Application | Comment | Organism |
---|---|---|
medicine | isoform c-Abl kinase activity is required for regulation of the estrogen receptor alpha function, and a Y52F/Y219F mutant estrogen receptor, unable to be phosphorylated by c-Abl, leads to reduced breast cancer cell growth and invasion | Homo sapiens |
Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
ATP + [estrogen receptor alpha]-L-tyrosine | Homo sapiens | - |
ADP + [estrogen receptor alpha]-L-tyrosine phosphate | estrogen receptor alpha associates with c-Abl nonreceptor tyrosine kinase. The direct interaction is mediated by two PXXP motifs of estrogen receptor alpha and the c-Abl SH3 domain. Estrogen receptor alpha can be phosphorylated on residues Y52 and Y219. Phosphorylation by c-Abl stabilizes estrogen recptor alpha, resulting in enhanced estrogen receptor alpha transcriptional activity and increased expression of endogenous target genes. Phosphorylation at the Y219 site affects DNA binding and dimerization by estrogen receptor alpha. c-Abl kinase activity is required for regulation of the estrogen receptor alpha function, and a Y52F/Y219F mutant estrogen receptor leads to reduced breast cancer cell growth and invasion | ? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | P00519 | ABL1 | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
ATP + [estrogen receptor alpha]-L-tyrosine | - |
Homo sapiens | ADP + [estrogen receptor alpha]-L-tyrosine phosphate | estrogen receptor alpha associates with c-Abl nonreceptor tyrosine kinase. The direct interaction is mediated by two PXXP motifs of estrogen receptor alpha and the c-Abl SH3 domain. Estrogen receptor alpha can be phosphorylated on residues Y52 and Y219. Phosphorylation by c-Abl stabilizes estrogen recptor alpha, resulting in enhanced estrogen receptor alpha transcriptional activity and increased expression of endogenous target genes. Phosphorylation at the Y219 site affects DNA binding and dimerization by estrogen receptor alpha. c-Abl kinase activity is required for regulation of the estrogen receptor alpha function, and a Y52F/Y219F mutant estrogen receptor leads to reduced breast cancer cell growth and invasion | ? | |
ATP + [estrogen receptor alpha]-L-tyrosine | - |
Homo sapiens | ADP + [estrogen receptor alpha]-L-tyrosine phosphate | estrogen receptor alpha associates with c-Abl nonreceptor tyrosine kinase. The direct interaction is mediated by two PXXP motifs of estrogen receptor alpha and the c-Abl SH3 domain. Estrogen receptor alpha can be phosphorylated on residues Y52 and Y219. Phosphorylation by c-Abl stabilizes estrogen receptor alpha, resulting in enhanced estrogen receptor alpha transcriptional activity and increased expression of endogenous target genes. Phosphorylation at the Y219 site affects DNA binding and dimerization by estrogen receptor alpha | ? |
Synonyms | Comment | Organism |
---|---|---|
c-ABL | - |
Homo sapiens |