ID:MYLK2_HUMAN DESCRIPTION: RecName: Full=Myosin light chain kinase 2, skeletal/cardiac muscle; Short=MLCK2; EC=2.7.11.18; FUNCTION: Implicated in the level of global muscle contraction and cardiac function. Phosphorylates a specific serine in the N- terminus of a myosin light chain. CATALYTIC ACTIVITY: ATP + [myosin light-chain] = ADP + [myosin light-chain] phosphate. SUBUNIT: May interact with centrin. SUBCELLULAR LOCATION: Cytoplasm. Note=Colocalizes with phosphorylated myosin light chain (RLCP) at filaments of the myofibrils. TISSUE SPECIFICITY: Heart and skeletal muscles. Increased expression in the apical tissue compared to the interventricular septal tissue. DISEASE: Defects in MYLK2 are a cause of familial hypertrophic cardiomyopathy (CMH) [MIM:192600]; also designated FHC or HCM. Familial hypertrophic cardiomyopathy is a hereditary heart disorder characterized by ventricular hypertrophy, which is usually asymmetric and often involves the interventricular septum. The symptoms include dyspnea, syncope, collapse, palpitations, and chest pain. They can be readily provoked by exercise. The disorder has inter- and intrafamilial variability ranging from benign to malignant forms with high risk of cardiac failure and sudden cardiac death. SIMILARITY: Belongs to the protein kinase superfamily. CAMK Ser/Thr protein kinase family. SIMILARITY: Contains 1 protein kinase domain.
The RNAfold program from the Vienna RNA Package is used to perform the secondary structure predictions and folding calculations. The estimated folding energy is in kcal/mol. The more negative the energy, the more secondary structure the RNA is likely to have.
ModBase Predicted Comparative 3D Structure on Q9H1R3
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Orthologous Genes in Other Species
Orthologies between human, mouse, and rat are computed by taking the best BLASTP hit, and filtering out non-syntenic hits. For more distant species reciprocal-best BLASTP hits are used. Note that the absence of an ortholog in the table below may reflect incomplete annotations in the other species rather than a true absence of the orthologous gene.
US Server
