S100P

Chr 4

S100 calcium binding protein P

Also known as: MIG9

The protein encoded by this gene is a member of the S100 family of proteins containing 2 EF-hand calcium-binding motifs. S100 proteins are localized in the cytoplasm and/or nucleus of a wide range of cells, and involved in the regulation of a number of cellular processes such as cell cycle progression and differentiation. S100 genes include at least 13 members which are located as a cluster on chromosome 1q21; however, this gene is located at 4p16. This protein, in addition to binding Ca2+, also binds Zn2+ and Mg2+. This protein may play a role in the etiology of prostate cancer. [provided by RefSeq, Jul 2008]

1
Active trials
47
Pubs (1 yr)
86
P/LP submissions
0%
P/LP missense
1.82
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryS100P
Population Constraint (gnomAD)
Low constraint (pLI 0.03) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
86 unique Pathogenic / Likely Pathogenic· 17 VUS of 104 total submissions
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Clinical Trials
1 active or recruiting trial — potential therapeutic options may be available

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.82LOEUF
pLI 0.033
Z-score 0.29
OE 0.80 (0.311.82)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.38Z-score
OE missense 1.14 (0.931.41)
63 obs / 55.1 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.80 (0.311.82)
00.351.4
Missense OE1.14 (0.931.41)
00.61.4
Synonymous OE0.93
01.21.6
LoF obs/exp: 2 / 2.5Missense obs/exp: 63 / 55.1Syn Z: 0.28
DN
0.84top 10%
GOF
0.89top 5%
LOF
0.1895th %ile

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

GOFprediction above median
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.

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

ClinVar Variant Classifications

104 submitted variants in ClinVar

Classification Summary

Pathogenic81
Likely Pathogenic5
VUS17
Benign1
81
Pathogenic
5
Likely Pathogenic
17
VUS
1
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
81
0
81
Likely Pathogenic
0
0
5
0
5
VUS
0
14
3
0
17
Likely Benign
0
0
0
0
0
Benign
0
0
0
1
1
Total014891104

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

View in ClinVar →

Protein Context — Lollipop Plot

S100P · protein map & ClinVar variants

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

Clinical Literature
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