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1 m that pericytes can differentiate along the chondrocytic and adipocytic lineages in vivo, these cell
2 lcium phosphate material is deposited in the chondrocytic and fibrocytic matrices.
3 e syndrome, CPA6 is expressed in a number of chondrocytic and nervous tissues during embryogenesis.
4 chymal precursor cells for selecting between chondrocytic and osteoblastic fates as well as a mechani
5 ted ATX and B10/PDNP3 expression in central (chondrocytic) and, to a lesser degree, peripheral (fibro
6 ls capable of differentiating to osteocytic, chondrocytic, and adipocytic lineages when stimulated un
7 lated with cells of irregular shape and less-chondrocytic appearance, contained abundant intracellula
8 ively reproduced the experimentally observed chondrocytic arrangements in growth plate of each of the
9 d evaluated its activity in osteoblastic and chondrocytic cell culture models.
10 ined in primary murine chondrocytes, a human chondrocytic cell line (T/C-28a2), primary human chondro
11 n chondrocytes from OA cartilage and a human chondrocytic cell line C28/I2 but was up-regulated by th
12 ) rapidly affects protein translation in the chondrocytic cell line SW1353.
13 lase (PLSCR1), during maturation of a murine chondrocytic cell line, N1511.
14 rid system and a cDNA library derived from a chondrocytic cell line.
15 differentiating cells in the lymphocytic and chondrocytic cell lineages.
16 cytes by generating stably transfected mouse chondrocytic cell lines.
17 is we studied the effects of Wnt on cultured chondrocytic cells and differentiating limb-bud mesenchy
18 that viperin is expressed in differentiating chondrocytic cells and regulates their protein secretion
19      Using primary chondrocytes and T/C-28a2 chondrocytic cells as model systems, we report that prol
20 monstrate that induction of MMP-1 by IL-1 in chondrocytic cells depends on unique combinations of sig
21  indicate a possible synovial origin for the chondrocytic cells found in rheumatoid pannus.
22 ecan in both notochord cells and surrounding chondrocytic cells of presumptive inner annuli and verte
23 ift assay using nuclear extracts from TMC-23 chondrocytic cells revealed that the NF-kappaB subunits
24                         Exposure of T/C-28a2 chondrocytic cells to fluid shear results in co-regulati
25 irs of sites eliminated enhancer activity in chondrocytic cells, as did the mutation of any one of th
26 ressed SOX9 activated these enhancers in non-chondrocytic cells, as it also activates the Col2a1 enha
27 ever, in normal or immortalized (e.g. ATDC5) chondrocytic cells, Runx2 expression is suppressed durin
28 ansfection of TG2 site-directed mutants into chondrocytic cells, we observed that wild type TG2, and
29                                        Using chondrocytic cells, we previously determined that IL-1 i
30 ction by proinflammatory cytokine-stimulated chondrocytic cells.
31  viperin-CXCL10-TGF-beta/SMAD2/3 axis in CHH chondrocytic cells.
32 es that occur during cytokine stimulation of chondrocytic cells.
33 n the medial part of menisci, which contains chondrocytic cells.
34 cers and can activate these enhancers in non-chondrocytic cells.
35 ondrocytes, and immortalized human articular chondrocytic CH-8 cells were transfected with CXCR1/CXCR
36 accharides induced a dose-dependent state of chondrocytic chondrolysis, including near-total loss of
37 m to mesoderm, before differentiating into a chondrocytic culture comprising cell aggregates.
38           However, the cells were capable of chondrocytic differentiation and formed cartilage tissue
39 n growth plate chondrocytes stimulates their chondrocytic differentiation and maturation toward hyper
40           We demonstrate that this defect in chondrocytic differentiation can be attributed to lack o
41 ker expression and aberrant osteoblastic and chondrocytic differentiation in a TEAD-dependent fashion
42 eration and saturation density but repressed chondrocytic differentiation.
43 steoblastic differentiation while repressing chondrocytic differentiation.
44 is SNP resides in an enhancer that regulates chondrocytic expression of PKDCC - a gene encoding a tyr
45 cyte proliferation and maturation, increased chondrocytic expression of Rankl, matrix metalloproteina
46 e understanding the coordinate regulation of chondrocytic genes.
47 FR) are thought to be negative regulators of chondrocytic growth, as exemplified by achondroplasia an
48 embryo fibroblasts could be induced into the chondrocytic lineage ex vivo, but these cells failed to
49 , commitment of cells to the osteoblastic or chondrocytic lineage may involve inhibition of alternati
50 f Wnt signaling diverts differentiation to a chondrocytic lineage.
51 rentiation within either the osteoblastic or chondrocytic lineage.
52  as melanocytic, adipocytic, osteocytic, and chondrocytic lineages, which recapitulates the plasticit
53  formed nodules and expressed high levels of chondrocytic marker proteins when cultured on Pln.
54 cription of osterix, notochordal markers and chondrocytic markers by 60-80%.
55 xpression and protein production in terms of chondrocytic markers when compared with unpurified dermi
56  as evidenced by lack of expression of other chondrocytic markers, such as aggrecan and collagen type
57 , suggesting that, in the majority of cases, chondrocytic miRNAs do not directly regulate target RNA
58                                              Chondrocytic MMP-3, but not MMP-7, was required for disc
59 idenced by the formation of large numbers of chondrocytic nodules on aggrecan-coated surfaces.
60 fferentiate exclusively into the adipocytic, chondrocytic, or osteocytic lineages.
61  provide new insights into the regulation of chondrocytic, osteoblastic, and osteoclastic differentia
62            BMP-4-expressing MDSCs acquired a chondrocytic phenotype in vitro more effectively than di
63 e ability of transplanted cells to acquire a chondrocytic phenotype.
64 operties of cartilage or the regulation of a chondrocytic phenotype.
65 mad and MAPK pathways in expression of early chondrocytic phenotypes and identify important changes i
66 of relative positioning of the proliferative chondrocytic population based on ciliary orientation.
67 ee-dimensional orientation patterns that the chondrocytic primary cilium forms in articular cartilage
68 search investigates the role of the immotile chondrocytic primary cilium in the growth plate.
69 on of Col2a1 and possibly other genes of the chondrocytic program.
70   Furthermore, inhibitory effects of FGF2 on chondrocytic proliferation were partially reduced in p21
71 regulatory response to genotoxic stress in a chondrocytic survival pathway is potentially also releva
72  The functional effects of miR-146a on human chondrocytic, synovial, and microglia cells were studied
73 ivities, achieved via direct transfection of chondrocytic TC28 and meniscal cells, both induced matri
74 ce of the Notch ligand Jag1, vSMCs acquire a chondrocytic transcriptional repertoire that can lead to
75 n deposition in the arterial wall upon osteo/chondrocytic transformation of vascular smooth muscle ce
76 knee OA articular cartilage and the central (chondrocytic) zone of OA menisci.
77                                          The chondrocytic zones of the growth plates also appeared no