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1 genic differentiation, release of calcifying matrix vesicles).
2 aphy are agglomerations of smaller calcified matrix vesicles.
3  V-, VI- and alkaline phosphatase-containing matrix vesicles.
4 on of hydroxyapatite inside membrane-limited matrix vesicles.
5 ed protein known to mediate Ca2+ influx into matrix vesicles.
6 eotide pyrophosphatase activity in cells and matrix vesicles.
7 eedles of hydroxyapatite in conjunction with matrix vesicles.
8         We propose that, unlike bone-derived matrix vesicles, a large population of EVs implicated in
9  of mineralization-competent cell fragments (matrix vesicles and apoptotic bodies).
10            Annexin V is a major component of matrix vesicles and has a role in mediating the influx o
11 n qualitatively modulate their production of matrix vesicles and only when induced to initiate minera
12 hemical cross-linking analysis revealed that matrix vesicles and phosphatidylserine-rich liposomes in
13  V-, VI- and alkaline phosphatase-containing matrix vesicles, and the initiation of mineralization by
14 s made even more intriguing by the fact that matrix vesicles are also present in nonmineralizing tiss
15                                              Matrix vesicles are lipid bilayer-enclosed structures th
16 oteins, and these spheres are unlikely to be matrix vesicles as reported for collagen calcification i
17 tion on collagen fibrils and the presence of matrix vesicles, as has been described in calcified vasc
18 the production and release of annexin V-rich matrix vesicles by mineralizing chondrocytes were accomp
19 ultures showed the presence of extracellular matrix vesicles, calcifying collagen fibrils, and nodula
20 ice reflects the lack of ANK activity in the matrix vesicle compartment.
21                     The nucleational core of matrix vesicles contains a complex (CPLX) of phosphatidy
22               Since the lipid composition of matrix vesicles differs from that of the plasma membrane
23    Microcalcifications appear to derive from matrix vesicles enriched in calcium-binding proteins tha
24        Vascular calcification initiates with matrix vesicle formation and mineralization following a
25                                              Matrix vesicles have a critical role in the initiation o
26      The phosphatidylserine-rich membrane of matrix vesicles in vivo may thus offer an ideal speciali
27                          Interestingly, only matrix vesicles isolated from RA-treated cells that cont
28 ated by PHOSPHO1 and likely does not rely on matrix vesicle-mediated initiation of mineralization.
29  concert to generate phosphocholine from the matrix vesicle membrane during skeletal mineralization.
30 cilitate crystal growth after rupture of the matrix vesicle membrane; it may also offer a smooth tran
31 pathological mineralization are initiated by matrix vesicles, membrane-enclosed particles released fr
32 mal otoconial and otolith formation based on matrix vesicle mineralization in bone which we believe t
33                                              Matrix vesicles (MV) are lipid bilayer-enclosed nanoscal
34         While previous studies revealed that matrix vesicles (MV) contain a nucleational core (NC) th
35                                              Matrix vesicles (MV) play a key role in the initiation o
36 nexins II, V, and VI are major components of matrix vesicles (MV), i.e. particles that have the criti
37 rocytes release plasma membrane (PM) derived matrix vesicles (MV), which are the site of initial hydr
38 , and the mineralizing potential of released matrix vesicles (MV).
39 d growth in the interior of membrane-limited matrix vesicles (MVs) and by propagating the crystals on
40                                              Matrix vesicles (MVs) are involved in de novo mineral fo
41 tes that calcification by isolated mammalian matrix vesicles (MVs) can be initiated by ATP.
42                                              Matrix vesicles (MVs) in the growth plate bind to cartil
43 Inorganic phosphate (Pi) accumulation within matrix vesicles (MVs) is a fundamental stage in the prec
44 mally occurs within the lumen of TNSALP-rich matrix vesicles (MVs) of growth cartilage, bone, and den
45 rystals were initiated, as is normal, within matrix vesicles (MVs) of the growth plate and bone of TN
46  calcification and the subsequent release of matrix vesicles (MVs), precursors of microcalcification.
47                                              Matrix vesicles (MVs), secreted by vascular smooth muscl
48                                              Matrix vesicles (MVs), structures that accumulate Ca2+ d
49 nd in association with meniscal cell-derived matrix vesicles (MVs).
50 A6) are quantitatively major proteins of the matrix vesicle nucleational core that is responsible for
51 hment of annexin V-mediated Ca2+ influx into matrix vesicles or liposomes.
52    Thus, we tested the novel hypothesis that matrix vesicles produced and released by mineralizing ce
53                            The regulation of matrix vesicle production is poorly understood but is th
54 ation, will release mineralization-competent matrix vesicles rich in annexin V and alkaline phosphata
55  mice and that NPP1 but not ANK localizes to matrix vesicles, suggesting that failure of ANK deficien
56 eralizing chondrocytes produced and released matrix vesicles that exhibited similar round shape, smoo
57  cholesterol is an integral component of the matrix vesicles that nucleate calcium mineral, we examin
58 of vascular calcification are not known, but matrix vesicles, the nucleation sites for calcium crysta
59 c bodies with (45)Ca demonstrated that, like matrix vesicles, they can concentrate calcium.
60                                     Isolated matrix vesicles were incubated in synthetic cartilage ly
61 ondrocytes released mineralization-competent matrix vesicles, which contained significantly higher am
62                In addition, lack of AnxA6 in matrix vesicles, which initiate the mineralization proce

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