KIFAP3
Kinesin-associated protein 3
Also known as: FLA3, KAP-1, KAP3, KIFA3_HUMAN, SMAP
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q92845
- Gene
- KIFAP3
- Ensembl
- ENSG00000075945
- Chromosome
- 1
- Canonical length
- 792 aa
- Protein class
- Plasma proteins, Predicted intracellular proteins
- Subcellular location
- Nucleoplasm,Microtubules,Basal body
OverviewNCBI Gene
The small G protein GDP dissociation stimulator (smg GDS) is a regulator protein having two activities on a group of small G proteins including the Rho and Rap1 family members and Ki-Ras; one is to stimulate their GDP/GTP exchange reactions, and the other is to inhibit their interactions with membranes. The protein encoded by this gene contains 9 'Armadillo' repeats and interacts with the smg GDS protein through these repeats. This protein, which is highly concentrated around the endoplasmic reticulum, is phosphorylated by v-src, and this phosphorylation reduces the affinity of the protein for smg GDS. It is thought that this protein serves as a linker between human chromosome-associated polypeptide (HCAP) and KIF3A/B, a kinesin superfamily protein in the nucleus, and that it plays a role in the interaction of chromosomes with an ATPase motor protein. Several transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Mar 2011]
Canonical amino-acid sequenceUniProt
792 residues, UniProt reviewed canonical sequence.
>Q92845|KIFAP3
1 MQGEDARYLK RKVKGGNIDV HPSEKALIVH YEVEATILGE MGDPMLGERK ECQKIIRLKS
61 LNANTDITSL ARKVVEECKL IHPSKLNEVE QLLYYLQNRR DSLSGKEKKE KSSKPKDPPP
121 FEGMEIDEVA NINDMDEYIE LLYEDIPDKV RGSALILQLA RNPDNLEELL LNETALGALA
181 RVLREDWKQS VELATNIIYI FFCFSSFSQF HGLITHYKIG ALCMNIIDHE LKRHELWQEE
241 LSKKKKAVDE DPENQTLRKD YEKTFKKYQG LVVKQEQLLR VALYLLLNLA EDTRTELKMR
301 NKNIVHMLVK ALDRDNFELL ILVVSFLKKL SIFMENKNDM VEMDIVEKLV KMIPCEHEDL
361 LNITLRLLLN LSFDTGLRNK MVQVGLLPKL TALLGNDNYK QIAMCVLYHI SMDDRFKSMF
421 AYTDCIPQLM KMLFECSDER IDLELISFCI NLAANKRNVQ LICEGNGLKM LMKRALKFKD
481 PLLMKMIRNI SQHDGPTKNL FIDYVGDLAA QISNDEEEEF VIECLGTLAN LTIPDLDWEL
541 VLKEYKLVPY LKDKLKPGAA EDDLVLEVVI MIGTVSMDDS CAALLAKSGI IPALIELLNA
601 QQEDDEFVCQ IIYVFYQMVF HQATRDVIIK ETQAPAYLID LMHDKNNEIR KVCDNTLDII
661 AEYDEEWAKK IQSEKFRWHN SQWLEMVESR QMDESEQYLY GDDRIEPYIH EGDILERPDL
721 FYNSDGLIAS EGAISPDFFN DYHLQNGDVV GQHSFPGSLG MDGFGQPVGI LGRPATAYGF
781 RPDEPYYYGY GSLocalizationUniProt · AlphaFold · HPA
Whether an antibody against KIFAP3 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)
- 0.31
- Highest tissue expression
- 60 nTPM
Expression across tissuesHPA
Tissue
- cerebral cortex: 60 nTPM
- retina: 52 nTPM
- hypothalamus: 50 nTPM
- heart muscle: 48 nTPM
- hippocampal formation: 38 nTPM
- midbrain: 38 nTPM
Single-cell type
- platelets: 395 nCPM
- late spermatids: 319 nCPM
- early spermatids: 262 nCPM
- other brain neurons: 257 nCPM
- adrenal medulla cells: 255 nCPM
- thyrotrophs: 237 nCPM
Immune cell
- NK-cell: 22 nTPM
- non-classical monocyte: 20 nTPM
- T-reg: 19 nTPM
- basophil: 17 nTPM
- naive CD8 T-cell: 15 nTPM
- MAIT T-cell: 15 nTPM
Brain region
- cerebral cortex: 112 nTPM
- hypothalamus: 106 nTPM
- pons: 99 nTPM
- medulla oblongata: 94 nTPM
- white matter: 90 nTPM
- hippocampal formation: 88 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)
- 0.54
- gnomAD pLI
- 0
- gnomAD missense Z
- 1.91
- DepMap mean gene effect
- 0.01
- DepMap dependency class
- selective
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 10% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- anterograde dendritic transport of neurotransmitter receptor complex
- cardiac muscle cell apoptotic process
- cilium organization
- intracellular protein localization
- microtubule-based movement
- microtubule-based process
- negative regulation of cardiac muscle cell apoptotic process
- negative regulation of neuroblast proliferation
- negative regulation of thymocyte apoptotic process
- neuroblast proliferation
- plus-end-directed vesicle transport along microtubule
- protein-containing complex assembly
- signal transduction
- thymocyte apoptotic process
- positive regulation of calcium-dependent cell-cell adhesion
Molecular functions
Cellular components
- axoneme
- centrosome
- ciliary basal body
- ciliary tip
- ciliary transition zone
- cilium
- condensed nuclear chromosome
- cytosol
- dendrite cytoplasm
- endoplasmic reticulum
- glutamatergic synapse
- Golgi apparatus
- kinesin II complex
- microtubule cytoskeleton
- periciliary membrane compartment
- photoreceptor connecting cilium
- photoreceptor inner segment
- photoreceptor outer segment
- postsynapse
Protein domainsUniProt · Pfam · InterPro
- Armadillo
- Armadillo-like helical
- Armadillo-type fold
- Kinesin-associated protein 3
- Kinesin-associated protein (KAP)
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of KIFAP3 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 KIFAP3 as an antibody target. Whether an autoantibody or antibody against KIFAP3 could matter depends on whether native KIFAP3 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
KIFAP3 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 KIFAP3 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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