Seroatlas · Human Serome Atlas

IFTAP

Intraflagellar transport-associated protein

Also known as: C11orf74, FLJ38678, HEPIS, IFTAP_HUMAN, NWC

Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene

Protein identityUniProt · HPA

UniProt accession: Q86VG3
Gene: IFTAP
Ensembl: ENSG00000166352
Chromosome: 11
Canonical length: 221 aa
Protein class: Predicted intracellular proteins
Subcellular location: Aggresome,Cytosol

OverviewNCBI Gene

This gene encodes a protein that was identified as a cellular interacting partner of non-structural protein 10 of the severe acute respiratory syndrome coronavirus (SARS-CoV). The encoded protein may function as a negative regulator of transcription. There is a pseudogene for this gene on chromosome 1. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Mar 2013]

Canonical amino-acid sequenceUniProt

221 residues, UniProt reviewed canonical sequence.

>Q86VG3|IFTAP
     1  MSAHMSGLEI MDEDQLIKDV LDKFLNCHEQ TYDEEFLNTF THLSQEDHVS KRGVFGTDSS
    61  ENIFTSAKVT HKNEADDYHL RNKTIFLRTS SQCLEEQVDN FLDLEDLDMD EEIKPQMSED
   121  LLLLPGEVEQ DVSTSIPSCI PFVAQPPTCE VKPKPSVKRM DKQTEEILGD EVQLFSLDEE
   181  FDYDNVMLTS KFSPAEIENI KELCKQQKRK DTSPDLEKSC D

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against IFTAP 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): 0.67
Highest tissue expression: 88 nTPM

Expression across tissuesHPA

Tissue

choroid plexus: 88 nTPM
thyroid gland: 77 nTPM
testis: 47 nTPM
heart muscle: 39 nTPM
tongue: 39 nTPM
skeletal muscle: 38 nTPM

Single-cell type

late primary spermatocytes: 332 nCPM
choroid plexus epithelial cells: 255 nCPM
late spermatids: 243 nCPM
respiratory ciliated cells: 186 nCPM
fallopian tube ciliated cells: 185 nCPM
early spermatids: 162 nCPM

Immune cell

plasmacytoid DC: 29 nTPM
myeloid DC: 21 nTPM
classical monocyte: 18 nTPM
intermediate monocyte: 15 nTPM
non-classical monocyte: 15 nTPM
NK-cell: 14 nTPM

Brain region

choroid plexus: 43 nTPM
cerebral cortex: 14 nTPM
midbrain: 13 nTPM
thalamus: 13 nTPM
white matter: 13 nTPM
basal ganglia: 13 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): 1.66
gnomAD pLI: 0
DepMap mean gene effect: 0.04
DepMap dependency class: none

Cancer expressionTCGA

Across TCGA tumor cohorts, this protein is over-expressed in roughly 5% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).

OntologyGO

Biological processes

Molecular functions

intraciliary transport particle A binding

Cellular components

Protein domainsUniProt · Pfam · InterPro

Intraflagellar transport-associated protein
Intraflagellar transport-associated protein

KeywordsUniProt

Phosphoprotein

InteractionsUniProt · HPA

Protein binding partners of IFTAP in the human serome: UniProt-annotated complex subunits plus reported interactors. Each links to its own Seroatlas record.

IFT122

Antibody and autoantibody relevanceSeroatlas analysis

Seroatlas reads IFTAP as an antibody target. Whether an autoantibody or antibody against IFTAP could matter depends on whether native IFTAP is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

IFTAP 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 IFTAP as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

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