FN3KRP
Ketosamine-3-kinase
Also known as: FLJ12171, FN3KL, KT3K_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q9HA64
- Gene
- FN3KRP
- Ensembl
- ENSG00000141560
- Chromosome
- 17
- Canonical length
- 309 aa
- Protein class
- Enzymes, Metabolic proteins, Plasma proteins, Predicted intracellular proteins
- Subcellular location
- Nucleoplasm
OverviewNCBI Gene
A high concentration of glucose can result in non-enzymatic oxidation of proteins by reaction of glucose and lysine residues (glycation). Proteins modified in this way are less active or functional. This gene encodes an enzyme which catalyzes the phosphorylation of psicosamines and ribulosamines compared to the neighboring gene which encodes a highly similar enzyme, fructosamine-3-kinase, which has different substrate specificity. The activity of both enzymes may result in deglycation of proteins to restore their function. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Mar 2012]
Canonical amino-acid sequenceUniProt
309 residues, UniProt reviewed canonical sequence.
>Q9HA64|FN3KRP
1 MEELLRRELG CSSVRATGHS GGGCISQGRS YDTDQGRVFV KVNPKAEARR MFEGEMASLT
61 AILKTNTVKV PKPIKVLDAP GGGSVLVMEH MDMRHLSSHA AKLGAQLADL HLDNKKLGEM
121 RLKEAGTVGR GGGQEERPFV ARFGFDVVTC CGYLPQVNDW QEDWVVFYAR QRIQPQMDMV
181 EKESGDREAL QLWSALQLKI PDLFRDLEII PALLHGDLWG GNVAEDSSGP VIFDPASFYG
241 HSEYELAIAG MFGGFSSSFY SAYHGKIPKA PGFEKRLQLY QLFHYLNHWN HFGSGYRGSS
301 LNIMRNLVKLocalizationUniProt · AlphaFold · HPA
Whether an antibody against FN3KRP 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)
- 0.26
- Highest tissue expression
- 50 nTPM
Expression across tissuesHPA
Tissue
- spinal cord: 50 nTPM
- midbrain: 41 nTPM
- amygdala: 41 nTPM
- cerebral cortex: 40 nTPM
- hippocampal formation: 39 nTPM
- basal ganglia: 38 nTPM
Single-cell type
- cytotrophoblasts: 122 nCPM
- migrating cytotrophoblasts: 95 nCPM
- syncytiotrophoblasts: 64 nCPM
- extravillous trophoblasts: 50 nCPM
- esophageal basal cells: 47 nCPM
- hofbauer cells: 45 nCPM
Immune cell
- plasmacytoid DC: 36 nTPM
- naive CD4 T-cell: 33 nTPM
- basophil: 32 nTPM
- NK-cell: 32 nTPM
- eosinophil: 31 nTPM
- T-reg: 30 nTPM
Brain region
- white matter: 40 nTPM
- basal ganglia: 32 nTPM
- cerebellum: 31 nTPM
- medulla oblongata: 31 nTPM
- spinal cord: 31 nTPM
- thalamus: 28 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)
- 1.54
- gnomAD pLI
- 0
- gnomAD missense Z
- -0.33
- 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
Molecular functions
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads FN3KRP as an antibody target. Whether an autoantibody or antibody against FN3KRP could matter depends on whether native FN3KRP is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
FN3KRP 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 FN3KRP as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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