Seroatlas · Human Serome Atlas

LITAF

Lipopolysaccharide-induced tumor necrosis factor-alpha factor

Also known as: FLJ38636, LITAF_HUMAN, PIG7, SIMPLE, TP53I7

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

Protein identityUniProt · HPA

UniProt accession
Q99732
Gene
LITAF
Ensembl
ENSG00000189067
Chromosome
16
Canonical length
161 aa
Protein class
Disease related genes, Human disease related genes, Predicted intracellular proteins, Predicted membrane proteins
Subcellular location
Nucleoplasm,Golgi apparatus,Vesicles

OverviewNCBI Gene

Lipopolysaccharide is a potent stimulator of monocytes and macrophages, causing secretion of tumor necrosis factor-alpha (TNF-alpha) and other inflammatory mediators. This gene encodes lipopolysaccharide-induced TNF-alpha factor, which is a DNA-binding protein and can mediate the TNF-alpha expression by direct binding to the promoter region of the TNF-alpha gene. The transcription of this gene is induced by tumor suppressor p53 and has been implicated in the p53-induced apoptotic pathway. Mutations in this gene cause Charcot-Marie-Tooth disease type 1C (CMT1C) and may be involved in the carcinogenesis of extramammary Paget's disease (EMPD). Multiple alternatively spliced transcript variants have been found for this gene. [provided by RefSeq, Dec 2014]

Canonical amino-acid sequenceUniProt

161 residues, UniProt reviewed canonical sequence.

>Q99732|LITAF
     1  MSVPGPYQAA TGPSSAPSAP PSYEETVAVN SYYPTPPAPM PGPTTGLVTG PDGKGMNPPS
    61  YYTQPAPIPN NNPITVQTVY VQHPITFLDR PIQMCCPSCN KMIVSQLSYN AGALTWLSCG
   121  SLCLLGCIAG CCFIPFCVDA LQDVDHYCPN CRALLGTYKR L

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against LITAF 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)
0.52
Highest tissue expression
200 nTPM

Expression across tissuesHPA

Tissue

  • urinary bladder: 200 nTPM
  • bone marrow: 195 nTPM
  • lung: 187 nTPM
  • appendix: 156 nTPM
  • kidney: 145 nTPM
  • adipose tissue: 130 nTPM

Single-cell type

  • neutrophils: 7,072 nCPM
  • monocytes: 847 nCPM
  • extravillous trophoblasts: 764 nCPM
  • nk-cells: 677 nCPM
  • macrophages: 622 nCPM
  • salivary acinar cells: 619 nCPM

Immune cell

  • neutrophil: 2,587 nTPM
  • total PBMC: 584 nTPM
  • basophil: 510 nTPM
  • gdT-cell: 461 nTPM
  • memory CD8 T-cell: 413 nTPM
  • naive CD8 T-cell: 382 nTPM

Brain region

  • white matter: 184 nTPM
  • medulla oblongata: 165 nTPM
  • pons: 137 nTPM
  • basal ganglia: 132 nTPM
  • cerebellum: 131 nTPM
  • thalamus: 130 nTPM

DiseaseUniProt · ClinVar · IEDB · PubMed

Four sources answering four different questions about LITAF.

Disease | AllUniProt

Conditions LITAF is implicated in, by any mechanism.

  • Charcot-Marie-Tooth disease, demyelinating, type 1C (CMT1C) MIM:601098

Disease | GeneticClinVar

8 pathogenic / likely-pathogenic of 311 ClinVar records.

Conditions with pathogenic or likely-pathogenic variants.

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)
1.28
gnomAD pLI
0.03
gnomAD missense Z
0.22
DepMap mean gene effect
0.05
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

Cellular components

Protein domainsUniProt · Pfam · InterPro

KeywordsUniProt

InteractionsUniProt · HPA

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

LITAF is annotated at the cell surface, where native LITAF 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 LITAF as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

Canonical record: https://seroatlas.com/gene/LITAF. Study-independent annotations aggregated from UniProt, Human Protein Atlas, PubMed, IEDB, Pfam, InterPro, Gene Ontology, AlphaFold, gnomAD, DepMap, ClinVar, TCGA. Catalog release seroatlas-reviewed-human-uniprot-20260313.

Seroatlas is the reference for exploring autoantibody and antibody serology at the human-protein level: the autoreactome and human serome, multiplex serology (HuProt, HuScan, VirScan, PhIP-Seq).

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