RPS6KA1

Chr 1

ribosomal protein S6 kinase A1

Also known as: HU-1, MAPKAPK1, MAPKAPK1A, RSK, RSK1, p90Rsk

The protein is a serine/threonine kinase that phosphorylates substrates in MAPK signaling pathways, regulates translation through ribosomal protein S6 phosphorylation, and modulates mTOR signaling to control cellular proliferation, survival, and differentiation. Mutations cause Coffin-Lowry syndrome, an X-linked disorder characterized by intellectual disability, distinctive facial features, and progressive skeletal abnormalities. The gene is highly constrained against loss-of-function variants (pLI = 0.0019, LOEUF = 0.515), consistent with its role in fundamental cellular processes.

OMIMResearchSummary from RefSeq, UniProt
MultiplemechanismLOEUF 0.52
Clinical SummaryRPS6KA1
Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.32) despite low pLI — interpret in context.
📋
ClinVar Variants
4 unique Pathogenic / Likely Pathogenic· 94 VUS of 130 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.52LOEUF
pLI 0.002
Z-score 3.88
OE 0.32 (0.200.52)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
2.99Z-score
OE missense 0.61 (0.550.67)
279 obs / 459.6 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.32 (0.200.52)
00.351.4
Missense OE0.61 (0.550.67)
00.61.4
Synonymous OE0.96
01.21.6
LoF obs/exp: 12 / 37.7Missense obs/exp: 279 / 459.6Syn Z: 0.48
DN
0.74top 25%
GOF
0.72top 25%
LOF
0.3164th %ile

This gene has evidence for multiple mechanisms of pathogenicity (dominant-negative and gain-of-function). Both the Badonyi & Marsh prediction and the broader genomic evidence point to dominant-negative as the predominant mechanism. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

DNprediction above median
GOFprediction above median

Note: In-silico variant effect predictors (SIFT, PolyPhen, REVEL, CADD) may underestimate pathogenicity of missense variants in genes with GOF or DN mechanisms. Consider functional evidence and clinical context.

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

ClinVar Variant Classifications

130 submitted variants in ClinVar

Classification Summary

Pathogenic4
VUS94
Likely Benign5
4
Pathogenic
94
VUS
5
Likely Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
4
0
4
Likely Pathogenic
0
0
0
0
0
VUS
0
87
7
0
94
Likely Benign
0
3
0
2
5
Benign
0
0
0
0
0
Total090112103

LoF = frameshift, stop gained/lost, canonical splice · Counts from ClinVar esearch · Updated hourly

View in ClinVar →

Protein Context — Lollipop Plot

RPS6KA1 · 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.

Search ClinicalTrials.gov →
Clinical Literature
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