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FTCD

formimidoyltransferase cyclodeaminase

The FTCD gene provides instructions for an enzyme crucial in the final steps of histidine breakdown, primarily functioning in the liver. The FTCD gene encodes the formimidoyltransferase-cyclodeaminase enzyme, which plays a bifunctional role in metabolism.

Chromosome 21q22.3 Autosomal recessive HGNC:3974 Tier C
FTCD 21q22.3 p arm q arm 21

FTCD is located on the long (q) arm of chromosome 21, at band 21q22.3. Arm ratio per GRCh38 - banding schematic.

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Overview

The FTCD gene provides genetic instructions for creating an enzyme known as formimidoyltransferase-cyclodeaminase. This enzyme is primarily located in the liver, though smaller quantities are also found in the kidneys and testes. The formimidoyltransferase-cyclodeaminase enzyme is considered bifunctional because it carries out two distinct enzymatic activities, both of which are critical for the breakdown of the amino acid histidine.

What the gene does

The formimidoyltransferase-cyclodeaminase enzyme, encoded by the FTCD gene, performs two key enzymatic functions. Its first role is as a transferase, moving a group of atoms from one molecule to another. Specifically, it converts formiminoglutamate (FIGLU) into 5-formiminotetrahydrofolate, a process that also yields the amino acid glutamate. The enzyme's second function is that of a deaminase, which involves removing a group of nitrogen and hydrogen atoms from molecules. In this capacity, it transforms 5-formiminotetrahydrofolate into another tetrahydrofolate molecule. These tetrahydrofolate molecules are vital for carrying one-carbon units, which are necessary for the synthesis of purines and pyrimidines, the fundamental building blocks of DNA and RNA. Both of these enzymatic actions constitute the final two steps in the metabolic pathway for breaking down the amino acid histidine.

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Chromosome location

The FTCD gene is situated on chromosome 21 at position 21q22.3. This specific location on the long arm (q) of chromosome 21 indicates its genomic address within the human genome.

Protein structure

The formimidoyltransferase-cyclodeaminase protein is composed of 541 amino acids and exhibits a modular structure. It includes a Formiminotransferase N-subdomain spanning amino acids 1-181 and a Formiminotransferase C-subdomain from amino acids 182-326. These are followed by a short Linker region from amino acids 327-334. The protein's second enzymatic activity is attributed to the Cyclodeaminase/cyclohydrolase domain, which comprises amino acids 335-541.

Domain map · 541 amino acids
Formiminotransferase N-subdomain (1–181)Formiminotransferase C-subdomain (182–326)Linker (327–334)Cyclodeaminase/cyclohydrolase (335–541)Formiminotransferase N1–181Formiminotransferase C182–326Cyclodeaminase/cyclohy335–5411~271541
Region - functional region
🧬 Explore 3D structure on AlphaFold
UniProt:O95954Length:541 aaStructure:AlphaFold

Key variants

Genetic variations within the FTCD gene can alter the function of the formimidoyltransferase-cyclodeaminase enzyme. These variants, sometimes referred to as mutations, can influence the enzyme's ability to perform its metabolic roles. Identifying and characterising these genetic changes is important for understanding their potential impact on health.

The table below shows the top 9 pathogenic or likely-pathogenic variants currently classified in ClinVar for FTCD.
View all on ClinVar →

Sample of pathogenic variants

9 pathogenic / likely-pathogenic variants from ClinVar, ranked by review status (expert-panel-reviewed first). This is a sample; recurrent founder variants in a specific population may not appear here - see the full ClinVar listing via the link above.

Variant (HGVS) Protein change Classification Evidence Associated condition
c.1031_1061del
Deletion
p.Val344fs Pathogenic/Likely pathogenic ★★☆☆ Glutamate formiminotransferase deficiency
c.1607T>A
single nucleotide variant
p.Leu536Ter Pathogenic/Likely pathogenic ★★☆☆ Glutamate formiminotransferase deficiency
c.211C>T
single nucleotide variant
p.Arg71Ter Pathogenic/Likely pathogenic ★★☆☆ FTCD-related disorder
c.293dup
Duplication
p.Val99fs Pathogenic/Likely pathogenic ★★☆☆ Glutamate formiminotransferase deficiency
c.763C>T
single nucleotide variant
p.Arg255Ter Pathogenic ★★☆☆ Inborn genetic diseases
c.990dup
Duplication
p.Pro331fs Pathogenic/Likely pathogenic ★★☆☆ Inborn genetic diseases
g.(?_47565311)_(47575437_?)del
Deletion
- Pathogenic ★☆☆☆ Glutamate formiminotransferase deficiency
c.1082_1083insTCGGC
Insertion
p.Ala362fs Pathogenic ★☆☆☆ Glutamate formiminotransferase deficiency
c.613dup
Duplication
p.Glu205fs Pathogenic ★☆☆☆ Glutamate formiminotransferase deficiency

Evidence stars indicate ClinVar review status. Individual variant interpretation should always be performed by a qualified clinical laboratory - many variants remain classified as Variants of Uncertain Significance (VUS) pending more research.

Associated conditions

Variants in the FTCD gene are associated with glutamate formiminotransferase deficiency. This inherited metabolic disorder can lead to elevated levels of formiminoglutamate (FIGLU) detectable in urine. Historically, the condition was described with both mild and severe presentations, although some individuals with FTCD gene variants may not experience obvious health problems.

No disease links recorded for this gene in our reference set.

Inheritance pattern

Conditions caused by pathogenic FTCD variants typically follow autosomal recessive inheritance.

♀ Carrier parent 1 altered copy ♂ Carrier parent 1 altered copy Affected Carrier Carrier Unaffected Affected Carrier Unaffected Circles = females · Squares = males

When both parents are carriers, each child has a 25% chance of being affected, 50% of being a carrier, and 25% of being unaffected.

Carrier frequency by population How common is heterozygous FTCD carrier status across ancestry groups?

UK clinical status

The FTCD gene is recognised within the UK's genomic healthcare framework, as evidenced by its inclusion in NHS England's PanelApp. It is listed with a 'green' status on panels such as DDG2P, Intellectual disability, Likely inborn error of metabolism, and Undiagnosed metabolic disorders (R98), indicating strong evidence of its association with these conditions.

Frequently asked questions

What does the FTCD gene do?

The FTCD gene provides instructions for an enzyme called formimidoyltransferase-cyclodeaminase. This enzyme is bifunctional, playing a key role in the final stages of breaking down the amino acid histidine, primarily in the liver.

What is glutamate formiminotransferase deficiency?

Glutamate formiminotransferase deficiency is an inherited condition caused by variants in the FTCD gene. It can lead to increased levels of formiminoglutamate (FIGLU) in the urine due to impaired histidine metabolism.

Where is the FTCD gene located?

The FTCD gene is located on chromosome 21, specifically at position 21q22.3. This is its designated address within the human genome.

References

  1. Mao Y, Vyas NK, Vyas MN. Structure of the bifunctional and Golgi-associated formiminotransferase cyclodeaminase octamer. The EMBO journal. 2004. PMID: 15272307
  2. Hilton JF, Christensen KE, Watkins D. The molecular basis of glutamate formiminotransferase deficiency. Human mutation. 2003. PMID: 12815595
  3. Solans A, Estivill X, de la Luna S. Cloning and characterization of human FTCD on 21q22.3, a candidate gene for glutamate formiminotransferase deficiency. Cytogenetics and cell genetics. 2000. PMID: 10773664
Educational content. This page is not medical or genetic advice, is not individually reviewed by a clinician for each reader, and should not replace a consultation with a qualified healthcare professional or genetic counsellor. If you are considering genetic testing or acting on a test result, book a consultation.
Data sources Last updated 27 September 2026. Content compiled from HGNC · MedlinePlus Genetics · ClinGen · Genomics England PanelApp · NHS National Genomic Test Directory · ClinVar · UniProt · AlphaFold .