megacolon/tyrosine

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Signalling of the Ret receptor tyrosine kinase through the c-Jun NH2-terminal protein kinases (JNKS): evidence for a divergence of the ERKs and JNKs pathways induced by Ret.

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The RET proto-oncogene encodes a functional receptor tyrosine kinase (Ret) for the Glial cell line Derived Neurotrophic Factor (GDNF). RET is involved in several neoplastic and non-neoplastic human diseases. Oncogenic activation of RET is detected in human papillary thyroid tumours and in multiple

Grb2 binding to the different isoforms of Ret tyrosine kinase.

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The RET proto-oncogene encodes two isoforms of a receptor tyrosine kinase which plays a role in neural crest and kidney development. Ret ligands have been recently identified as the neuron survival factor GDNF (Glial-Derived Neurotrophic Factor) and Neurturin. Somatic rearrangements of RET,

Tyrosine 1062 of RET-MEN2A mediates activation of Akt (protein kinase B) and mitogen-activated protein kinase pathways leading to PC12 cell survival.

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The RET tyrosine kinase is a functional receptor for neurotrophic ligands of the glial cell line-derived neurotrophic factor (GDNF) family. Loss of function of RET is associated with congenital megacolon or Hirschsprung's disease, whereas germ-line point mutations causing RET activation are

Mutation analysis of the RET receptor tyrosine kinase in Hirschsprung disease.

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Hirschsprung disease (HSCR), or congenital aganglionic megacolon, is the most common cause of congenital bowel obstruction with an incidence of 1 in 5000 live births. Recently, linkage of an incompletely penetrant, dominant form of HSCR was reported, followed by identification of mutations in the

Neurotrophic factor receptor RET: structure, cell biology, and inherited diseases.

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RET (REarranged during Transfection) is a transmembrane receptor tyrosine kinase that is activated by a complex consisting of a soluble glial cell line-derived neurotrophic factor (GDNF) family ligand (GFL) and a glycosyl phosphatidylinositol-anchored co-receptor, GDNF family receptors alpha

Hirschsprung's disease genes and the development of the enteric nervous system.

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Hirschsprung's disease or aganglionic megacolon causes chronic, congenital obstipation at an incidence of 1 per 5000 live births. Two approaches have been vital to the present understanding of the pathogenesis and genetic background of the disease: disease linkage analyses and mouse models of

Analysis of the RET gene in subjects with sporadic Hirschsprung's disease.

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BACKGROUND Hirschsprung's disease (HSCR), or aganglionic megacolon, is a hereditable disease of the enteric nervous system. It is an embryonic developmental disorder characterized by the absence of ganglion cells in the lower enteric plexus. Gut motility is compromised in HSCR, with consequent risk

Assignment of mouse Gfra1, the homologue of a new human HSCR candidate gene, to the telomeric region of mouse chromosome 19.

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Glial cell line-derived neurotrophic factor (Gdnf) and its alpha receptor (Gfra1) interact with the Ret receptor triggering its tyrosine kinase activity. As Gdnf and Ret have been linked to the development of Hirschsprung disease (HSCR), it seems likely that Gfra1 could also be a susceptibility gene

Cell-autonomous and cell non-autonomous signaling through endothelin receptor B during melanocyte development.

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The endothelin receptor B gene (Ednrb) encodes a G-protein-coupled receptor that is expressed in a variety of cell types and is specifically required for the development of neural crest-derived melanocytes and enteric ganglia. In humans, mutations in this gene are associated with Waardenburg-Shah

Intestinal ganglioneuromatosis: mucosal and transmural types. A clinicopathologic and immunohistochemical study of six cases.

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Six cases of intestinal ganglioneuromatosis (GN) included in this study reveal the occurrence of two morphologic patterns. Transmural GN was characterized by neural hyperplasia in all layers of the bowel wall with predominant involvement of the myenteric plexus. It was found in three patients

[Molecular genetics of Hirschsprung disease: a model of multigenic neurocristopathy].

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Hirschsprung's disease (HSCR, aganglionic megacolon) is a frequent congenital malformation regarded as a multigenic neurocristopathy. Three susceptibility genes have been recently identified in HSCR, namely the RET proto-oncogene, the endothelin B receptor (EDNRB) gene, and the endothelin 3 (EDN3)

[From monogenic to polygenic: model of Hirschsprung disease].

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Genomic structure of the gene for the SH2 and pleckstrin homology domain-containing protein GRB10 and evaluation of its role in Hirschsprung disease.

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Hirschsprung disease (HSCR), or congenital aganglionic megacolon, is the most frequent cause of congenital bowel obstruction. Germline mutations in the RET receptor tyrosine kinase have been shown to cause HSCR. Mice that carry null alleles for RET or for its ligand, glial cell line-derived

[Mutations of RET proto-oncogene in Hirschsprung disease].

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Hirschsprung's disease (HSCR) is a common condition (1 in 5,000 live births) resulting in intestinal obstruction in neonates and megacolon in infants and adults. This disease has been ascribed to the absence of autonomic ganglion cells, which are derived from the neural crest, in the terminal

The insulin receptor substrate (IRS)-1 recruits phosphatidylinositol 3-kinase to Ret: evidence for a competition between Shc and IRS-1 for the binding to Ret.

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Tyrosine 1062 of Ret, which represents an intracytoplasmic docking site for multiple signaling molecules, is essential for Ret-mediated activation of phosphatidylinositol 3-Kinase (PI3-K). PI3-K, in turn, has been implicated in inducing cell survival and neoplastic transformation mediated by Ret. We

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