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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 maps to chromosome 12p near D12S363.
9 MGP mRNA was assayed by relative quantitative and real-t
10 MGP overexpression reduced vascular BMP activity, athero
11 MGP promoter activity was also stimulated by BMP-4 in a
12 MGP protein is active and functions as an inhibitor of B
13 MGP requires to be activated by gamma-glutamyl carboxyla
14 MGP was a candidate on the basis of its localization to
15 MGP was also released into the medium and removed by ult
16 MGP/BMP2 colocalization was analyzed by confocal microsc
17 metallointercalator complex 1-Rh(MGP)2phi5+ [MGP = 4-(guanidylmethyl)-1,10-phenanthroline; phi = phen
20 agulation factor carboxylation and abolished MGP carboxylation at the physiological concentration of
21 vus and 20 E. gallinarum isolates) acidified MGP, 41 of 46 (89%) were LM and ARA positive, and 45 of
22 hanism represented by the presence of active MGP appears to be compromised in glaucomatous tissue.
24 trate, methyl-alpha-D-glucopyranoside (alpha-MGP), stimulated release, whereas the SGLT1 inhibitor ph
28 we discuss how this can be implemented in an MGP framework and illustrate its application to simple m
29 years ago from the duplication of an ancient MGP gene and may exhibit intermediate functional feature
30 is expressed in endothelial cells (EC), and MGP deficiency results in developmental defects suggesti
32 fication inhibitory activities of fetuin and MGP may be related to their ability to form stable compl
33 ain structure to fetuin and, like fetuin and MGP, contains several residues of phosphoserine and accu
35 inhibited BMP-dependent neuronal growth and MGP expression increased in sympathetic neurons during t
38 fication and characterization of both OC and MGP from the Adriatic sturgeon, a ray-finned fish charac
42 TDC5 cells with inducible sense or antisense MGP cDNA constructs, we found that overexpression of MGP
44 had twice as much arterial calcification as MGP(-/-) OPN(+/+) at 2 wk, and over 3 times as much at 4
52 rrected the craniofacial anomalies caused by MGP deficiency, suggesting a local role for MGP in the d
53 identified by Luminex (for types detected by MGP PCR) or direct sequencing or cloning before sequenci
54 elial-epithelial interactions, maintained by MGP, are essential in pulmonary cell differentiation.
55 n of the calcification mechanism mediated by MGP could be used to regulate resistance and elevated IO
56 mRNAs were not detected in either calcified MGP(-/-) or noncalcified wild-type (MGP(+/+)) vessels.
60 ssociate with reduced levels of carboxylated MGP, and inhibitory effects of quercetin do not involve
61 n, shown by mass spectrometry not to contain MGP, was found to be recognized by anti-MGP antibodies.
69 ybridization demonstrated that the genes for MGP and Ank were expressed locally in vibrissae, whereas
71 accumulation overlap with those reported for MGP; OC was detected in bone cells and mineralized struc
79 ification of methyl-alpha-D-glucopyranoside (MGP), and rapid motility (RM), for differentiating isola
81 for atherosclerosis, levels of BMP-4, HSP70, MGP, and interleukin-6 were elevated in the aortic wall.
88 ults suggest that BMP and calcium binding in MGP are independent but functionally intertwined process
89 The importance of elastin calcification in MGP null vascular disease is highlighted by significant
90 se calcification of vascular medial cells in MGP deficient aortas and the increase in expression of a
91 osclerotic lesion formation was decreased in MGP-deficient mice, which may be explained by a dramatic
98 stribution and accumulation typical of known MGPs, and it contains seven possible Gla residues that w
99 lyethylene glycol (PEG) to form cross-linked MGP-polyurethane (PUR) networks, these materials are cap
103 content, increased ALP, decreased normalized MGP expression and lower gamma-carboxylase activity.
105 further studied in matrix GLA protein null (MGP(-/-)) mice whose arteries spontaneously calcify.
111 ynthesis and that the gamma-carboxylation of MGP is necessary for its binding to the serum mineral co
116 ed VEGF expression, we studied the effect of MGP on the activity of transforming growth factor (TGF)-
118 tion of ALK1 signaling induced expression of MGP in addition to that of VEGF, allowing for negative f
119 onal, more acidic Ser-phosphorylated form of MGP believed to be the product of Golgi casein kinase.
121 eriments show that the anti-ECMM function of MGP requires four amino acids which are gamma-carboxylat
123 se-dependent, that a progressive increase of MGP levels ceased to be stimulatory and instead turned i
127 s induced by TGF-beta1, but the induction of MGP preceded that of VEGF, consistent with a promoting e
130 Increased BMP activity due to the lack of MGP induces expression of the activin receptor-like kina
134 his work suggests that coordinated levels of MGP are required for chondrocyte differentiation and mat
141 constructs, we found that overexpression of MGP in maturing chondrocytes and underexpression of MGP
142 The data suggest that phosphorylation of MGP dictates different transport routes for MGP in VSMCs
144 lar localization of BMP-2 in the presence of MGP, binding assays were performed on whole cells and ce
148 ct on ALK1 expression and the stimulation of MGP and VEGF expression were dependent on signaling by t
151 on intracellular processing and transport of MGP to become an extracellular binding protein for bone
152 maturing chondrocytes and underexpression of MGP in proliferative and hypertrophic chondrocytes induc
157 ation) from a former manufactured gas plant (MGP) site was treated in a laboratory scale bioreactor (
160 methyl-D-glucose-containing polysaccharides (MGPs), synthetic 6-O-methyl-D-glucose-containing polysac
161 ain reactions with modified general primers (MGP) and Forslund-Antonsson primers (FAP) and identified
162 based on multiple-output Gaussian processes (MGPs), which are a flexible non-parametric Bayesian mode
163 Matrix gamma-carboxyglutamic acid protein (MGP) is a member of the vitamin K-dependent protein fami
164 Matrix gamma-carboxyglutamic acid protein (MGP) is a mineral-binding extracellular matrix protein s
166 is and is antagonized by matrix Gla protein (MGP) and crossveinless 2 (CV2), both induced by the acti
167 MP-4; the BMP inhibitors matrix Gla protein (MGP) and Noggin; activin-like kinase receptor (ALK)1, -2
168 Osteocalcin (OC) and matrix Gla protein (MGP) are considered evolutionarily related because they
169 sis of the properties of matrix Gla protein (MGP) as a vitamin K-dependent calcification inhibitor.
170 eral, 80% fetuin, and 2% matrix Gla protein (MGP) by weight, and the presence of the complex in serum
184 the proteins fetuin and matrix Gla protein (MGP) that was initially discovered in serum of rats trea
185 show that deficiency of matrix Gla protein (MGP), a BMP inhibitor, causes induction of Notch ligands
186 nduced the expression of matrix Gla protein (MGP), a regulator of BMP function in the vascular system
187 sulting from the loss of matrix Gla protein (MGP), causes ectopic hepatic differentiation in the pulm
188 ion in the expression of matrix Gla protein (MGP), osteopontin (OPN), and vascular calcification-asso
192 itive immunostaining for matrix-gla-protein (MGP), fetuin-A, and ankylosis protein (Ank) as well as a
193 ent with binding models in which Lambda-1-Rh(MGP)2phi5+ (Lambda-Rh) traps the recognition site 5'-CAT
194 e symmetric metallointercalator complex 1-Rh(MGP)2phi5+ [MGP = 4-(guanidylmethyl)-1,10-phenanthroline
195 obility assays demonstrated that Lambda-1-Rh(MGP)2phi5+ at 120 nM competes 50% of yAP-1 binding to th
197 , the preferred binding site for Lambda-1-Rh(MGP)2phi5+ was engineered into the AP-1 recognition elem
198 , including geometric isomers of Lambda-1-Rh(MGP)2phi5+, show no specific binding to the target site
199 a high-affinity binding site for Lambda-1-Rh(MGP)2phi5+, whereas the native ARE showed no interaction
201 nist warfarin prevents the increase in serum MGP after etidronate injection, which shows that the inc
202 tion, which shows that the increase in serum MGP is due to new synthesis and that the gamma-carboxyla
208 othelial cells with N-terminally FLAG-tagged MGP and used immunoprecipitation and liquid chromatograp
213 Studies of MGP-deficient mice suggest that MGP is an inhibitor of extracellular matrix calcificatio
216 nthesis inhibitor cyclohexamide suggest that MGP, OPN, and VCAF mRNA abundance are controlled at diff
220 ere infected with an adenovirus carrying the MGP construct, which produced non-gamma-carboxylated MGP
221 e suggests that a common polymorphism of the MGP promoter influences binding of the AP-1 complex, whi
225 concentration = cMGP/[cMGP + uncarboxylated MGP]) was lower in cases than in controls (0.58+/-0.02 v
226 s had higher plasma levels of uncarboxylated MGP (ucMGP) and carboxylated MGP (cMGP) than controls.
233 ts in vascular calcification associated with MGP dysfunction and emphasize the need for a comprehensi
236 estern blot analyses were cross-reacted with MGP N-terminal- and conformational-specific antibodies.
237 the Ins2(Akita/+) mice by breeding them with MGP transgenic mice, which increased aortic BMP inhibiti
238 without loss of function and that zebrafish MGP, which lacks upstream Gla residues, did not function
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