EC Number   |
General Information |
Reference |
|---|
   2.7.11.17 | evolution |
calcium/calmodulin-dependent protein kinase IV (CAMKIV) is a member of Ser/Thr protein kinase family |
740003 |
| 2.7.11.17 | evolution |
the enzyme belongs to the serine/threonine protein kinase family |
740158 |
| 2.7.11.17 | malfunction |
after CASK silencing, single calcium channel recordings show an increase of the voltage-gated calcium channel Cav1.2 open probability explaining the increase of the whole-cell current |
740268 |
| 2.7.11.17 | malfunction |
autoactivation of CCaMK by mutation of Thr271. The complete absence of the EF-hand domains leads to unregulated Thr271 phosphorylation and deactivation of the protein |
741158 |
| 2.7.11.17 | malfunction |
calcium/calmodulin-dependent protein kinase 2 inhibition or knockdown ameliorates the basic calcium phosphate-induced changes in sry-box 9, indian hedgehog, type X collagen, interleukin-6 and matrix metalloproteinase 13 expression |
760806 |
| 2.7.11.17 | malfunction |
Camk2b-/- mice, which lack the beta isoform of calcium/calmodulin-dependent protein kinase 2 (CAMK2B), show very severe locomotion deficits, while global deletion of Camk2b in the adult mouse causes only mild locomotion deficits, suggesting that the severe locomotion deficits of Camk2b-/- mice are largely of developmental origin. Early onset deletion of Camk2b in cerebellum, striatum or forebrain do not recapitulate the locomotion deficits, suggesting that these deficits cannot be attributed to a single brain area. Most hippocampal phenotypes observed in Camk2b-/- mutants require CAMK2B protein, but not its enzymatic function |
-, 741420 |
| 2.7.11.17 | malfunction |
CaMKIIalpha inhibition protects from NO-induced neuronal cell death. Isozyme mutation of either site, Cys280 or Cys289, abolishes autonomous Ca2+-independent activity of the isozyme |
740722 |
| 2.7.11.17 | malfunction |
chronic overactivity of CaMKII is associated with left ventricular hypertrophy and dysfunction and lethal arrhythmias |
703089 |
| 2.7.11.17 | malfunction |
deletion causes decreased vascular smooth muscle proliferation, neointimal formation, and programmatic changes in cell cycle control, including increased p21 protein expression and decreased cdk activity |
722742 |
| 2.7.11.17 | malfunction |
enzyme deletion leads to growth defects in different media and increased sensitivity to several environmental stresses, including H2O2, menadione, SDS, and Congo red; they also reduced the ability to produce conidia and traps, thus causing a deficiency in nematicidal ability as well. Moreover, the mutants exhibit hypersensitivity to heat shock and ultraviolet-radiation stresses compared with the wild type strain |
-, 760420 |
