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Canine gene

FAS

Human counterpart: FAS

FAS is a gene catalogued in the canine genome. Here is its canonical identity across the genomics world and, where documented, its human counterpart.

In the reference databases

FAS as it is catalogued across the genomics world. Each link is the canonical record, so this gene composes with everything those resources know.

The human counterpart

In humans, this gene's counterpart is FAS. That ortholog is what connects FAS to a century of human medical genetics. The dog and human proteins are 49% identical (a lower-confidence 1:1 call, shown for transparency, not hidden).

In people, FAS rarely tolerates loss-of-function variation (gnomAD v4.1 constraint, LOEUF 0.37), a sign it does important, dosage-sensitive work.

In people, variants in the FAS gene have conflicting classifications in ClinVar, and none is expert-reviewed. The evidence is unsettled, not that variants here are benign.

In dogs, 4 of 1,572 Dog10K variants in this gene sit at a position kept conserved across 241 mammals (the exhaustive scan), candidates worth a closer look, never a diagnosis.

Translational evidence balance
balanced · 0

Dog and human evidence are symmetric here, a validated cross-species footprint. Coverage, not importance. D = 1 dog vs H = 1 human cited disease channels.

Medicine face

Q4 · both planes dark

FAS

Two planes on one gene. Disagreement is the reading, not a hole to fill.Neither plane holds a filled product row. The empty cells are the instrument.

Canine plane

Coverage

dark · below bar

dark_in_all_frames

Spectra

4 named streams agree. A recount, not a medicine vote.

Open Spectra

Canine bridge

We hold no OMIA phene for this gene.

Lookup · Discovery · Frontier

Lookup cleared (human P/LP signal exists below the 3-star expert-review bar; moderate-confidence anchor (Landrum et al. 2018)). Discovery absent. A candidate never fills a drug row. Frontier cause below bar.

Medicine plane

Mechanism

Receptor for TNFSF6/FASLG.

Full function description, 4 more sentences
  • The adapter molecule FADD recruits caspase CASP8 to the activated receptor.
  • The resulting death-inducing signaling complex (DISC) performs CASP8 proteolytic activation which initiates the subsequent cascade of caspases (aspartate-specific cysteine proteases) mediating apoptosis.
  • FAS-mediated apoptosis may have a role in the induction of peripheral tolerance, in the antigen- stimulated suicide of mature T-cells, or both.
  • The secreted isoforms 2 to 6 block apoptosis (in vitro).

Source UniProt via Open Targets · PMID 19118384 · PMID 7533181 · PMID 9184224

TP53 Regulates Transcription of Death Receptors and Ligands · Dimerization of procaspase-8 · RIPK1-mediated regulated necrosis · FasL/ CD95L signaling · Regulation by c-FLIP · Caspase activation via Death Receptors in the presence of ligand · Reactome

Molecules

Open Targets 26.06 returns no drug or clinical candidate for this target. The empty list is the reading.

Canine trials

unqueryable

We hold no canine registry row. The AVMA Veterinary Clinical Trials Registry is the index that would hold one. This station is unqueryable until that ingest exists. That is not evidence that nobody runs trials in dogs.

PK / tox station

stub

This station is not wired. No PK or tox numbers.

This is not a treatment recommendation and not a claim about any individual dog.

Molecule direction and mechanism of action include ChEMBL (CC BY-SA 3.0).

Coverage · Spectra · Frontier

Research tools for this gene
Dog10K lookup Candidate models AVCG classification table

Lookup and discovery are candidate-framed research surfaces. Classification renders AVCG grades we cite; Sniff does not score variants with a model of its own.

On the numbers

Per-breed allele frequencies across the atlas are surfaced for the trait loci Sniff has verified a direction-of-effect for. For FAS we show the cited identity and disease associations, and we would rather show you exactly that than a frequency we cannot yet interpret honestly. See the gene catalog for trait loci with frequency views and every disease-linked gene page.

How to cite this page

Gene identity and disease associations are grounded in OMIA (CC-BY) and the open Sniff Atlas. Full citation formats at sniff.world/cite.

Last updated
Sources: OMIA · Sniff gene crossrefs · Ensembl / NCBI / HGNC · gnomAD v4.1 (Karczewski 2020) · ClinVar (Landrum 2018) · Dog10K (Meadows 2023) · Zoonomia 241-way phyloP (Christmas 2023)