FOXI2
Forkhead box protein I2
Also known as: FLJ46831, FOXI2_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q6ZQN5
- Gene
- FOXI2
- Ensembl
- ENSG00000186766
- Chromosome
- 10
- Canonical length
- 318 aa
- Protein class
- Predicted intracellular proteins, Transcription factors
OverviewNCBI Gene
Predicted to enable DNA-binding transcription factor activity, RNA polymerase II-specific and RNA polymerase II cis-regulatory region sequence-specific DNA binding activity. Predicted to be involved in anatomical structure morphogenesis; cell differentiation; and regulation of transcription by RNA polymerase II. Predicted to be located in chromatin. [provided by Alliance of Genome Resources, Jul 2025]
Canonical amino-acid sequenceUniProt
318 residues, UniProt reviewed canonical sequence.
>Q6ZQN5|FOXI2
1 MATYCDDLGP SSAPPGQAQA TAHPPGYEPG DLGAVGGGPL LWVNAPALSP KSYASGPGPA
61 PPYAAPSYGA PGPLLGAPGG LAGADLAWLS LSGQQELLRL VRPPYSYSAL IAMAIQSAPL
121 RKLTLSQIYQ YVAGNFPFYK RSKAGWQNSI RHNLSLNDCF KKVPRDEDDP GKGNYWTLDP
181 NCEKMFDNGN FRRKRKRRAE ASAAVRSGAR SVGGAEAPAL EPPSAACLDL QASPSPSAPE
241 AATCFSGFAS AMSALAGGLG TFPGGLAGDF SFGRRPPTVA THAPQTLNPS PGFAPGHQTA
301 AAGFRLSHLL YSREGTEVLocalizationUniProt · AlphaFold · HPA
Whether an antibody against FOXI2 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)
- 0.6
- Highest tissue expression
- 2.8 nTPM
Expression across tissuesHPA
Tissue
- kidney: 2.8 nTPM
- esophagus: 1.8 nTPM
- cervix: 1.6 nTPM
- pituitary gland: 1.1 nTPM
- parathyroid gland: 0.8 nTPM
- salivary gland: 0.8 nTPM
Single-cell type
- salivary ionocytes: 22 nCPM
- epididymal clear cells: 20 nCPM
- respiratory ionocytes: 18 nCPM
- esophageal apical cells: 5.8 nCPM
- thymic myoid cells: 4.1 nCPM
- renal collecting duct intercalated cells: 3 nCPM
Immune cell
- basophil: 0 nTPM
- classical monocyte: 0 nTPM
- eosinophil: 0 nTPM
- gdT-cell: 0 nTPM
- intermediate monocyte: 0 nTPM
- MAIT T-cell: 0 nTPM
Brain region
- hypothalamus: 0.8 nTPM
- medulla oblongata: 0.5 nTPM
- spinal cord: 0.4 nTPM
- cerebellum: 0.3 nTPM
- cerebral cortex: 0.3 nTPM
- choroid plexus: 0.3 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)
- 1.85
- gnomAD pLI
- 0
- gnomAD missense Z
- -0.09
- DepMap mean gene effect
- 0.06
- DepMap dependency class
- none
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 3% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- anatomical structure morphogenesis
- cell differentiation
- regulation of transcription by RNA polymerase II
Molecular functions
- DNA-binding transcription factor activity, RNA polymerase II-specific
- RNA polymerase II cis-regulatory region sequence-specific DNA binding
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads FOXI2 as an antibody target. Whether an autoantibody or antibody against FOXI2 could matter depends on whether native FOXI2 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
FOXI2 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 FOXI2 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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