

87 MGP dictates different transport routes for MGP in VSMCs.

88 The main advantages that follow from MGPs approach include the natural non-parametric represe

89 All three mutations predict a non-functional MGP.

90 The matrix GLA (MGP) gene has been found to be among the 10 most highly

91 g the inhibitor of calcification matrix Gla (MGP) in the trabecular meshwork cells.

92 When methyl-alpha-D-glucopyranoside (MGP) molecules are reacted with hexamethylene diisocyana

93 ification of methyl-alpha-D-glucopyranoside (MGP), and rapid motility (RM), for differentiating isola

94 We investigated how MGP carboxylation influences the risk of calciphylaxis i

95 for atherosclerosis, levels of BMP-4, HSP70, MGP, and interleukin-6 were elevated in the aortic wall.

96 Human MGP is a 10-kD skeletal extracellular matrix (ECM) prote

97 c EC with increasing concentrations of human MGP (hMGP) for 24 h.

98 orphisms in the promoter region of the human MGP gene.

99 F (IGFBP6, CTSK, LGALS1, and CCN3), and iAF (MGP, COMP, SPP1, GSN, SOD2, DCN, FN1, TIMP3, WDR73, and

100 ndem mass spectrometric analysis to identify MGP-binding proteins.

101 In MGP a subpopulation of neurons exhibiting low NR2D signa

102 ion, and the development of cerebral AVMs in MGP null (Mgp(-/-)) mice.

103 ults suggest that BMP and calcium binding in MGP are independent but functionally intertwined process

104 The importance of elastin calcification in MGP null vascular disease is highlighted by significant

105 se calcification of vascular medial cells in MGP deficient aortas and the increase in expression of a

106 osclerotic lesion formation was decreased in MGP-deficient mice, which may be explained by a dramatic

107 Mice deficient in MGP alone (MGP(-/-) OPN(+/+)) showed calcification of th

108 Our data indicate that mutations in MGP are responsible for KS and confirm its role in the r

109 ndings support that heterozygous variants in MGP altering the Cys19 residue cause autosomal dominant

110 d families with two heterozygous variants in MGP, both altering the cysteine 19 residue to phenylalan

111 ontains structural features usually found in MGPs (e.g. a putative phosphorylated propeptide).

112 Increased MGP expression inhibited BMP-dependent neuronal growth a

113 n effect that may be limited by ALK1-induced MGP.

114 cted that BMP4 and BMP9 and their inhibitors MGP (matrix gamma-carboxyglutamic acid [Gla] protein) an

115 tein the most gamma-carboxylated among known MGPs.

116 stribution and accumulation typical of known MGPs, and it contains seven possible Gla residues that w

117 lyethylene glycol (PEG) to form cross-linked MGP-polyurethane (PUR) networks, these materials are cap

118 Mechanistically, MGP deficiency increased BMP activity in lungs.

119 a vitamin K-dependent enzyme, which mediates MGP carboxylation.

120 In the mouse model, MGP null vascular disease presents as calcifying cartila

121 ross generation (CGP) and multigenerational (MGP) plasticity have been identified as mechanisms of ac

122 thered publicly available information on NGS-MGP from 5 commercial laboratories for the following: ca

123 generation sequencing multigene panels (NGS-MGP) from 5 commercial laboratories to inform ophthalmol

124 prospective diagnostic yield studies of NGS-MGPs will aid in making decisions of panel selection for

125 The genetic testing of CASAs using NGS-MGPs is complicated, owing to their number, variety, and

126 content, increased ALP, decreased normalized MGP expression and lower gamma-carboxylase activity.

127 soluble in serum, was identified as a novel MGP-binding protein.

128 further studied in matrix GLA protein null (MGP(-/-)) mice whose arteries spontaneously calcify.

129 treatment of cells led to loss of ability of MGP to bind BMP-4.

130 The ability of MGP to inhibit calcification requires the activity of a

131 Acidification of MGP was therefore the single most useful test for differ

132 evere COVID-19 due to impaired activation of MGP and endothelial protein S, respectively.

133 evere COVID-19 due to impaired activation of MGP and endothelial protein S, respectively.

134 As a result, activation of MGP by gamma-glutamyl carboxylase is diminished, allowin

135 Mutational analysis of MGP in three unrelated probands identified three differe

136 ynthesis and that the gamma-carboxylation of MGP is necessary for its binding to the serum mineral co

137 Aortic content of MGP mRNA was increased 5-fold in renal failure but did n

138 The effect of MGP mutagenesis on vascular calcification was determined

139 This study showed that the effect of MGP on ALK1 signaling and VEGF expression in bovine aort

140 To quantify the effect of MGP on BMP-2 activity, we assayed for alkaline phosphata

141 ed VEGF expression, we studied the effect of MGP on the activity of transforming growth factor (TGF)-

142 antibodies to TGF-beta blocked the effect of MGP on VEGF expression.

143 Oscillations in the expression of MGP and CV2 were detected in endothelial cells in vitro,

144 tion of ALK1 signaling induced expression of MGP in addition to that of VEGF, allowing for negative f

145 Immunohistochemistry showed expression of MGP, but not THBS2 in submucosa in UC and CD.

146 GFbeta1 and BMP9 stimulate the expression of MGP, which limits the enhanced ALK1 induction by counter

147 onal, more acidic Ser-phosphorylated form of MGP believed to be the product of Golgi casein kinase.

148 Both forms of MGP were found in the cytosolic and microsomal fractions

149 eriments show that the anti-ECMM function of MGP requires four amino acids which are gamma-carboxylat

150 ) does not display the anti-ECMM function of MGP.

151 To examine the impact of MGP on the onset and progression of CKD, various mouse m

152 se-dependent, that a progressive increase of MGP levels ceased to be stimulatory and instead turned i

153 vels on ALK1 expression and the induction of MGP and VEGF.

154 l interfering RNA abolished the induction of MGP and VEGF.

155 cts of quercetin do not involve induction of MGP carboxylation.

156 s induced by TGF-beta1, but the induction of MGP preceded that of VEGF, consistent with a promoting e

157 Inhibition of MGP resulted in smaller and less vascularized xenografts

158 Because lack of MGP also causes arterial calcification, our findings dem

159 Increased BMP activity due to the lack of MGP induces expression of the activin receptor-like kina

160 In contrast, raising the serum level of MGP does not affect mineralization of any ECM.

161 High levels of MGP (>15-fold excess), however, resulted in pronounced e

162 ing studies showed that inhibitory levels of MGP abolished BMP-2 receptor binding.

163 his work suggests that coordinated levels of MGP are required for chondrocyte differentiation and mat

164 Low levels of MGP relative to BMP-2 (<1-fold excess) resulted in mild

165 Enhancing levels of MGP resulted in increased Smad1 activation.

166 Inhibitory levels of MGP yielded increased matrix binding of BMP-2, suggestin

167 Loss of MGP or its BMP4-binding capacity disrupted the retinal v

168 ependent gamma-carboxylation modification of MGP.

169 However, overexpression of MGP during the hypertrophic phase has no effect on chond

170 Overexpression of MGP in HTM cells reduced ALP activity in a model of BMP2

171 constructs, we found that overexpression of MGP in maturing chondrocytes and underexpression of MGP

172 The data suggest that phosphorylation of MGP dictates different transport routes for MGP in VSMCs

173 ed to identify a larger soluble precursor of MGP or an intracellular carrier protein for MGP.

174 lar localization of BMP-2 in the presence of MGP, binding assays were performed on whole cells and ce

175 Further, down-regulation of MGP by shRNA does not alter the effect of quercetin.

176 To determine the role of MGP in EC, we cultured bovine aortic EC with increasing

177 e of this study was to determine the role of MGP in the vasculature of the lungs and kidneys.

178 )-injured kidneys are the primary sources of MGP production.

179 ct on ALK1 expression and the stimulation of MGP and VEGF expression were dependent on signaling by t

180 Studies of MGP-deficient mice suggest that MGP is an inhibitor of e

181 Synthesis of MGP is increased in renal failure and deficiency of GlaM

182 on intracellular processing and transport of MGP to become an extracellular binding protein for bone

183 maturing chondrocytes and underexpression of MGP in proliferative and hypertrophic chondrocytes induc

184 mined the effects of vitamin K deficiency on MGP carboxylation.

185 Only MGP proteins with preserved ability to bind and inhibit

186 We used MGP transgenic or MGP-deficient mice bred to apolipoprotein E mice, a mode

187 thelial population with signs of oscillatory MGP expression in developing vasculature supported the i

188 pallidus (LGP), and medial globus pallidus (MGP).

189 ation) from a former manufactured gas plant (MGP) site was treated in a laboratory scale bioreactor (

190 Unlike plants, MGP-PUR networks require no photo-initiated reactions, a

191 In the mammalian growth plate, MGP is expressed by proliferative and late hypertrophic

192 methyl-D-glucose-containing polysaccharides (MGPs), synthetic 6-O-methyl-D-glucose-containing polysac

193 ain reactions with modified general primers (MGP) and Forslund-Antonsson primers (FAP) and identified

194 ed, multivariate genotype-phenotype (process MGP) approach to determine the overall contributions to

195 based on multiple-output Gaussian processes (MGPs), which are a flexible non-parametric Bayesian mode

196 Matrix gamma-carboxyglutamic acid protein (MGP) is a member of the vitamin K-dependent protein fami

197 Matrix gamma-carboxyglutamic acid protein (MGP) is a mineral-binding extracellular matrix protein s

198 ts of matrix gamma-carboxyglutamate protein (MGP).

199 is and is antagonized by matrix Gla protein (MGP) and crossveinless 2 (CV2), both induced by the acti

200 MP-4; the BMP inhibitors matrix Gla protein (MGP) and Noggin; activin-like kinase receptor (ALK)1, -2

201 est an important role of matrix Gla protein (MGP) and thrombospondin 2 (THBS2) in fibrosis in various

202 Osteocalcin (OC) and matrix Gla protein (MGP) are considered evolutionarily related because they

203 sis of the properties of matrix Gla protein (MGP) as a vitamin K-dependent calcification inhibitor.

204 eral, 80% fetuin, and 2% matrix Gla protein (MGP) by weight, and the presence of the complex in serum

205 ing and/or inhibition of matrix Gla protein (MGP) carboxylation.

206 unction mutations in the matrix Gla protein (MGP) gene.

207 Matrix GLA protein (MGP) has been identified as a calcification inhibitor in

208 Matrix GLA protein (MGP) has previously been shown to enhance expression of

209 Mutations in matrix Gla protein (MGP) have been correlated with vascular calcification.

210 Matrix Gla protein (MGP) is a 14-kD extracellular matrix protein of the mine

211 Matrix Gla protein (MGP) is a potent inhibitor of vascular calcification.

212 Matrix Gla protein (MGP) is a vitamin K-dependent post-translationally modif

213 Matrix Gla protein (MGP) is an antagonist of BMPs that is highly expressed i

214 Matrix Gla protein (MGP) is an inhibitor of vascular calcification but its m

215 Matrix GLA protein (MGP) is expressed in endothelial cells (EC), and MGP def

216 Matrix GLA protein (MGP) is ubiquitously expressed with high accumulation in

217 t mice were crossed with matrix Gla protein (MGP) mutant mice.

218 he loss of BMP inhibitor matrix Gla protein (MGP) shows induction of Hoxd3.

219 s and expressed elevated matrix GLA protein (MGP) that mediated enhanced tumor angiogenesis.

220 the proteins fetuin and matrix Gla protein (MGP) that was initially discovered in serum of rats trea

221 show that deficiency of matrix Gla protein (MGP), a BMP inhibitor, causes induction of Notch ligands

222 ased expression of serum matrix Gla protein (MGP), a potent inhibitor of soft tissue calcification, i

223 nduced the expression of matrix Gla protein (MGP), a regulator of BMP function in the vascular system

224 sulting from the loss of matrix Gla protein (MGP), causes ectopic hepatic differentiation in the pulm

225 eric coagulation factor, matrix Gla protein (MGP), or osteocalcin as VKD reporter proteins, and then

226 ion in the expression of matrix Gla protein (MGP), osteopontin (OPN), and vascular calcification-asso

227 Vitamin K also activates matrix Gla protein (MGP), which protects against pulmonary and vascular elas

228 s, in part, prevented by matrix Gla protein (MGP).

229 ors osteonectin (ON) and matrix Gla protein (MGP).

230 to reduced fetuin-A and matrix gla-protein (MGP) levels.

231 itive immunostaining for matrix-gla-protein (MGP), fetuin-A, and ankylosis protein (Ank) as well as a

232 [FIX]) or calcification (matrix Gla protein [MGP]) were reacted in the presence of a challenge VKD pr

233 ent with binding models in which Lambda-1-Rh(MGP)2phi5+ (Lambda-Rh) traps the recognition site 5'-CAT

234 e symmetric metallointercalator complex 1-Rh(MGP)2phi5+ [MGP = 4-(guanidylmethyl)-1,10-phenanthroline

235 obility assays demonstrated that Lambda-1-Rh(MGP)2phi5+ at 120 nM competes 50% of yAP-1 binding to th

236 The metallointercalator Lambda-1-Rh(MGP)2phi5+ binds tightly and specifically to the site 5'

237 , the preferred binding site for Lambda-1-Rh(MGP)2phi5+ was engineered into the AP-1 recognition elem

238 , including geometric isomers of Lambda-1-Rh(MGP)2phi5+, show no specific binding to the target site

239 a high-affinity binding site for Lambda-1-Rh(MGP)2phi5+, whereas the native ARE showed no interaction

240 the native ARE requires 3 microM Lambda-1-Rh(MGP)2phi5+.

241 -sectional study of patients with CKD, serum MGP levels were found to be associated with albuminuria

242 nist warfarin prevents the increase in serum MGP after etidronate injection, which shows that the inc

243 tion, which shows that the increase in serum MGP is due to new synthesis and that the gamma-carboxyla

244 ression were independent of changes in serum MGP.

245 138C) is significantly correlated with serum MGP levels in human subjects.

246 Silencing MGP by siRNA resulted in ALP activity that was increased

247 Since MGP is an insoluble matrix protein, this work has focuse

248 Sturgeon MGP shows a primary structure, post-translation modifica

249 odel expressing hemagglutinin epitope-tagged MGP, it was identified that pericytes in healthy kidneys

250 othelial cells with N-terminally FLAG-tagged MGP and used immunoprecipitation and liquid chromatograp

251 significantly earlier (4.4 +/- 0.2 wk) than MGP(-/-) OPN(+/+) counterparts (6.6 +/- 1.0 wk).

252 The fact that MGP is present in the general circulation raises the que

253 on of Matrix gla protein (Mgp) revealed that MGP is an inhibitor of ECMM.

254 These results suggest that MGP is a BMP-2 regulatory protein.

255 Studies of MGP-deficient mice suggest that MGP is an inhibitor of extracellular matrix calcificatio

256 Together, these results suggest that MGP modulates BMP activity.

257 Together, the results suggest that MGP plays a role in EC function, altering the response t

258 nthesis inhibitor cyclohexamide suggest that MGP, OPN, and VCAF mRNA abundance are controlled at diff

259 sed matrix binding of BMP-2, suggesting that MGP inhibits BMP-2 in part via matrix association.

260 This work suggests that MGP expression in myofibroblasts exacerbates renal fibro

261 The MGP promoter fragment resulted in beta-galactosidase exp

262 Directed expression by the MGP gene promoter specifically to the trabecular meshwor

263 ere infected with an adenovirus carrying the MGP construct, which produced non-gamma-carboxylated MGP

264 Biallelic loss-of-function variants in the MGP gene cause Keutel syndrome, an autosomal recessive d

265 e suggests that a common polymorphism of the MGP promoter influences binding of the AP-1 complex, whi

266 However, the fraction of total MGP that was carboxylated (relative cMGP concentration =

267 ting CAC, independent of its effect on total MGP concentrations.

268 alcified MGP(-/-) or noncalcified wild-type (MGP(+/+)) vessels.

269 ndent MGP (desphospho-uncarboxylated [dp-uc] MGP) and prothrombin (PIVKA-II) were measured inversely

270 concentration = cMGP/[cMGP + uncarboxylated MGP]) was lower in cases than in controls (0.58+/-0.02 v

271 s had higher plasma levels of uncarboxylated MGP (ucMGP) and carboxylated MGP (cMGP) than controls.

272 We used MGP transgenic or MGP-deficient mice bred to apolipoprot

273 MP-2, we performed immunoprecipitation using MGP and BMP-2 tagged with FLAG and c-Myc.

274 ification in cartilage and arterial vessels, MGP's function in human TM was investigated.

275 The objective was to determine whether MGP also binds other proteins, which could interfere wit

276 To test whether MGP affects BMP-induced differentiation, three sets of e

277 esults showed co-precipitation of BMP-2 with MGP.

278 ts in vascular calcification associated with MGP dysfunction and emphasize the need for a comprehensi

279 eries was greatly up-regulated compared with MGP wild-types.

280 Treatment of the ATDC5 cultures with MGP antiserum during the proliferative phase leads to th

281 estern blot analyses were cross-reacted with MGP N-terminal- and conformational-specific antibodies.

282 the Ins2(Akita/+) mice by breeding them with MGP transgenic mice, which increased aortic BMP inhibiti

283 without loss of function and that zebrafish MGP, which lacks upstream Gla residues, did not function