EC Number   |
General Information |
Reference |
|---|
   2.7.10.1 | malfunction |
Mer deficiency is associated with increased renal inflammation when mice are challenged with nephrotoxic serum |
761659 |
| 2.7.10.1 | metabolism |
Eph receptor tyrosine kinases are activated upon ephrin binding via a sequential and ordered autophosphorylation process where residue YJM2 is phosphorylated first, followed by YJM1, and, finally by Yact. The Eph kinase activity most closely correlates with the phosphorylation status of the juxtamembrane region and not that of the activation loop. Eph kinase activity is primarily correlated with phosphorylation of residue YJM2 and not of the adjacent YJM1 |
722019 |
| 2.7.10.1 | metabolism |
high levels of receptor tyrosine kinases in CCM3-deficient cells increases their susceptibility to tyrosine kinase inhibition |
760669 |
| 2.7.10.1 | metabolism |
phosphorylation of the protein chaperone small glutamine-rich tetratricopeptide repeat-containing protein alpha at Ser305 is essential for isoform platelet-derived growth factor receptor PDGFRalpha stabilization and cell survival in PDGFRalpha-dependent cancer cells |
723768 |
| 2.7.10.1 | physiological function |
although receptor tyrosine kinase EphB2 is not directly involved in the amyloid beta-induced depletion of NMDA-type glutamate receptors, increasing its expression may counteract this pathogenic process through a neuronal activity- and PDZ-dependent regulation of AMPA-type glutamate receptors |
738691 |
| 2.7.10.1 | physiological function |
brain-derived neurotrophic factor and TrkB signaling activates Narp expression alone |
704659 |
| 2.7.10.1 | physiological function |
EphA2 receptor tyrosine kinase plays a central role in the regulation of cell adhesion and guidance |
738611 |
| 2.7.10.1 | physiological function |
ERBB4 plays a key role in the survival of ERBB2C cancer cells after they develop resistance to ERBB2 inhibitors, lapatinib and trastuzumab |
737992 |
| 2.7.10.1 | physiological function |
hepatocyte growth factor expression leads to autocrine activation of its receptor tyrosine kinase, MET, in nearly half of the acute myeloid leukemia cell lines and clinical samples studied. Genetic depletion of hepatocyte growth factor or MET potently inhibits the growth and survival of hepatocyte growth factor-expressing acute myeloid leukemia cells. Leukemic cells treated with the specific MET kinase inhibitor crizotinib develop resistance due to compensatory upregulation of hepatocyte growth factor expression, leading to restoration of MET signaling. In cases of acute myeloid leukemia where MET is coactivated with other tyrosine kinases, such as fibroblast growth factor receptor 1, concomitant inhibition of FGFR1 and MET blocks compensatory hepatocyte growth factor upregulation, resulting in sustained logarithmic cell kill both in vitro and in xenograft models in vivo |
723254 |
| 2.7.10.1 | physiological function |
Kruppel-like factor 11 inhibits prostaglandin E2 synthesis via transcriptional silencing of the promoter of cytosolic phospholipase A2, this function of Kruppel-like factor 11 can be reversed by epidermal growth factor receptor-AKT-mediated post-translational modification of threonine 56 |
704651 |
