SDHB

Chr 1ADIsolated casesAR

succinate dehydrogenase complex iron sulfur subunit B

Also known as: CWS2, IP, MC2DN4, PGL4, PPGL4, SDH, SDH1, SDH2

The protein functions as the iron-sulfur subunit of succinate dehydrogenase complex II, converting succinate to fumarate in the citric acid cycle and transferring electrons to the oxidative phosphorylation pathway. Mutations cause autosomal dominant pheochromocytoma/paraganglioma syndrome 4, gastrointestinal stromal tumors, and autosomal recessive mitochondrial complex II deficiency. The pathogenic mechanism involves loss of tumor suppressor function, leading to mitochondrial dysfunction and disrupted oxygen sensing through HIF1 transcription factor stabilization.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt, Mechanism
MultiplemechanismAD/Isolated cases/ARLOEUF 0.824 OMIM phenotypes
Clinical SummarySDHB
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Gene-Disease Validity (ClinGen)
mitochondrial disease · ARDefinitive

Definitive — sufficient evidence for diagnostic panels

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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Clinical Trials
1 active or recruiting trial — potential therapeutic options may be available
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GeneReview available — SDHB
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
0.82LOEUF
pLI 0.000
Z-score 2.13
OE 0.47 (0.280.82)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
-0.10Z-score
OE missense 1.02 (0.901.17)
158 obs / 154.4 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.47 (0.280.82)
00.351.4
Missense OE1.02 (0.901.17)
00.61.4
Synonymous OE1.00
01.21.6
LoF obs/exp: 9 / 19.0Missense obs/exp: 158 / 154.4Syn Z: 0.02
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveSDHB-related pheochromocytomaGOFAD
definitiveSDHB-related gastrointestinal stromal tumorLOFAD
definitiveSDHB-related paraganglioma and gastric stromal sarcomaLOFAD
DN
0.77top 25%
GOF
0.5562th %ile
LOF
0.3452th %ile

This gene has evidence for multiple mechanisms of pathogenicity (dominant-negative and loss-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
LOF1 literature citation

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

LOFGross SDHB deletions in patients with paraganglioma detected by multiplex PCR: a possible hot spot?PMID:16258955

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

ClinVar Variant Classifications

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

SDHB · protein map & ClinVar variants

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

3D Protein StructureAlphaFold
Clinical Literature
Open Research Assistant →
Key Publications
Landmark & review papers · by relevance
PubMed
Top 5 results · since 2015Search PubMed ↗