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1 an impaired ability to differentiate towards cardiac mesoderm.
2 n factor cascade to direct the generation of cardiac mesoderm.
3 s), GATA4 was shown to promote endoderm, not cardiac mesoderm.
4 late the Wnt in mesendoderm specification to cardiac mesoderm.
5 ing during mesoderm specification and in pre-cardiac mesoderm.
6 ch signaling during the prepatterning of the cardiac mesoderm.
7 spatial specificity of eve expression in the cardiac mesoderm.
8 hereas the Lbe cells are expanded within the cardiac mesoderm.
9 ose is critical to direct the cell fate into cardiac mesoderm.
10 recisely targeted gene expression within the cardiac mesoderm.
11 xpression that specify cell types within the cardiac mesoderm.
12 d work in parallel to FGF signaling from the cardiac mesoderm.
13 sors and in tissues involved in induction of cardiac mesoderm.
14 of a combinatorial mechanism to specify the cardiac mesoderm.
15 subset of ME genes that is required to form cardiac mesoderm.
16 n important role for QKI in the formation of cardiac mesoderm.
17 le for Quaking (QKI) in the specification of cardiac mesoderm.
18 are observed between definitive endoderm and cardiac mesoderm.
19 y and contribute to different subsets of non-cardiac mesoderm.
20 a molecular pathway regulating the posterior cardiac mesoderm and demonstrate that cardiovascular def
21 nhibition did not generate lateral plate and cardiac mesoderm and favored instead somitic differentia
22 P-TFI and II), is initially activated in the cardiac mesoderm and is subsequently restricted to cells
23 of the yolk sac; the distal region generates cardiac mesoderm and node-derived axial mesendoderm; and
24 the AIP can induce cardiac identity from non-cardiac mesoderm and that it can pattern this by specify
27 lls (hESCs) and derived definitive endoderm, cardiac mesoderm, and ectoderm cell lineages, we detect
28 tration threshold of FGFs emanating from the cardiac mesoderm are involved in patterning the foregut
29 GF2, but not FGF8, was sufficient to replace cardiac mesoderm as an inducer of the liver gene express
30 Remarkably, knockout of QKI disrupts the cardiac mesoderm-associated alternative splicing program
32 ory framework for the differentiation of the cardiac mesoderm, beginning at the 110-cell stage, and e
33 primarily by regulating cell fate within the cardiac mesoderm between muscular and non-muscular cell
34 erminants influence the specification of the cardiac mesoderm, both by inhibiting inductive signals r
35 l, mutually redundant role in specifying the cardiac mesoderm (CM) as eliminating the functions of bo
36 specify the yolk sac haemogenic endothelium, cardiac mesoderm, definitive endoderm, and axial mesoder
37 ranscription factors involved in somitic and cardiac mesoderm development in diverse bilaterians.
38 as a classical Polycomb protein during early cardiac mesoderm differentiation by repressing pluripote
42 haracterized by absence of prechordal plate, cardiac mesoderm, endoderm and ventral neuroectoderm.
43 we uncover complex interactions between the cardiac mesoderm, endoderm, and the rest of the embryo,
45 s is both necessary and sufficient to direct cardiac mesoderm formation in frog embryos and human emb
46 elopmental pathway in which pannier promotes cardiac mesoderm formation, and pointed acts subsequentl
48 to the interface between the pharyngeal and cardiac mesoderm, identify the transcription factor code
49 essed in endoderm underlying the presumptive cardiac mesoderm in amphibian, bird, and mammalian embry
54 required for formation of both visceral and cardiac mesoderm, including formation of the dorsal vess
57 that Rho kinase transcripts were enriched in cardiac mesoderm, lateral plate mesoderm and the neural
60 xposure of YAP(-/-) hESCs to Activin induces cardiac mesoderm markers (BAF60c and HAND1) without acti
61 captured EYFP+ cells that strongly expressed cardiac mesoderm markers and cardiac transcription facto
62 nscription factor 1 (MESP1; from mesoderm to cardiac mesoderm), meis homeobox 1 (MEIS1) and GATA-bind
64 nderlying early stages (ie, from mesoderm to cardiac mesoderm) of cardiomyocyte differentiation remai
65 rt defects (CHDs) are the result of abnormal cardiac mesoderm or cardiac neural crest development.
67 xhibited transcriptional profiles resembling cardiac mesoderm progressing towards cardiomyocyte fates
68 therefore conclude that proper maturation of cardiac mesoderm requires GATA-6, which functions to mai
72 and the rescue of jumu mutations by ectopic cardiac mesoderm-specific expression of neb demonstrate
76 kx2-5 is among the earliest known markers of cardiac mesoderm that is central to the regulatory pathw
77 rased from most genes at the transition from cardiac mesoderm to cardiac progenitor cells but is pres
78 but how the pathway switches from promoting cardiac mesoderm to restricting cardiomyocyte progenitor
79 d acts downstream of GATA factors in the pre-cardiac mesoderm to specify lineage commitment of cardio
86 during mesoderm specification and in the pre-cardiac mesoderm, we find a previously unrecognized role
87 rmal cells maintain contact with nascent pre-cardiac mesoderm, we hypothesized that direct physical c
88 at co-expression of these three genes in the cardiac mesoderm, which also involves cross-regulation,
89 y broad regions of mesoderm, including early cardiac mesoderm, which are derived from Tbx1-expressing
91 e importance of mesendoderm specification to cardiac mesoderm, which needs precisely regulation of Wn
92 to hepatic specification, direct contact of cardiac mesoderm with ventral endoderm is required to in