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Gene

FGA

fibrinogen alpha chain

Summary

Cytogenetic location
4q31.3
Coordinates
Chromosome 4: 154,585,275–154,590,742 (GRCh38)
Exons
5 exons across 5.5 kb
Protein
644 amino acids
Inheritance
Autosomal dominant
MANE Select transcript
ENST00000403106.8NM_021871.4
Locus type
gene with protein product
  • Very high
  • Confident
  • Low
  • Very low

Reference genomeGRCh38

Positions on gene and variant pages follow this choice, in this browser.

Curated reports relevant to this gene

  • Congenital Afibrinogenemia

    • Congenital Fibrinogen Deficiency

      Congenital deficiencies of fibrinogen are coagulation disorders characterized by bleeding symptoms ranging from mild to severe resulting from reduced quantity and/or quality of circulating fibrinogen. Afibrinogenemia (complete absence of fibrinogen) and hypofibrinogenemia (reduced plasma fibrinogen concentration) correspond to quantitative anomalies of fibrinogen while dysfibrinogenemia corresponds to a functional anomaly of fibrinogen. Hypo- and dysfibrinogenemia may be frequently combined (hypodysfibrinogenemia).

      • ClinGen rates the link definitive
      • 4 GenCC submitters rate it definitive or strong

  • Hereditary Amyloidosis

    • Autosomal dominant

      Hereditary amyloidosis refers to a group of inherited conditions that make up one of the subtypes of amyloidosis. Hereditary amyloidosisis characterized by the deposit of an abnormal protein called amyloid in multiple organs of the body where it should not be, which causes disruption of organ tissue structure and function. In hereditary amyloidosis, amyloid deposits most often occur in tissues of the heart, kidneys, and nervous system. While symptoms of hereditary amyloidosis may appear in childhood, most individuals do not experience symptoms until adulthood. There are many types of hereditary amyloidosis associated with different gene mutations and abnormal proteins. The most common type of hereditary amyloidosis is transthyretin amyloidosis (ATTR), a condition in which the amyloid deposits are most often made up of the transthyretin protein which is made in the liver. Other examplesof hereditary amyloidosis include, but are not limited to, apolipoprotein AI amyloidosis (A ApoAI), gelsolin amyloidosis (A Gel), lysozyme amyloidosis (A Lys), cystatin C amyloidosis (A Cys), fibrinogen Aα-chain amyloidosis (A Fib), and apolipoprotein AII amyloidosis (A ApoAII).

      • 2 GenCC submitters rate it definitive or strong
      What knowing changes

      Tafamidis (kinetic stabilizer), patisiran (RNAi), vutrisiran (RNAi), inotersen (antisense), liver transplantation

Inheritance

Autosomal dominant
One changed copy, from either parent, is enough. A parent who has one passes it on to each child with a one-in-two chance.

How FGA is laid out

  • Coding sequence
  • Untranslated region
  • Intron
  • Direction of transcription
  • Known disease-causing sites
Chromosome 4, with a bracket where FGA sits. FGA and 6 genes near it on chromosome 4, from 154,088,009 to 155,088,008.Chromosome 44q31.3p16.3p16.2p16.1p15.33p15.32p15.31p15.2p15.1p14p13p12p11q11q12q13.1q13.2q13.3q21.1q21.21q21.22q21.23q21.3q22.1q22.2q22.3q23q24q25q26q27q28.1q28.2q28.3q31.1q31.21q31.22q31.23q31.3q32.1q32.2q32.3q33q34.1q34.2q34.3q35.1q35.2154.2 Mb154.4 Mb154.6 Mb154.8 Mb155 MbDCHS2: 154,231,742–154,491,804, reverse strandDCHS2PLRG1: 154,535,005–154,550,415, reverse strandPLRG1FGB: 154,562,952–154,572,807, forward strandFGBFGA: 154,585,275–154,590,742, reverse strandFGAFGG: 154,604,058–154,612,967, reverse strandFGGLRAT: 154,626,945–154,753,158, forward strandLRATRBM46: 154,781,213–154,828,813, forward strandRBM46Diagram of FGA: 5 exons on the reverse strand of chromosome 4Exon 5: 17 known disease-causing sitesExon 4: 4 known disease-causing sitesExon 3: 2 known disease-causing sitesExon 2: 5 known disease-causing sitesExon 5: 154,585,275–154,586,918, 1,644 basesExon 4: 154,587,512–154,587,657, 146 basesExon 3: 154,588,793–154,588,976, 184 basesExon 2: 154,589,437–154,589,562, 126 basesExon 1: 154,590,634–154,590,742, 109 bases543215′3′

Exons of the gene's MANE Select transcript (release v1.5), from NCBI and EMBL-EBI, on the GRCh38 reference genome.

Chromosome bands from UCSC's GRCh38 ideogram (2022-10-29).

Nearby genes from Ensembl release 116, on GRCh38.

Exons make up 2.2 kb of the gene's 5.5 kb; 1,935 of those bases code for the protein.

How a genome test reads FGA

32

positions in FGA where ClinVar classes a change as pathogenic or likely pathogenic

None of them falls in a region short reads find hard.

A whole genome covers all 5.5 kb of FGA, introns included, not only the 2.2 kb of exons.

Where this comes from

  • HGNC: the gene's symbol, name, other symbols and location.
  • MANE Select v1.5, from NCBI and EMBL-EBI: the transcript, its exons and coding sequence.
  • GenCC and ClinGen, released 2026-10-16: which conditions the gene is linked to, and how strongly.
  • The ACMG secondary findings list, SF v3.2.
  • ClinVar and the GIAB stratifications: known disease-causing sites, and the regions short reads find hard.
  • The Human Phenotype Ontology, release 2026-09-01: the traits linked to the gene. Find out more at hpo.jax.org.
  • Data release 2026.10.16-c6eea6bf.

Cite this page

APA

Dante Labs. (n.d.). FGA gene: fibrinogen alpha chain. Retrieved 16 October 2026, from https://dantelabs.com/genes/fga

Vancouver

Dante Labs. FGA gene: fibrinogen alpha chain [Internet]. [cited 16 October 2026]. Available from: https://dantelabs.com/genes/fga

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