DOK2
Docking protein 2
Also known as: Dok-2, DOK2_HUMAN, p56dok-2
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- O60496
- Gene
- DOK2
- Ensembl
- ENSG00000147443
- Chromosome
- 8
- Canonical length
- 412 aa
- Protein class
- Predicted intracellular proteins
- Subcellular location
- Plasma membrane
OverviewNCBI Gene
The protein encoded by this gene is constitutively tyrosine phosphorylated in hematopoietic progenitors isolated from chronic myelogenous leukemia (CML) patients in the chronic phase. It may be a critical substrate for p210(bcr/abl), a chimeric protein whose presence is associated with CML. This encoded protein binds p120 (RasGAP) from CML cells. [provided by RefSeq, Jul 2008]
Canonical amino-acid sequenceUniProt
412 residues, UniProt reviewed canonical sequence.
>O60496|DOK2
1 MGDGAVKQGF LYLQQQQTFG KKWRRFGASL YGGSDCALAR LELQEGPEKP RRCEAARKVI
61 RLSDCLRVAE AGGEASSPRD TSAFFLETKE RLYLLAAPAA ERGDWVQAIC LLAFPGQRKE
121 LSGPEGKQSR PCMEENELYS SAVTVGPHKE FAVTMRPTEA SERCHLRGSY TLRAGESALE
181 LWGGPEPGTQ LYDWPYRFLR RFGRDKVTFS FEAGRRCVSG EGNFEFETRQ GNEIFLALEE
241 AISAQKNAAP ATPQPQPATI PASLPRPDSP YSRPHDSLPP PSPTTPVPAP RPRGQEGEYA
301 VPFDAVARSL GKNFRGILAV PPQLLADPLY DSIEETLPPR PDHIYDEPEG VAALSLYDSP
361 QEPRGEAWRR QATADRDPAG LQHVQPAGQD FSASGWQPGT EYDNVVLKKG PKLocalizationUniProt · AlphaFold · HPA
Whether an antibody against DOK2 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
- Cell surface
- Secreted
- No
- Transmembrane segments
- 0
- Mean surface accessibility (rSASA)
- 0.51
- Highest tissue expression
- 44 nTPM
Expression across tissuesHPA
Tissue
- spleen: 44 nTPM
- appendix: 25 nTPM
- lymph node: 25 nTPM
- lung: 24 nTPM
- bone marrow: 18 nTPM
- thymus: 15 nTPM
Single-cell type
- platelets: 559 nCPM
- hofbauer cells: 202 nCPM
- kupffer cells: 187 nCPM
- cdc: 166 nCPM
- nk-cells: 146 nCPM
- monocytes: 141 nCPM
Immune cell
- eosinophil: 1,569 nTPM
- total PBMC: 809 nTPM
- intermediate monocyte: 624 nTPM
- T-reg: 599 nTPM
- non-classical monocyte: 583 nTPM
- basophil: 579 nTPM
Brain region
- thalamus: 7 nTPM
- choroid plexus: 3.5 nTPM
- cerebral cortex: 2.8 nTPM
- midbrain: 1.5 nTPM
- pons: 1.4 nTPM
- white matter: 1.3 nTPM
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)
- 1.07
- gnomAD pLI
- 0
- gnomAD missense Z
- -0.86
- DepMap mean gene effect
- 0.11
- DepMap dependency class
- none
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 4% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- cell surface receptor protein tyrosine kinase signaling pathway
- cell surface receptor signaling pathway
- Ras protein signal transduction
- signal transduction
Molecular functions
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of DOK2 in the human serome: UniProt-annotated complex subunits plus reported interactors. Each links to its own Seroatlas record.
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads DOK2 as an antibody target. Whether an autoantibody or antibody against DOK2 could matter depends on whether native DOK2 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
DOK2 is annotated at the cell surface, where native DOK2 is exposed to circulating antibodies and is a prime autoantibody target that could block, deplete, or overstimulate it.
Annotation status
The present source text does not explicitly label DOK2 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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