RPS17

Chr 15

ribosomal protein S17

Also known as: DBA4, RPS17L, RPS17L1, RPS17L2, S17, eS17

Ribosomes, the organelles that catalyze protein synthesis, consist of a small 40S subunit and a large 60S subunit. Together these subunits are composed of four RNA species and approximately 80 structurally distinct proteins. This gene encodes a ribosomal protein that is a component of the 40S subunit. The protein belongs to the S17E family of ribosomal proteins and is located in the cytoplasm. Mutations in this gene cause Diamond-Blackfan anemia 4. Alternative splicing of this gene results in multiple transcript variants. As is typical for genes encoding ribosomal proteins, there are multiple processed pseudogenes of this gene dispersed through the genome. [provided by RefSeq, Apr 2014]

GeneReviewsResearchGenerating clinical summary…
Multiplemechanism
Clinical SummaryRPS17
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ClinVar Variants
7 unique Pathogenic / Likely Pathogenic· 17 VUS of 38 total submissions
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GeneReview available — RPS17
Authoritative clinical overview · Recommended first read
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Some data sources returned errors (1)

omim: Error: OMIM fetch failed: 429

Population Genetics & Constraint

Constraint data not available from gnomAD.

This gene — mechanism propensity

DN
0.6453th %ile
GOF
0.2597th %ile
LOF
0.52top 25%

This gene has evidence for multiple mechanisms of pathogenicity (loss-of-function and dominant-negative). The Badonyi & Marsh model scores dominant-negative highest among its predictions, but genomic evidence (constraint, ClinVar variant spectrum, and literature) most strongly supports loss-of-function (haploinsufficiency). Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

LOF1 literature citation · 57% of P/LP variants are LoF · ClinGen HI: Sufficient evidence for dosage pathogenicity
DNprediction 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.

Literature Evidence

LOFRibosomal protein gene deletions in Diamond-Blackfan anemia1

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312. Mechanism ranking also informed by gnomAD constraint, ClinVar, and ClinGen data.

References

  1. 1.PMID 22045982

ClinVar Variant Classifications

38 submitted variants in ClinVar

Classification Summary

Pathogenic5
Likely Pathogenic2
VUS17
Likely Benign8
Benign5
Conflicting1
5
Pathogenic
2
Likely Pathogenic
17
VUS
8
Likely Benign
5
Benign
1
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
3
1
1
0
5
Likely Pathogenic
1
1
0
0
2
VUS
1
11
3
2
17
Likely Benign
0
0
2
6
8
Benign
0
0
5
0
5
Conflicting
1
Total51311838

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

View in ClinVar →

24 pathogenic / likely-pathogenic (of 28) ClinVar copy-number / structural variants overlap RPS17 — these span large chromosomal regions, not the gene specifically, and are excluded from the counts above. Explore in CNV tools →

Protein Context — Lollipop Plot

RPS17 · 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.

Search ClinicalTrials.gov →