DGKG
Diacylglycerol kinase gamma
Also known as: DAGK3, DGKG_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- P49619
- Gene
- DGKG
- Ensembl
- ENSG00000058866
- Chromosome
- 3
- Canonical length
- 791 aa
- Protein class
- Enzymes, Metabolic proteins, Plasma proteins, Predicted intracellular proteins
- Subcellular location
- Vesicles,Plasma membrane
OverviewNCBI Gene
This gene encodes an enzyme that is a member of the type I subfamily of diacylglycerol kinases, which are involved in lipid metabolism. These enzymes generate phosphatidic acid by catalyzing the phosphorylation of diacylglycerol, a fundamental lipid second messenger that activates numerous proteins, including protein kinase C isoforms, Ras guanyl nucleotide-releasing proteins and some transient receptor potential channels. Diacylglycerol kinase gamma has been implicated in cell cycle regulation and in the negative regulation of macrophage differentiation in leukemia cells. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008]
Canonical amino-acid sequenceUniProt
791 residues, UniProt reviewed canonical sequence.
>P49619|DGKG
1 MGEERWVSLT PEEFDQLQKY SEYSSKKIKD ALTEFNEGGS LKQYDPHEPI SYDVFKLFMR
61 AYLEVDLPQP LSTHLFLAFS QKPRHETSDH PTEGASNSEA NSADTNIQNA DNATKADEAC
121 APDTESNMAE KQAPAEDQVA ATPLEPPVPR SSSSESPVVY LKDVVCYLSL LETGRPQDKL
181 EFMFRLYDSD ENGLLDQAEM DCIVNQMLHI AQYLEWDPTE LRPILKEMLQ GMDYDRDGFV
241 SLQEWVHGGM TTIPLLVLLG MDDSGSKGDG RHAWTMKHFK KPTYCNFCHI MLMGVRKQGL
301 CCTYCKYTVH ERCVSRNIPG CVKTYSKAKR SGEVMQHAWV EGNSSVKCDR CHKSIKCYQS
361 VTARHCVWCR MTFHRKCELS TLCDGGELRD HILLPTSICP ITRDRPGEKS DGCVSAKGEL
421 VMQYKIIPTP GTHPLLVLVN PKSGGRQGER ILRKFHYLLN PKQVFNLDNG GPTPGLNFFR
481 DTPDFRVLAC GGDGTVGWIL DCIDKANFAK HPPVAVLPLG TGNDLARCLR WGGGYEGGSL
541 TKILKDIEQS PLVMLDRWHL EVIPREEVEN GDQVPYSIMN NYFSIGVDAS IAHRFHVMRE
601 KHPEKFNSRM KNKLWYFEFG TSETFAATCK KLHDHIELEC DGVGVDLSNI FLEGIAILNI
661 PSMYGGTNLW GENKKNRAVI RESRKGVTDP KELKFCVQDL SDQLLEVVGL EGAMEMGQIY
721 TGLKSAGRRL AQCASVTIRT NKLLPMQVDG EPWMQPCCTI KITHKNQAPM MMGPPQKSSF
781 FSLRRKSRSK DLocalizationUniProt · AlphaFold · HPA
Whether an antibody against DGKG can act on the native protein depends on physical access: surface and secreted proteins are reachable by circulating antibodies, intracellular proteins usually are not.
- Antibody reachability
- Intracellular
- Secreted
- No
- Transmembrane segments
- 0
- Mean surface accessibility (rSASA)
- 0.32
- Highest tissue expression
- 26 nTPM
Expression across tissuesHPA
Tissue
- cerebellum: 26 nTPM
- cerebral cortex: 12 nTPM
- bone marrow: 8.8 nTPM
- heart muscle: 8.5 nTPM
- hippocampal formation: 8.4 nTPM
- epididymis: 7.6 nTPM
Single-cell type
- bergmann glia: 1,728 nCPM
- oligodendrocyte progenitor cells: 820 nCPM
- astrocytes: 530 nCPM
- somatotrophs: 445 nCPM
- vascular smooth muscle cells: 438 nCPM
- cardiomyocytes: 422 nCPM
Immune cell
- neutrophil: 2.6 nTPM
- classical monocyte: 2.1 nTPM
- myeloid DC: 1.5 nTPM
- non-classical monocyte: 1.5 nTPM
- eosinophil: 1.2 nTPM
- intermediate monocyte: 1.2 nTPM
Brain region
- cerebellum: 74 nTPM
- pons: 60 nTPM
- hippocampal formation: 59 nTPM
- basal ganglia: 52 nTPM
- cerebral cortex: 49 nTPM
- white matter: 43 nTPM
DiseaseUniProt · ClinVar · IEDB · PubMed
Four sources answering four different questions about DGKG.
Disease | GeneticClinVar
1 pathogenic / likely-pathogenic of 155 ClinVar records.
Conditions with pathogenic or likely-pathogenic variants.
Genetic constraint and essentialitygnomAD · DepMap
Does the body need this protein intact? Low LOEUF or a strong DepMap dependency means loss or blockade of the protein is likely to be felt.
- gnomAD LOEUF (loss-of-function intolerance)
- 0.82
- gnomAD pLI
- 0
- gnomAD missense Z
- 0.12
- DepMap mean gene effect
- -0.01
- DepMap dependency class
- none
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 8% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- diacylglycerol metabolic process
- glycerolipid metabolic process
- intracellular signal transduction
- lipid phosphorylation
- negative regulation of phospholipase C/protein kinase C signal transduction
- phosphatidic acid biosynthetic process
- phospholipase C-activating G protein-coupled receptor signaling pathway
- platelet activation
- regulation of dendrite development
Molecular functions
- ATP binding
- ATP-dependent diacylglycerol kinase activity
- calcium ion binding
- lipid binding
- zinc ion binding
Cellular components
Protein domainsUniProt · Pfam · InterPro
- Diacylglycerol kinase, accessory domain
- Diacylglycerol kinase, catalytic domain
- EF-hand domain
- Protein kinase C-like, phorbol ester/diacylglycerol-binding domain
- EF-hand domain pair
- NAD kinase/diacylglycerol kinase-like domain superfamily
- Inorganic polyphosphate/ATP-NAD kinase, N-terminal
- EF-Hand 1, calcium-binding site
- Diacylglycerol kinase type I, N-terminal
- Diacylglycerol kinase
- DGK type I, N-terminal domain superfamily
- C1-like domain superfamily
- Phorbol esters/diacylglycerol binding domain (C1 domain)
- Diacylglycerol kinase accessory domain
- Diacylglycerol kinase catalytic domain
- Diacylglycerol kinase N-terminus
- Diacylglycerol kinase gamma, second protein kinase C conserved region 1
KeywordsUniProt
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads DGKG as an antibody target. Whether an autoantibody or antibody against DGKG could matter depends on whether native DGKG is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
DGKG is annotated as predominantly intracellular. Intracellular proteins are common autoantibody markers, becoming visible to the immune system after cell injury or altered processing, but are usually markers of disease rather than direct drivers.
Annotation status
The present source text does not explicitly label DGKG as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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