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The protein encoded by EDN3 is a member of the endothelin family. Additionally we are shipping Endothelin 3 Antibodies (81) and Endothelin 3 Proteins (6) and many more products for this protein.
Showing 7 out of 13 products:
This is the first report of the cDNA encoding the precursor protein of ET-3 in a non-mammalian species.
EDN3 expression in left internal mammary arteries depends on tissue harvesting technique.
Down-regulated expression of ET3 attenuates the malignant behaviors of human melanoma cells partially by decreasing the expression of SPARC (show SPARC ELISA Kits).
Waardenburg syndrome type II and mutations of EDNRB (show EDNRB ELISA Kits), EDN3 and SOX10 (show SOX10 ELISA Kits) genes are responsible for Waardenburg syndrome type IV. (review)
Our data showed that almost all patients, regardless of individual characteristics such as gender or age, expressed the endothelin receptor genes, but did not express the genes for ET-3.
Studies revealed hypermethylation of EDN2 (show EDN2 ELISA Kits) and EDN3 genes in human primary colon cancers and in a panel of human colon cancer cell lines. Epigenetic inactivation of ET-2 (show EDN2 ELISA Kits) and ET-3 occurs frequently in both rat and human colon cancers.
plasma levels of big ET-2 (show EDN2 ELISA Kits), and big ET-3 are markedly increased in patients with end stage renal disease on hemodialysis
A novel missense mutation in EDN3 and a deletion mutation in DMD (show DMD ELISA Kits) has been found in the same Indian family members affected with Waardenburg syndrome and Duchenne muscular dystrophy (show DMD ELISA Kits).
These data suggest that autocrine EDN3/EDNRB (show EDNRB ELISA Kits) signaling is essential for maintaining GSCs. Incorporating END3 (show EPHA3 ELISA Kits)/EDNRB (show EDNRB ELISA Kits)-targeted therapies into conventional cancer treatments may have clinical implication for the prevention of tumor recurrence.
ET-1 (show EDN1 ELISA Kits) and the ET-1 (show EDN1 ELISA Kits)/ET-3 ratio are elevated in cirrhotic patients with portopulmonary hypertension (PPHT) and that ET-1 (show EDN1 ELISA Kits) is associated with a poor outcome irrespective of PPHT.
Finding suggest that mutations in RET (show RET ELISA Kits) and NTRK3 (show NTRK3 ELISA Kits) acting together are necessary and sufficient for the appearance of Hirschsprung disease and that the EDN3 mutation acts as a phenotype modifier.
colonic migrating motor complexes occur in mice lacking the endothelin-3 gene
Enterocolitis causes profound lymphoid depletion in endothelin receptor B (show EDNRB ELISA Kits)- and endothelin 3-null mouse models of Hirschsprung-associated enterocolitis.
changes in spinal afferent innervation and visceral pain transmission from the aganglionic rectum in ls/ls mice with deletions of the endothelin-3 gene
EDN3 worked synergistically to induce melanocyte differentiation in vitro
a coordinate and balanced interaction between SOX10 (show SOX10 ELISA Kits), endothelin-3 and endothelin B receptor (show EDNRB ELISA Kits) is required for normal enteric nervous system and melanocyte development
Using quantitative real-time polymerase chain reaction (PCR) we demonstrated reduced levels of endothelin-3 mRNA in the male mouse bowel at the time that ENS precursors migrate into the colon.
an ENU-induced mutation in endothelin 3 results in a mouse model of Waardenburg syndrome type IV
Endothelin 3 induces skin pigmentation in a keratin-driven inducible mouse model.
Polymorphisms within the EDN3 gene are associated with meat color in the pig.
The protein encoded by this gene is a member of the endothelin family. Endothelins are endothelium-derived vasoactive peptides involved in a variety of biological functions. The active form of this protein is a 21 amino acid peptide processed from the precursor protein. The active peptide is a ligand for endothelin receptor type B (EDNRB). The interaction of this endothelin with EDNRB is essential for development of neural crest-derived cell lineages, such as melanocytes and enteric neurons. Mutations in this gene and EDNRB have been associated with Hirschsprung disease (HSCR) and Waardenburg syndrome (WS), which are congenital disorders involving neural crest-derived cells. Four alternatively spliced transcript variants encoding three distinct isoforms have been observed.
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