The ATMIN protein is a transcription factor that regulates ATM kinase activity and promotes DNA damage response through RAD51 foci formation and DYNLL1 gene activation. The gene is extremely intolerant to loss-of-function variants (pLI near 1.0), suggesting that mutations would likely cause severe developmental or neurological phenotypes, though specific disease associations have not yet been established in the provided data. The high constraint score indicates that pathogenic variants in this gene would be expected to have significant clinical consequences.

OMIMResearchSummary from RefSeq, UniProt
LOEUF 0.77
Clinical SummaryATMIN
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
Some data sources returned errors (1)

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Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.77LOEUF
pLI 0.000
Z-score 2.40
OE 0.47 (0.290.77)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
-0.73Z-score
OE missense 1.10 (1.021.19)
451 obs / 409.2 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.47 (0.290.77)
00.351.4
Missense OE1.10 (1.021.19)
00.61.4
Synonymous OE1.21
01.21.6
LoF obs/exp: 11 / 23.6Missense obs/exp: 451 / 409.2Syn Z: -2.16

ClinVar Variant Classifications

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

ATMIN · protein map & ClinVar variants

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

3D Protein StructureAlphaFold

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

No active trials found for this gene.

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Clinical Literature
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