KTI12

Chr 1

KTI12 chromatin associated homolog

Also known as: SBBI81, TOT4

The KTI12 protein binds ATP and is involved in tRNA wobble uridine modification, a process essential for proper protein synthesis. Mutations in this gene cause autosomal recessive intellectual disability with microcephaly and seizures, typically presenting in early childhood. The gene is not highly constrained against loss-of-function variants, which is consistent with its recessive inheritance pattern.

ResearchSummary from RefSeq
LOEUF 1.42
Clinical SummaryKTI12
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
1.42LOEUF
pLI 0.000
Z-score 0.73
OE 0.73 (0.401.42)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.50Z-score
OE missense 1.09 (0.981.22)
240 obs / 219.2 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.73 (0.401.42)
00.351.4
Missense OE1.09 (0.981.22)
00.61.4
Synonymous OE1.07
01.21.6
LoF obs/exp: 6 / 8.2Missense obs/exp: 240 / 219.2Syn Z: -0.56

ClinVar Variant Classifications

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

KTI12 · 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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Recent Gene-Specific Literature
Gene in title · MEDLINE · newest first
Europe PMC