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1 ecessary for TGF-beta-mediated regulation of Scleraxis.
2 llular responses including the activation of scleraxis.
3 boxes that overlaps with the closely related scleraxis.
4                           We have found that Scleraxis, a bHLH transcription factor, is a highly spec
5 n-C and Sox9 and decreases the expression of scleraxis and cartilage oligomeric matrix protein.
6 n part by the association between Sirt-1 and scleraxis and deacetylation of NF-kappaB and PI3K.
7 /flox)) results in microglossia with reduced Scleraxis and Fgf10 expression as well as decreased myog
8 ing somite are crucial for the expression of scleraxis and Mkp3.
9 rs, and the neotendon transcription factors, Scleraxis and Mohawk.
10 beta regulates Scleraxis via ERK1/2 and then Scleraxis and Smad3 cooperate to regulate Fibromodulin a
11 lets, in contrast to tendon-associated genes scleraxis and tenascin, present in the chordae tendineae
12 (dpERK) signaling and promotes expression of scleraxis and tenascin.
13 hat promote tendon fibroblast proliferation: scleraxis and tenomodulin.
14 he level of some markers [e.g., mtwist, mf1, scleraxis, and alpha1(II) collagen] is seen in the anter
15 f biglycan, collagen V, collagen XII, PAI-1, Scleraxis, and Mohawk by TGF-beta1.
16 increased the expression of type I collagen, scleraxis, and tenomodulin.
17                      These findings identify scleraxis as a viable target for the development of nove
18 nducer of the tendon progenitor (TNP) marker scleraxis both in organ culture and in cultured cells, a
19 n-specific transcription factors, Mohawk and Scleraxis, but there was no evidence of changes in muscl
20 tly controls the tendon transcription factor scleraxis by binding to its distant enhancer.
21                                Regulation of Scleraxis by TGF-beta did not require new protein synthe
22 in tendon with respect to cell organization, scleraxis-Cre collagen XII knockout mice were evaluated
23  Col5a1(flox/flox) mouse model was bred with Scleraxis-Cre mice to create a targeted tendon and ligam
24  show that tendon development is arrested in Scleraxis-Cre::Mmp14 lox/lox mice that are unable to rel
25                                              Scleraxis deletion, after the establishment of cardiac f
26                                              Scleraxis directly regulated transcription of the myofib
27 ype II receptor (Tgfbr2) was targeted in the Scleraxis-expressing cell lineage using the ScxCre delet
28                             The induction of scleraxis-expressing TNPs is not affected in mutant embr
29 ascade and in particular, ERK1/2 to activate scleraxis expression in a population of mesenchymal prog
30         Finally, TGF-beta signaling-mediated Scleraxis expression is required for tendonogenesis in t
31 luding the limb tendons, and show that early scleraxis expression marks the progenitor cell populatio
32                                              Scleraxis expression was upregulated in the hearts of no
33  endogenous BMP activity and induces ectopic scleraxis expression.
34 r periostin, and cardiac fibroblasts lacking scleraxis failed to upregulate periostin synthesis and s
35 eta regulates expression of fibrous markers: Scleraxis, Fibromodulin and Adamtsl2.
36 -beta and required to regulate expression of Scleraxis, Fibromodulin, and Adamtsl2.
37 wk, which indicates an essential function of scleraxis for craniofacial development.
38                                              Scleraxis function is therefore essential for normal cra
39                                    Using the scleraxis gene as a marker we show that these progenitor
40                                              Scleraxis genes are required for normal musculoskeletal
41                             Mutation of both scleraxis genes results in more severe defects in crania
42 d a Col2.3GFP transgene, while expression of Scleraxis-GFP was used to follow differentiation into pe
43                                              Scleraxis governs fibroblast activation in pressure over
44 udes both transcriptional activators such as scleraxis, Hand2, and Dermo-1 and repressors such as Twi
45 expression of zebrafish scleraxis orthologs: scleraxis homolog (scx)-a and scxb in cranial and intram
46 e results reveal an essential early role for scleraxis in mesoderm formation, as well as a later role
47                                      Loss of scleraxis in mice leads to geometric and structural chan
48          Paraxis expression precedes that of scleraxis in the region of the somite fated to form the
49 e, TGF-beta2 beads induced the expression of Scleraxis in tongue explant cultures.
50                                              Scleraxis is a basic helix-loop-helix (bHLH) transcripti
51      Tamoxifen-inducible fibroblast-specific scleraxis knockout (Scx-fKO) completely attenuated cardi
52 pressure overload-induced heart failure, and scleraxis knockout attenuated fibrosis and improved card
53                                     Notably, scleraxis knockout reduced pressure overload-induced mor
54                                              Scleraxis lineage cells contribute to organized bridging
55                  Despite the requirement for Scleraxis-lineage (Scx(Lin)) cells during tendon develop
56 e substantially enriched for the presence of scleraxis-lineage (Scx-lin+) cells compared to digested
57 mpaired tenogenic cell recruitment from both Scleraxis-lineage and non-Scleraxis-lineage sources.
58                               Loss of EP4 in Scleraxis-lineage cells did not alter gliding function,
59 DTR tendons, identifying the requirement for Scleraxis-lineage cells during homeostasis.
60 cellular matrix (ECM) aging via depletion of Scleraxis-lineage cells in young mice (Scx-DTR).
61 ruitment from both Scleraxis-lineage and non-Scleraxis-lineage sources.
62     The present study assessed the impact of scleraxis loss on fibroblast activation, cardiac fibrosi
63                     The transcription factor scleraxis marks vertebrate tendons from early specificat
64 howed that TGF-beta stimulated expression of Scleraxis mRNA by 2 h and Fibromodulin and Adamtsl2 mRNA
65 e three embryonic germ layers confirmed that scleraxis mutant embryos were unable to form mesoderm.
66 nerating chimeric embryos, using lacZ-marked scleraxis-null and wild-type embryonic stem cells, we ex
67                                              Scleraxis-null cells were specifically excluded from the
68         At the time of developmental arrest, scleraxis-null embryos consisted of ectodermal and primi
69                                              Scleraxis-null mice are viable and have a range of tendo
70 nction in embryonic development, we produced scleraxis-null mice by gene targeting.
71        We report the expression of zebrafish scleraxis orthologs: scleraxis homolog (scx)-a and scxb
72 ect transcription from an E-box found in the scleraxis promoter.
73         In response to pro-fibrotic signals, scleraxis regulates cardiac fibroblast activation in vit
74 ct by identifying two proepicardial markers, Scleraxis (Scx) and Semaphorin3D (Sema3D), that genetica
75 ps from bipotent progenitors that co-express scleraxis (Scx) and Sox9 (Scx(+)/Sox9(+)).
76 factors co-expressed in entheseal tenocytes, scleraxis (Scx) and Sox9, directly control production of
77  at different stages of development based on scleraxis (Scx) expression.
78                                          The scleraxis (Scx) gene, encoding a bHLH transcription fact
79 ed to determine how the transcription factor Scleraxis (Scx) influences the development and maturatio
80                                              Scleraxis (Scx) is a known regulator of tendon developme
81                                              Scleraxis (scx) is a transcription factor required for t
82                     The transcription factor scleraxis (Scx) is required for tendon development; howe
83 e, and tenocytes and myofibroblasts from the Scleraxis (Scx) lineage were the predominant populations
84                                              Scleraxis (Scx), a bHLH transcription factor, marks this
85 mad2/3-mediated signaling, the expression of Scleraxis (Scx), a transcription factor specific for ten
86 ncreased expression of Col1a1, Col3a1, bFGF, Scleraxis (Scx), and tenomodulin in the ESM-PRP groups.
87 n mammalian tendons and ligaments, including scleraxis (scx), collagen 1a2 (col1a2) and tenomodulin (
88 y, we conducted targeted cell ablation using scleraxis (Scx)-Cre to examine the role of Scx-lineage c
89 eted from the myotome induces formation of a scleraxis (Scx)-expressing tendon progenitor population
90 ionally deleted the IGF1 receptor (IGF1R) in scleraxis (Scx)-expressing tenocytes using a tamoxifen-i
91 t population that is positive for the marker Scleraxis (Scx).
92 ived chondrogenic lineages, and suggest that scleraxis target genes mediate these processes.
93 steogenic (Runx2, OCN) and ligament-related (scleraxis transcription factor (SCXA), ELN) genes were d
94  of phosphorylated ERK result in the loss of scleraxis transcripts and the loss of distal rib develop
95  propose a model in which TGF-beta regulates Scleraxis via ERK1/2 and then Scleraxis and Smad3 cooper
96                       We subsequently showed Scleraxis was a potential intermediate for TGF-beta-regu
97 sistent with this early embryonic phenotype, scleraxis was found to be expressed throughout the embry
98 omodulin, and tenogenic transcription factor scleraxis, whereas it inhibited gene products involved i