SCUBA

CAMK2D — Calcium/calmodulin dependent protein kinase II delta

CAMK2D belongs to a gene co-expression module in 4 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.

CAMK2D's module in each cell type

Cell typeModuleShares the module with
CD19⁺ B cellsBCR signaling/maturation
B cell maturation
ATP6V0A1, BCL11A, CD22, CLEC2D, DDHD1, DGKD, IL4R, ITPR1 +9 moreView in SCUBA
EndothelialQuiescent EC Identity
Endothelial cell development
ADRB1, CLU, CYP1B1, FAM20A, FOXP1, FZD6, GCHFR, GIPC2 +19 moreView in SCUBA
EnterocytesApicobasal polarity scaffold
Migration & adhesion
ADGRG7, DPYD, MAGI3, MAST2, MGAM2, NUMB, PATJ, PRELID2 +3 moreView in SCUBA
Mucosal-associated invariant T cellCalcium Signal Integration
TCR Signaling
ANKRD44, ARB2A, DOCK10, ELMO1, EXOC4, FCHSD2, FNDC3A, FOXN3 +20 more

About the gene

SynonymsCAMKD
Chromosome4: 113418054-113761927
Predicted locationIntracellular, Membrane
Essential geneNo
Protein classEnzymes, Plasma proteins, Predicted intracellular proteins, Predicted membrane proteins
Molecular functionCalmodulin-binding, Kinase, Serine/threonine-protein kinase, Transferase

Function

Calcium/calmodulin-dependent protein kinase involved in the regulation of Ca(2+) homeostatis and excitation-contraction coupling (ECC) in heart by targeting ion channels, transporters and accessory proteins involved in Ca(2+) influx into the myocyte, Ca(2+) release from the sarcoplasmic reticulum (SR), SR Ca(2+) uptake and Na(+) and K(+) channel transport. Targets also transcription factors and signaling molecules to regulate heart function. In its activated form, is involved in the pathogenesis of dilated cardiomyopathy and heart failure. Contributes to cardiac decompensation and heart failure by regulating SR Ca(2+) release via direct phosphorylation of RYR2 Ca(2+) channel on 'Ser-2808'. In the nucleus, phosphorylates the MEF2 repressor HDAC4, promoting its nuclear export and binding to 14-3-3 protein, and expression of MEF2 and genes involved in the hypertrophic program. Is essential for left ventricular remodeling responses to myocardial infarction. In pathological myocardial remodeling acts downstream of the beta adrenergic receptor signaling cascade to regulate key proteins involved in ECC. Regulates Ca(2+) influx to myocytes by binding and phosphorylating the L-type Ca(2+) channel subunit beta-2 CACNB2. In addition to Ca(2+) channels, can target and regulate the cardiac sarcolemmal Na(+) channel Nav1.5/SCN5A and the K+ channel Kv4.3/KCND3, which contribute to arrhythmogenesis in heart failure. Phosphorylates phospholamban (PLN/PLB), an endogenous inhibitor of SERCA2A/ATP2A2, contributing to the enhancement of SR Ca(2+) uptake that may be important in frequency-dependent acceleration of relaxation (FDAR) and maintenance of contractile function during acidosis. May participate in the modulation of skeletal muscle function in response to exercise, by regulating SR Ca(2+) transport through phosphorylation of PLN/PLB and triadin, a ryanodine receptor-coupling factor. In response to interferon-gamma (IFN-gamma) stimulation, catalyzes phosphorylation of STAT1, stimulating the JAK-STAT signaling pathway (By similarity).

Human Protein Atlas · Open Targets · UniProt

Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.