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1 xylase activity and in undercarboxylation of matrix gla protein.
2  may be related to loss of regulation of the matrix Gla protein.
3 osphatase, osteoprotegerin, osteopontin, and matrix Gla protein.
4 ar calcification, mice with gene deletion of matrix Gla protein, a bone morphogenetic protein (BMP)-i
5  express bone-associated genes (osteopontin, matrix gla protein, alkaline phosphatase, and the transc
6 s with MS globally expressed lower levels of matrix Gla protein and osteonectin, whereas alkaline pho
7 jury, suggesting a prominent association for matrix Gla protein and osteopontin in ABCC6-related dyst
8 -regulation of the mineralization inhibitors matrix Gla protein and osteopontin.
9 nd calcification inhibitors osteoprotegerin, matrix Gla protein, and osteopontin.
10 ally expressed in the lymphatic endothelium (matrix Gla protein, apolipoprotein D precursor, and sele
11  beta-catenin and induction of periostin and matrix gla protein but does not induce genes associated
12 e-specific gene SM22alpha and high levels of matrix Gla protein but little osteopontin mRNA.
13 s of mineralization, such as osteopontin and matrix Gla protein, but not osteocalcin, were concomitan
14 rboxylase activity results in a reduction of matrix gla protein carboxylation, thus allowing peripher
15 yte-like cells in calcified blood vessels of matrix Gla protein deficient (MGP(-/-)) mice.
16                                    Moreover, matrix Gla protein-depleted human aortic endothelial cel
17                               Enhancement of matrix Gla protein expression in Ins2Akita/+ mice, as me
18 values for six of the propeptides (factor X, matrix Gla protein, factor VII, factor IX, PRGP1, and pr
19 s, has evolved via animal models such as the matrix gla protein, knock-out, and the targeted overexpr
20 ntial for angiogenesis and is antagonized by matrix Gla protein (MGP) and crossveinless 2 (CV2), both
21 ssion of BMP-2 and BMP-4; the BMP inhibitors matrix Gla protein (MGP) and Noggin; activin-like kinase
22                         Osteocalcin (OC) and matrix Gla protein (MGP) are considered evolutionarily r
23 n proposed on the basis of the properties of matrix Gla protein (MGP) as a vitamin K-dependent calcif
24 sts of about 18% mineral, 80% fetuin, and 2% matrix Gla protein (MGP) by weight, and the presence of
25  beta-catenin signaling and/or inhibition of matrix Gla protein (MGP) carboxylation.
26  caused by loss-of-function mutations in the matrix Gla protein (MGP) gene.
27                                              Matrix GLA protein (MGP) has been identified as a calcif
28                                              Matrix GLA protein (MGP) has previously been shown to en
29                                 Mutations in matrix Gla protein (MGP) have been correlated with vascu
30                                              Matrix Gla protein (MGP) is a 14-kD extracellular matrix
31                                              Matrix Gla protein (MGP) is a potent inhibitor of vascul
32                                              Matrix Gla protein (MGP) is an antagonist of BMPs that i
33                                              Matrix Gla protein (MGP) is an inhibitor of vascular cal
34                                              Matrix GLA protein (MGP) is expressed in endothelial cel
35                                              Matrix GLA protein (MGP) is ubiquitously expressed with
36 ification, OPN mutant mice were crossed with matrix Gla protein (MGP) mutant mice.
37                              Inactivation of Matrix gla protein (Mgp) revealed that MGP is an inhibit
38 onding control tumors and expressed elevated matrix GLA protein (MGP) that mediated enhanced tumor an
39 hosphate mineral and the proteins fetuin and matrix Gla protein (MGP) that was initially discovered i
40             Here, we show that deficiency of matrix Gla protein (MGP), a BMP inhibitor, causes induct
41                      A candidate molecule is matrix GLA protein (Mgp), a mineral-binding ECM protein
42 arget contact also induced the expression of matrix Gla protein (MGP), a regulator of BMP function in
43 nary endothelium, resulting from the loss of matrix Gla protein (MGP), causes ectopic hepatic differe
44 f 5 less critical VKD proteins [osteocalcin, matrix Gla protein (Mgp), growth arrest specific protein
45  vitro; and a reduction in the expression of matrix Gla protein (MGP), osteopontin (OPN), and vascula
46  the mineral regulators osteonectin (ON) and matrix Gla protein (MGP).
47 scular disease and is, in part, prevented by matrix Gla protein (MGP).
48 ization capacity due to reduced fetuin-A and matrix gla-protein (MGP) levels.
49 c6-/- serum, and positive immunostaining for matrix-gla-protein (MGP), fetuin-A, and ankylosis protei
50 calcification in vivo was further studied in matrix GLA protein null (MGP(-/-)) mice whose arteries s
51 ein produced by extrahepatic tissues such as matrix Gla protein or osteocalcin.
52  (i.e. apolipoprotein E, vitamin D receptor, matrix Gla protein, peroxisome proliferator activated re
53      We notably found that undercarboxylated matrix Gla protein precisely colocalized within areas of
54 NA and calcification inhibitors fetuin-A and matrix Gla protein suggests a novel role for EVs in inte
55 hosphate mineral and the proteins fetuin and matrix Gla protein that was initially discovered in the
56                   Regulatory factors include matrix GLA protein, the phosphate cotransporter Pit-1, a
57 on molecule/GA733-2, Kop protease inhibitor, matrix gla protein, tissue inhibitor of metalloproteinas
58 ast growth factor 23 (FGF23), uncarboxylated matrix Gla protein (ucMGP), and fetuin-A are regulators
59 kin by specific antibodies demonstrated that matrix gla protein was found predominantly in undercarbo
60     BMP antagonists follistatin, noggin, and matrix Gla protein were expressed in cultured bovine and
61 hown to have abundant uncarboxylated form of matrix Gla protein, which allowed progressive tissue min
62 of both coagulation factors in the liver and matrix gla protein, which, in fully carboxylated form, i

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