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Carnitine-acylcarnitine translocase

Mammalian protein found in Homo sapiens From Wikipedia, the free encyclopedia

Carnitine-acylcarnitine translocase (CACT) is responsible for passive transport of carnitine and carnitine-fatty acid complexes and across the inner mitochondrial membrane as part of the carnitine shuttle system.

AliasesSLC25A20, CAC, CACT, Carnitine-acylcarnitine translocase, solute carrier family 25 member 20
End48,898,904 bp[1]
Quick facts SLC25A20, Identifiers ...
SLC25A20
Identifiers
AliasesSLC25A20, CAC, CACT, Carnitine-acylcarnitine translocase, solute carrier family 25 member 20
External IDsOMIM: 613698; MGI: 1928738; GeneCards: SLC25A20
Orthologs
DatabasesNCBI: entry; OMA: entry
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_000387

NM_020520

RefSeq (protein)

NP_000378

NP_065266

Location (UCSC)Chr 3: 48.86 – 48.9 MbChr 9: 108.54 – 108.56 Mb
PubMed search[3][4]
Wikidata
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SymbolSLC25A20
Alt. symbolsCACT
Quick facts solute carrier family 25 (carnitine/acylcarnitine translocase), member 20, Identifiers ...
solute carrier family 25 (carnitine/acylcarnitine translocase), member 20
Identifiers
SymbolSLC25A20
Alt. symbolsCACT
NCBI gene788
HGNC1421
OMIM212138
RefSeqNM_000387
UniProtO43772
Other data
LocusChr. 3 p21.31
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StructuresSwiss-model
DomainsInterPro
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Function

Fatty acyl–carnitine can diffuse from the cytosol across the porous outer mitochondrial membrane to the intermembrane space, but must utilize CACT to cross the nonporous inner mitochondrial membrane and reach the mitochondrial matrix.[5] CACT is a cotransporter, returning one molecule of carnitine from the matrix to the intermembrane space as one molecule of fatty acyl–carnitine moves into the matrix.[6]

Clinical significance

A disorder is associated with carnitine-acylcarnitine translocase deficiency. This disorder disrupts the carnitine shuttle system from moving fatty acids across the mitochondrial membrane, leading to a decrease in fatty acid catabolism. The result is an accumulation of fatty acid within muscles and liver, decreased tolerance to long term exercise, inability to fast for more than a few hours, muscle weakness and wasting, and a strong acidic smell on the breath (due to protein catabolism).[7]

Acyl-CoA from cytosol to the mitochondrial matrix

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