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This is the first report of the cDNA encoding the precursor protein of ET-3 in a non-mammalian species.
the critical physiological role of the KIT-ET3-NO pathway in fulfilling high demand (exceeding basal level) of endothelium-dependent NO generation for coping with atherosclerosis, pregnancy, and aging, is reported.
genome-wide association studies in population of women in China: Data suggest that EDN3 (endothelin 3) and EDNRB (endothelin receptor type B (Montrer EDNRB Kits ELISA)) play important roles in the molecular mechanisms underlying cervical cancer.
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 (Montrer SPARC Kits ELISA).
Waardenburg syndrome type II and mutations of EDNRB (Montrer EDNRB Kits ELISA), EDN3 and SOX10 (Montrer SOX10 Kits ELISA) 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 (Montrer EDN2 Kits ELISA) and EDN3 genes in human primary colon cancers and in a panel of human colon cancer cell lines. Epigenetic inactivation of ET-2 (Montrer EDN2 Kits ELISA) and ET-3 occurs frequently in both rat and human colon cancers.
plasma levels of big ET-2 (Montrer EDN2 Kits ELISA), 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 (Montrer DMD Kits ELISA) has been found in the same Indian family members affected with Waardenburg syndrome and Duchenne muscular dystrophy (Montrer DMD Kits ELISA).
These data suggest that autocrine EDN3/EDNRB (Montrer EDNRB Kits ELISA) signaling is essential for maintaining GSCs. Incorporating END3 (Montrer EPHA3 Kits ELISA)/EDNRB (Montrer EDNRB Kits ELISA)-targeted therapies into conventional cancer treatments may have clinical implication for the prevention of tumor recurrence.
Control of differentiation of mouse enteric nervous system progenitor cells by EDN3 requires regulation of Ednrb (Montrer EDNRB Kits ELISA) expression by SOX10 (Montrer SOX10 Kits ELISA) and ZEB2 (Montrer ZEB2 Kits ELISA).
colonic migrating motor complexes occur in mice lacking the endothelin-3 gene
Enterocolitis causes profound lymphoid depletion in endothelin receptor B (Montrer EDNRB Kits ELISA)- 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 (Montrer SOX10 Kits ELISA), endothelin-3 and endothelin B receptor (Montrer EDNRB Kits ELISA) 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.
, endothelin 3
, lethal spotting