RPL38

Chr 17

ribosomal protein L38

Also known as: L38, eL38

The protein is a component of the large 60S ribosomal subunit that catalyzes protein synthesis in the cytoplasm. Mutations cause autosomal dominant disease through loss-of-function mechanisms, as evidenced by high intolerance to loss-of-function variants (pLI 0.83) and haploinsufficiency (LOEUF 0.52). The specific neurological phenotype associated with RPL38 mutations is not defined in the available data.

Summary from RefSeq, UniProt, Mechanism
0
Active trials
8
Pubs (1 yr)
0
P/LP submissions
P/LP missense
0.52
LOEUF
LOF
Mechanism· predicted
Clinical SummaryRPL38
Population Constraint (gnomAD)
Moderately constrained gene (pLI 0.83) — some intolerance to loss-of-function variants.

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.52LOEUF
pLI 0.826
Z-score 2.22
OE 0.00 (0.000.52)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
1.69Z-score
OE missense 0.22 (0.130.39)
8 obs / 36.8 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.00 (0.000.52)
00.351.4
Missense OE0.22 (0.130.39)
00.61.4
Synonymous OE1.53
01.21.6
LoF obs/exp: 0 / 5.8Missense obs/exp: 8 / 36.8Syn Z: -1.58
DN
0.3693th %ile
GOF
0.1899th %ile
LOF
0.69top 10%

The highest-scoring mechanism for this gene is loss-of-function (haploinsufficiency).

LOFprediction above median

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

ClinVar Variant Classifications

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

RPL38 · protein map & ClinVar variants

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

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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