M
Maureen Gendron-Maguire
Researcher at Roche Institute of Molecular Biology
Publications - 8
Citations - 3620
Maureen Gendron-Maguire is an academic researcher from Roche Institute of Molecular Biology. The author has contributed to research in topics: Gene & Null allele. The author has an hindex of 8, co-authored 8 publications receiving 3528 citations. Previous affiliations of Maureen Gendron-Maguire include University of Texas MD Anderson Cancer Center.
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Journal ArticleDOI
Distinct roles of the receptor tyrosine kinases Tie-1 and Tie-2 in blood vessel formation
Thomas N. Sato,Yuzuru Tozawa,Urban Deutsch,Karen Wolburg-Buchholz,Yuko Fujiwara,Maureen Gendron-Maguire,Thomas Gridley,Hartwig Wolburg,Werner Risau,Ying Qin +9 more
TL;DR: In vivo analyses of embryos deficient in Tie-2 showed that it is important in angiogen-esis, particularly for vascular network formation in endothelial cells, which contrasts with previous reports on Tie-1 function in vasculogenesis and/or endothelial cell survival.
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Embryonic Lethality and Vascular Defects in Mice Lacking the Notch Ligand Jagged1
Yingzi Xue,Xiang Gao,Claire E. Lindsell,Christine R. Norton,Bo Chang,Carol Hicks,Maureen Gendron-Maguire,Elizabeth B. Rand,Gerry Weinmaster,Thomas Gridley +9 more
TL;DR: The phenotype of Cm /+ mice is established as a contiguous gene deletion syndrome and it is demonstrated that Jag1 is essential for remodeling of the embryonic vasculature.
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Hoxa-2 mutant mice exhibit homeotic transformation of skeletal elements derived from cranial neural crest.
TL;DR: Analysis of stained skeletons revealed that homozygous mutant animals contained multiple cranial skeletal defects, including a duplication of the ossification centers of the bones of the middle ear.
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Goosecoid is not an essential component of the mouse gastrula organizer but is required for craniofacial and rib development
Jaime A. Rivera-Pérez,Moisés Mallo,Maureen Gendron-Maguire,Thomas Gridley,Richard R. Behringer +4 more
TL;DR: It is demonstrated that gsc is not essential for organizer activity in the mouse but is required later during embryogenesis for craniofacial and rib cage development and transplantation experiments suggest that the ovary does not provide gsc function to rescue gastrulation defects.
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Mice homozygous for a null mutation of activin beta B are viable and fertile
TL;DR: A null mutation is made in the mouse activin β B gene by deleting the portion of the gene encoding the proteolytic cleavage site and the majority of the coding region for the mature processed protein.