SQSTM1

Chr 5ADAR

sequestosome 1

Also known as: A170, DMRV, EBIAP, FTDALS3, NADGP, OSIL, PDB3, ZIP3

This gene encodes a multifunctional scaffolding protein that binds ubiquitin, regulates NF-kB signaling pathway activation, and functions in autophagy. Mutations cause autosomal dominant frontotemporal dementia and/or amyotrophic lateral sclerosis, distal myopathy with rimmed vacuoles, and Paget disease of bone, as well as autosomal recessive childhood-onset neurodegeneration with ataxia, dystonia, and gaze palsy. The pathogenic mechanism involves disrupted protein aggregation clearance and impaired autophagy processes.

Summary from RefSeq, OMIM, UniProt
Research Assistant →

Primary Disease Associations & Inheritance

Frontotemporal dementia and/or amyotrophic lateral sclerosis 3MIM #616437
AD
Myopathy, distal, with rimmed vacuolesMIM #617158
AD
Neurodegeneration with ataxia, dystonia, and gaze palsy, childhood-onsetMIM #617145
AR
Paget disease of bone 3MIM #167250
AD
2
Active trials
492
Pubs (1 yr)
0
P/LP submissions
P/LP missense
0.80
LOEUF
LOF
Mechanism· G2P
Clinical SummarySQSTM1
🧬
Gene-Disease Validity (ClinGen)
frontotemporal dementia and/or amyotrophic lateral sclerosis 3 · ADModerate

Moderate evidence — consider for supplementary testing

Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
💊
Clinical Trials
2 active or recruiting trials — potential therapeutic options may be available
📖
GeneReview available — SQSTM1
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.80LOEUF
pLI 0.001
Z-score 2.18
OE 0.44 (0.260.80)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
-0.94Z-score
OE missense 1.16 (1.061.28)
304 obs / 261.2 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.44 (0.260.80)
00.351.4
Missense OE1.16 (1.061.28)
00.61.4
Synonymous OE1.27
01.21.6
LoF obs/exp: 8 / 18.0Missense obs/exp: 304 / 261.2Syn Z: -2.24
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
limitedSQSTM1-related Paget disease of boneLOFAD
DN
0.6065th %ile
GOF
0.5367th %ile
LOF
0.4233th %ile

This gene has evidence for multiple mechanisms of pathogenicity (gain-of-function and loss-of-function). The Badonyi & Marsh model scores dominant-negative highest among its predictions, but genomic evidence (constraint, ClinVar variant spectrum, and literature) most strongly supports gain-of-function. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

GOF1 literature citation
LOF1 literature citation

Literature Evidence

GOFRea et al. (2006) demonstrated that transfection of the P392L mutation into HEK293 cells resulted in increased NFKB1 activity compared to wildtype, suggesting a gain of function.PMID:16813535
LOFOur results identify a novel pathogenic SQSTM1 S224X mutation in an atypical FTD patient accompanied with loss of SQSTM1/p62 protein expression probably due to SQSTM1 gene haploinsufficiency.PMID:29467647

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312.

ClinVar Variant Classifications

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

SQSTM1 · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

Clinical Literature
Open Research Assistant →