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<i>Pax9</i> is required for cardiovascular development and interacts with <i>Tbx1</i> in the pharyngeal endoderm to control 4 <sup>th</sup> pharyngeal arch artery morphogenesis

2019-03-14

Abstract excerpt

Developmental defects affecting the heart and aortic arch arteries are a key phenotype observed in DiGeorge syndrome patients and are caused by a microdeletion on chromosome 22q11. Heterozygosity of TBX1 , one of the deleted genes, is expressed throughout the pharyngeal arches and is considered a key component for the arch artery defects. Pax9 is expressed in the pharyngeal endoderm and is downregulated in Tbx1...

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Literature Corpus work
e9aba3c3-0c69-531f-8bbb-27c3876fd7c3
DOI
10.1101/576660
Open publication

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<i>Pax9</i> is required for cardiovascular development and interacts with <i>Tbx1</i> in the pharyngeal endoderm to control 4 <sup>th</sup> pharyngeal arch artery morphogenesisDOI 10.1101/576660
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