CYP11B1

Chr 8ARAD

cytochrome P450 family 11 subfamily B member 1

Also known as: CPN1, CYP11B, FHI, P450C11

This mitochondrial cytochrome P450 enzyme catalyzes the 11β-hydroxylation of steroid precursors to produce cortisol and corticosterone in the adrenal cortex. Mutations cause congenital adrenal hyperplasia due to 11β-hydroxylase deficiency (autosomal recessive) presenting in infancy with virilization and hypertension, or glucocorticoid-remediable aldosteronism (autosomal dominant) with early-onset hypertension. The gene shows low constraint to loss-of-function variation (pLI near zero), consistent with the recessive inheritance pattern of the classic form.

Summary from RefSeq, OMIM, UniProt
Research Assistant →

Primary Disease Associations & Inheritance

Adrenal hyperplasia, congenital, due to 11-beta-hydroxylase deficiencyMIM #202010
AR
Aldosteronism, glucocorticoid-remediableMIM #103900
AD
UniProtHyperaldosteronism, familial, 1
3
Active trials
64
Pubs (1 yr)
165
P/LP submissions
21%
P/LP missense
0.95
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryCYP11B1
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
113 unique Pathogenic / Likely Pathogenic· 178 VUS of 500 total submissions
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Clinical Trials
3 active or recruiting trials — potential therapeutic options may be available
📖
GeneReview available — CYP11B1
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.95LOEUF
pLI 0.000
Z-score 1.72
OE 0.60 (0.390.95)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
-1.56Z-score
OE missense 1.26 (1.151.37)
367 obs / 291.9 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.60 (0.390.95)
00.351.4
Missense OE1.26 (1.151.37)
00.61.4
Synonymous OE1.47
01.21.6
LoF obs/exp: 13 / 21.6Missense obs/exp: 367 / 291.9Syn Z: -4.03
DN
0.75top 25%
GOF
0.76top 25%
LOF
0.2288th %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

500 submitted variants in ClinVar

Classification Summary

Pathogenic49
Likely Pathogenic64
VUS178
Likely Benign193
Conflicting15
49
Pathogenic
64
Likely Pathogenic
178
VUS
193
Likely Benign
15
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
18
4
27
0
49
Likely Pathogenic
28
20
15
1
64
VUS
1
157
17
3
178
Likely Benign
0
3
94
96
193
Benign
0
0
0
0
0
Conflicting
15
Total47184153100499

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

View in ClinVar →

Protein Context — Lollipop Plot

CYP11B1 · protein map & ClinVar variants

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

Clinical Literature
Open Research Assistant →
Full-Text Mentions
NLP-detected gene mentions in article bodies · via PubTator3
PubTator3
Top 5 full-text resultsSearch PubTator3 ↗
Key Publications
Landmark & review papers · by relevance
PubMed
Top 5 results · since 2015Search PubMed ↗