GDF2

Chr 10AD

growth differentiation factor 2

Also known as: BMP-9, BMP9, HHT5

The encoded protein is a secreted TGF-beta superfamily ligand that acts as a potent inhibitor of angiogenesis and regulates cartilage and bone development through SMAD1 signaling in endothelial cells. Mutations cause hereditary hemorrhagic telangiectasia type 5, inherited in an autosomal dominant pattern. This gene shows low constraint against loss-of-function variants, suggesting tolerance to protein loss.

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

Telangiectasia, hereditary hemorrhagic, type 5MIM #615506
AD
0
Active trials
15
Pubs (1 yr)
73
P/LP submissions
6%
P/LP missense
0.98
LOEUF
DN
Mechanism· predicted
Clinical SummaryGDF2
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Gene-Disease Validity (ClinGen)
telangiectasia, hereditary hemorrhagic, type 5 · ADModerate

Moderate evidence — consider for supplementary testing

2 total gene-disease associations curated

Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
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ClinVar Variants
68 unique Pathogenic / Likely Pathogenic· 120 VUS of 460 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.98LOEUF
pLI 0.002
Z-score 1.63
OE 0.49 (0.270.98)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
0.46Z-score
OE missense 0.92 (0.831.02)
239 obs / 259.8 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.49 (0.270.98)
00.351.4
Missense OE0.92 (0.831.02)
00.61.4
Synonymous OE1.24
01.21.6
LoF obs/exp: 6 / 12.1Missense obs/exp: 239 / 259.8Syn Z: -2.08
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
limitedGDF2-related telangiectasia, hereditary haemorrhagicOTHERAD
DN
0.6453th %ile
GOF
0.4085th %ile
LOF
0.3161th %ile

The highest-scoring mechanism for this gene is dominant-negative.

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

460 submitted variants in ClinVar

Classification Summary

Pathogenic48
Likely Pathogenic20
VUS120
Likely Benign201
Benign47
Conflicting23
48
Pathogenic
20
Likely Pathogenic
120
VUS
201
Likely Benign
47
Benign
23
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
5
1
42
0
48
Likely Pathogenic
0
3
17
0
20
VUS
1
87
31
1
120
Likely Benign
0
13
16
172
201
Benign
0
1
45
1
47
Conflicting
23
Total6105151174459

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

View in ClinVar →

Protein Context — Lollipop Plot

GDF2 · 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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