SCUBA

DAPK2 — Death associated protein kinase 2

DAPK2 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.

DAPK2's module in each cell type

Cell typeModuleShares the module with
CD4⁺ T cellsCytotoxic effector
Cytotoxicity
ADAP1, ALOX5AP, AOAH, CD244, CMIP, CPNE7, CRTAM, DOCK5 +15 moreView in SCUBA
EnterocytesJunctional Hippo/TGF-beta signaling
Migration & adhesion
AFDN, BACH1, CCNL1, DST, PELI2, SMAD3, UACA, WWC1View in SCUBA
Gamma-delta T cellsGut-homing Residence
Tissue residence
ADAM28, ASB2, ATP8B4, CAPG, CCR9, CD101, CD9, DENND1B +8 more
Natural Killer cellsNK Checkpoint Receptors
Immune regulation
CD7, CD96, CRACR2B, ECH1, ECI2, ISYNA1, KIR2DL4, MAP4 +5 moreView in SCUBA

About the gene

SynonymsDRP-1, MGC119312
Chromosome15: 63907036-64072033
Predicted locationIntracellular, Membrane
Essential geneNo
Protein classEnzymes, Predicted intracellular proteins, Predicted membrane proteins
Molecular functionCalmodulin-binding, Kinase, Serine/threonine-protein kinase, Transferase
Biological processApoptosis

Function

Calcium/calmodulin-dependent serine/threonine kinase involved in multiple cellular signaling pathways that trigger cell survival, apoptosis, and autophagy. Regulates both type I apoptotic and type II autophagic cell death signals, depending on the cellular setting. The former is caspase-dependent, while the latter is caspase-independent and is characterized by the accumulation of autophagic vesicles. Acts as a mediator of anoikis and a suppressor of beta-catenin-dependent anchorage-independent growth of malignant epithelial cells. May play a role in granulocytic maturation. Regulates granulocytic motility by controlling cell spreading and polarization. Isoform 2 is not regulated by calmodulin. It can phosphorylate MYL9. It can induce membrane blebbing and autophagic cell death

Human Protein Atlas · Open Targets · UniProt

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