id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
work_j7kpdr5srze47kmsl2scd6h4c4	L. de Pontual	Noradrenergic neuronal development is impaired by mutation of the proneural HASH-1 gene in congenital central hypoventilation syndrome (Ondine's curse)	2003	8	.pdf	application/pdf	4458	836	71	consequences of HASH-1 mutations, we developed an in vitro model of noradrenergic differentiation in neuronal progenitors derived from the mouse vagal neural crest, reproducing in vitro the HASH–PHOX–RET All HASH-1 mutant alleles impaired noradrenergic neuronal development, when overexpressed Thus, HASH-1 mutations may contribute to the CCHS phenotype in rare cases, mutant HASH-1 alleles induced the impairment of noradrenergic neuronal development. HASH-1 gene mutations was detected in a panel of 120 HASH-1 expression in early human development expression of HASH-1 in early human development (Fig. 2). HASH-1 adenoviral constructs (Fig. 4), as shown by GFP of HASH-1 gene mutations for the noradrenergic lineage neuronal development could be expected with HASH-1 gene the expression pattern of HASH-1 in the developing human (A) HASH-1 gene mutations. (A) HASH-1 gene mutations. HASH-1 gene expression in developing human embryos. In vitro culture model of mouse vagal neural crest cells to analyze the HASH-1–PHOX2B/PHOX2A cascade controlling.	./cache/work_j7kpdr5srze47kmsl2scd6h4c4.pdf	./txt/work_j7kpdr5srze47kmsl2scd6h4c4.txt