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1                                              ActRIIA stimulates Smad1 activation in a kinase-dependen
2                                              ActRIIA(+/-)B(+/-) animals lack axial defects, but have
3                                              ActRIIA/B blockade approximately doubles the muscle incr
4 tudies revealed that MT2 cleaves ALK2, ALK3, ActRIIA, Bmpr2, Hfe, and, to a lesser extent, Hjv and Tf
5 idin-induction pathway, including Hjv, Alk3, ActRIIA, and Hfe, when overexpressed in hepatoma cells.
6 growth differentiation factor 11 (GDF11), an ActRIIA ligand, was increased in splenic erythroblasts f
7  demonstrates however that both ActRIIB- and ActRIIA-deficient mice display a hypertrophic phenotype.
8 nt findings demonstrate that both BMPRII and ActRIIA are necessary for endoglin-mediated suppression
9 ptors, we also tested the role of BMPRII and ActRIIA as the type II receptor candidates for the three
10 ansfected with RGMa utilized both BMPRII and ActRIIA for BMP2 or BMP4 signaling.
11 sfection of small hairpin RNA for BMPRII and ActRIIA in MC3T3 cells suppressed the signaling of GDF6,
12 le receptor through the use of specific anti-ActRIIA or anti-ActRIIB antibodies achieves only a parti
13 umab (BYM338), as a human dual-specific anti-ActRIIA/ActRIIB antibody, at the molecular and cellular
14 the muscle increase of GDF8 blockade, and as ActRIIA/B responds to multiple other TGFbeta-family memb
15  by X-ray analysis, bimagrumab binds to both ActRIIA and ActRIIB ligand binding domains in a competit
16 xial vertebrae, and that Gdf11 binds to both ActRIIA and ActRIIB, and induces phosphorylation of Smad
17  the activins are capable of binding to both ActRIIA and ActRIIB, with different affinities.
18 ary benefits comparable to those elicited by ActRIIA-Fc.
19 atercept is an activin receptor type IIA-Fc (ActRIIA-Fc) fusion protein that improves cardiopulmonary
20                                 Furthermore, ActRIIA-Fc normalized pulmonary macrophage infiltration
21 Mt2S762A, had reduced interactions with Hjv, ActRIIA, and Hfe.
22  two type I (ALK2 and ALK3) and two type II (ActRIIA and BMPR2) BMP receptors.
23 eport that RAP-011, an activin receptor IIA (ActRIIA) ligand trap, improved ineffective erythropoiesi
24 on of invasion: activin A receptor type IIA (ActRIIA) and bone morphogenetic protein receptor type II
25 (BMPRII), but not activin receptor type IIA (ActRIIA) or ActRIIB, based on changes in BMP signaling b
26  we observed similar gastrulation defects in ActRIIA(-/-)nodal(+/-) double mutants, which, if they de
27                               Interestingly, ActRIIA is the predominant BMP type II receptor expresse
28 s myostatin, and activin A are the two major ActRIIA/B ligands mediating muscle minimization.
29  therapeutic anti-inflammatory activities of ActRIIA-Fc that, together with its known anti-proliferat
30 ollecting ducts, we observed coexpression of ActRIIA, Dragon, and BMP4 but not BMPRII.
31 ation of the soluble extracellular domain of ActRIIA fused to a murine IgG2a-Fc, increases bone forma
32 in mice/monkeys matches the muscle growth of ActRIIA/B blockade.
33 These findings demonstrate the importance of ActRIIA in addition to ActRIIB in mediating myostatin an
34               Three high-affinity ligands of ActRIIA-Fc each induced macrophage activation in vitro,
35 er, the cellular and molecular mechanisms of ActRIIA-Fc action are incompletely understood.
36 ngs suggest that RGMa facilitates the use of ActRIIA by endogenous BMP2 and BMP4 ligands that otherwi
37 not ActRIIB, and HJV enhances utilization of ActRIIA by BMP-2 and BMP-4.
38 via BMPRII and that increased utilization of ActRIIA leads to generation of an enhanced BMP signal.
39 to augment muscle growth by blocking GDF8 or ActRIIA/B.
40 he crystal structure of the type II receptor ActRIIA with dorsomorphin and demonstrate that dorsomorp
41 s signaling through the BMP type II receptor ActRIIA.
42 eptor for activin, type II activin receptor (ActRIIA), by administration of the soluble extracellular
43 ies that ActRIIB and its subfamily receptor, ActRIIA, cooperatively mediate the Gdf11 signal in patte
44         Here, mutations of activin receptors ActRIIA and ActRIIB are shown to disrupt the development
45 and betaB subunits and the activin receptors ActRIIA and ActRIIB was demonstrated by RT-PCR.
46  the three type II TGF-beta family receptors ActRIIA, ActRIIB, and BMPRII have been implicated in ALK
47 n that the type II TGF-beta family receptors ActRIIA, ActRIIB, and BMPRII interact with a large group
48 V selectively uses the BMP type II receptors ActRIIA and BMPRII, but not ActRIIB, and HJV enhances ut
49               The type II activin receptors, ActRIIA and ActRIIB, have been shown to play critical ro
50 ves activation of type II activin receptors, ActRIIA/B, which yield profound muscle growth in humans
51 on, and RGMa-mediated BMP signaling required ActRIIA expression.
52                          We demonstrate that ActRIIA and BMPRII physically interact, and that each al
53               Further analyses revealed that ActRIIA(-/-)ActRIIB(+/-) and about 15% of the ActRIIA(-/
54 en together, these observations suggest that ActRIIA ligand traps may have therapeutic relevance in b
55 both receptor mutations by interbreeding the ActRIIA and ActRIIB knockout mutants.
56 ctRIIA(-/-)ActRIIB(+/-) and about 15% of the ActRIIA(-/-) embryos failed to form an elongated primiti
57 iation factor 8 (GDF8)/myostatin, acting via ActRIIA/B receptors, is the best-characterized negative
58 the key second negative regulator acting via ActRIIA/B, as blockade of both GDF8 and ActA in mice/mon
59                   Therapeutic treatment with ActRIIA-Fc-but not with a vasodilator-strikingly reverse