BMP1

Chr 8AR

bone morphogenetic protein 1

Also known as: OI13, PCOLC, PCP, PCP2, TLD

This metalloprotease processes extracellular matrix precursor proteins including procollagens I, II, and III and activates lysyl oxidase, which is essential for collagen cross-linking and proper bone and cartilage formation. Biallelic mutations cause autosomal recessive osteogenesis imperfecta type XIII, characterized by bone fragility and skeletal deformities. The gene is highly constrained against loss-of-function variation (LOEUF 0.456), indicating that complete loss of protein function is likely not tolerated.

Summary from RefSeq, OMIM, UniProt
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Primary Disease Associations & Inheritance

Osteogenesis imperfecta, type XIIIMIM #614856
AR
0
Active trials
51
Pubs (1 yr)
53
P/LP submissions
4%
P/LP missense
0.46
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryBMP1
Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.30) despite low pLI — interpret in context.
📋
ClinVar Variants
51 unique Pathogenic / Likely Pathogenic· 126 VUS of 600 total submissions
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GeneReview available — BMP1
Authoritative clinical overview · Recommended first read
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Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.46LOEUF
pLI 0.001
Z-score 4.74
OE 0.30 (0.200.46)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
1.99Z-score
OE missense 0.78 (0.730.84)
512 obs / 655.0 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.30 (0.200.46)
00.351.4
Missense OE0.78 (0.730.84)
00.61.4
Synonymous OE1.02
01.21.6
LoF obs/exp: 16 / 53.3Missense obs/exp: 512 / 655.0Syn Z: -0.28
DN
0.76top 25%
GOF
0.7125th %ile
LOF
0.2968th %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

600 submitted variants in ClinVar

Classification Summary

Pathogenic39
Likely Pathogenic12
VUS126
Likely Benign370
Benign25
Conflicting11
39
Pathogenic
12
Likely Pathogenic
126
VUS
370
Likely Benign
25
Benign
11
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
4
2
33
0
39
Likely Pathogenic
7
0
5
0
12
VUS
1
107
16
2
126
Likely Benign
0
10
124
236
370
Benign
0
0
21
4
25
Conflicting
11
Total12119199242583

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

View in ClinVar →

Protein Context — Lollipop Plot

BMP1 · 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 →
Clinical Literature
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