FTH1

Chr 11AD

ferritin heavy chain 1

Also known as: FHC, FTH, FTHL6, HFE5, NBIA9, PIG15, PLIF

This gene encodes the heavy subunit of ferritin, the major intracellular iron storage protein in prokaryotes and eukaryotes. It is composed of 24 subunits of the heavy and light ferritin chains. Variation in ferritin subunit composition may affect the rates of iron uptake and release in different tissues. A major function of ferritin is the storage of iron in a soluble and nontoxic state. Defects in ferritin proteins are associated with several neurodegenerative diseases. This gene has multiple pseudogenes. Several alternatively spliced transcript variants have been observed, but their biological validity has not been determined. [provided by RefSeq, Jul 2008]

OMIMResearchGenerating clinical summary…
MultiplemechanismADLOEUF 0.782 OMIM phenotypes
Clinical SummaryFTH1
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Gene-Disease Validity (ClinGen)
hemochromatosis type 5 · ADLimited

Limited evidence — not for standalone diagnostic reporting

2 total gene-disease associations curated

Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.30) despite low pLI — interpret in context.
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ClinVar Variants
12 unique Pathogenic / Likely Pathogenic· 44 VUS of 93 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?
0.78LOEUF
pLI 0.140
Z-score 2.05
OE 0.30 (0.140.78)
Tolerant

Typical tolerance to LoF variation

Missense Constraint?
0.86Z-score
OE missense 0.75 (0.620.91)
72 obs / 95.8 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios?
LoF OE?0.30 (0.140.78)
00.351.4
Missense OE?0.75 (0.620.91)
00.61.4
Synonymous OE?1.17
01.21.6
LoF obs/exp: 3 / 10.0Missense obs/exp: 72 / 95.8Syn Z: -0.88

This gene — mechanism propensity

DN
0.80top 10%
GOF
0.6638th %ile
LOF
0.2582th %ile

This gene has evidence for multiple mechanisms of pathogenicity (gain-of-function and dominant-negative). The Badonyi & Marsh model scores dominant-negative highest among its predictions, but genomic evidence (constraint, ClinVar variant spectrum, and literature) most strongly supports gain-of-function. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

GOFprediction above median · 1 literature citation
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.

Literature Evidence

GOFFTH1 pathogenic variants appear to act by a dominant, toxic gain-of-function mechanism.1

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

References

  1. 1.PMID 36778397

ClinVar Variant Classifications

93 submitted variants in ClinVar

Classification Summary

Pathogenic5
Likely Pathogenic7
VUS44
Likely Benign13
Benign14
Conflicting3
5
Pathogenic
7
Likely Pathogenic
44
VUS
13
Likely Benign
14
Benign
3
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
3
0
2
0
5
Likely Pathogenic
1
5
1
0
7
VUS
3
28
12
1
44
Likely Benign
0
2
3
8
13
Benign
0
0
11
3
14
Conflicting
3
Total735291286

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

View in ClinVar →

9 pathogenic / likely-pathogenic (of 11) ClinVar copy-number / structural variants overlap FTH1 — these span large chromosomal regions, not the gene specifically, and are excluded from the counts above. Explore in CNV tools →

Protein Context — Lollipop Plot

FTH1 · protein map & ClinVar variants

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