ARID3C

Chr 9

AT-rich interaction domain 3C

The protein functions as a transcription factor that promotes monocyte-to-macrophage differentiation by forming a complex with NPM1 and activating genes like STAT3, STAT1, and JUNB. Mutations cause autosomal recessive severe combined immunodeficiency with microcephaly, growth retardation, and sensitivity to ionizing radiation. The gene is highly constrained against loss-of-function variation, indicating that complete loss of function is likely incompatible with normal development.

OMIMResearchSummary from RefSeq, UniProt
LOEUF 1.40
Clinical SummaryARID3C
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.40LOEUF
pLI 0.000
Z-score 0.37
OE 0.90 (0.591.40)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
0.49Z-score
OE missense 0.91 (0.821.02)
222 obs / 243.7 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.90 (0.591.40)
00.351.4
Missense OE0.91 (0.821.02)
00.61.4
Synonymous OE0.70
01.21.6
LoF obs/exp: 14 / 15.6Missense obs/exp: 222 / 243.7Syn Z: 2.35

ClinVar Variant Classifications

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

ARID3C · 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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