MLYCD
Malonyl-CoA decarboxylase, mitochondrial
Also known as: DCMC_HUMAN, hMCD, MCD
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- O95822
- Gene
- MLYCD
- Ensembl
- ENSG00000103150
- Chromosome
- 16
- Canonical length
- 493 aa
- Protein class
- Disease related genes, Enzymes, Human disease related genes, Metabolic proteins, Potential drug targets, Predicted intracellular proteins
- Quaternary structure
- Homotetramer
OverviewNCBI Gene
The product of this gene catalyzes the breakdown of malonyl-CoA to acetyl-CoA and carbon dioxide. Malonyl-CoA is an intermediate in fatty acid biosynthesis, and also inhibits the transport of fatty acyl CoAs into mitochondria. Consequently, the encoded protein acts to increase the rate of fatty acid oxidation. It is found in mitochondria, peroxisomes, and the cytoplasm. Mutations in this gene result in malonyl-CoA decarboyxlase deficiency. [provided by RefSeq, Jul 2008]
Canonical amino-acid sequenceUniProt
493 residues, UniProt reviewed canonical sequence.
>O95822|MLYCD
1 MRGFGPGLTA RRLLPLRLPP RPPGPRLASG QAAGALERAM DELLRRAVPP TPAYELREKT
61 PAPAEGQCAD FVSFYGGLAE TAQRAELLGR LARGFGVDHG QVAEQSAGVL HLRQQQREAA
121 VLLQAEDRLR YALVPRYRGL FHHISKLDGG VRFLVQLRAD LLEAQALKLV EGPDVREMNG
181 VLKGMLSEWF SSGFLNLERV TWHSPCEVLQ KISEAEAVHP VKNWMDMKRR VGPYRRCYFF
241 SHCSTPGEPL VVLHVALTGD ISSNIQAIVK EHPPSETEEK NKITAAIFYS ISLTQQGLQG
301 VELGTFLIKR VVKELQREFP HLGVFSSLSP IPGFTKWLLG LLNSQTKEHG RNELFTDSEC
361 KEISEITGGP INETLKLLLS SSEWVQSEKL VRALQTPLMR LCAWYLYGEK HRGYALNPVA
421 NFHLQNGAVL WRINWMADVS LRGITGSCGL MANYRYFLEE TGPNSTSYLG SKIIKASEQV
481 LSLVAQFQKN SKLLocalizationUniProt · AlphaFold · HPA
Whether an antibody against MLYCD can act on the native protein depends on physical access: surface and secreted proteins are reachable by circulating antibodies, intracellular proteins usually are not.
- Antibody reachability
- Intracellular
- Secreted
- No
- Transmembrane segments
- 0
- Mean surface accessibility (rSASA)
- 0.3
- Highest tissue expression
- 20 nTPM
Expression across tissuesHPA
Tissue
- tongue: 20 nTPM
- heart muscle: 8.5 nTPM
- liver: 5.4 nTPM
- skeletal muscle: 5.3 nTPM
- pancreas: 4.8 nTPM
- choroid plexus: 3 nTPM
Single-cell type
- choroid plexus epithelial cells: 33 nCPM
- astrocytes: 31 nCPM
- bergmann glia: 31 nCPM
- myonuclei: 30 nCPM
- cone photoreceptor cells: 29 nCPM
- oligodendrocytes: 21 nCPM
Immune cell
- basophil: 0.5 nTPM
- eosinophil: 0.5 nTPM
- non-classical monocyte: 0.2 nTPM
- classical monocyte: 0.1 nTPM
- gdT-cell: 0.1 nTPM
- intermediate monocyte: 0.1 nTPM
Brain region
- thalamus: 11 nTPM
- choroid plexus: 10 nTPM
- medulla oblongata: 10 nTPM
- midbrain: 9.8 nTPM
- white matter: 9.6 nTPM
- basal ganglia: 9.5 nTPM
DiseaseUniProt · ClinVar · IEDB · PubMed
Four sources answering four different questions about MLYCD.
Disease | AllUniProt
Conditions MLYCD is implicated in, by any mechanism.
- Malonyl-CoA decarboxylase deficiency (MLYCD deficiency) MIM:248360
Disease | GeneticClinVar
69 pathogenic / likely-pathogenic of 755 ClinVar records.
Conditions with pathogenic or likely-pathogenic variants.
- Deficiency of malonyl-CoA decarboxylase
- Sarcoma
- Intellectual disability
- Familial cancer of breast
- MLYCD-related disorder
Genetic constraint and essentialitygnomAD · DepMap
Does the body need this protein intact? Low LOEUF or a strong DepMap dependency means loss or blockade of the protein is likely to be felt.
- gnomAD LOEUF (loss-of-function intolerance)
- 0.84
- gnomAD pLI
- 0
- gnomAD missense Z
- -1.76
- DepMap mean gene effect
- 0.06
- DepMap dependency class
- none
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 4% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- acetyl-CoA biosynthetic process
- acyl-CoA metabolic process
- fatty acid biosynthetic process
- fatty acid oxidation
- malonyl-CoA catabolic process
- positive regulation of fatty acid oxidation
- regulation of fatty acid beta-oxidation
- regulation of glucose metabolic process
- response to ischemia
- response to nutrient
Molecular functions
- identical protein binding
- malonyl-CoA decarboxylase activity
Cellular components
Protein domainsUniProt · Pfam · InterPro
- Malonyl-CoA decarboxylase, C-terminal
- Malonyl-CoA decarboxylase, N-terminal
- Malonyl-CoA decarboxylase, N-terminal domain superfamily
- Malonyl-CoA decarboxylase
- Malonyl-CoA decarboxylase, C-terminal catalytic domain superfamily
- Malonyl-CoA decarboxylase C-terminal domain
- Malonyl-CoA decarboxylase N-terminal domain
KeywordsUniProt
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads MLYCD as an antibody target. Whether an autoantibody or antibody against MLYCD could matter depends on whether native MLYCD is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
MLYCD is annotated as predominantly intracellular. Intracellular proteins are common autoantibody markers, becoming visible to the immune system after cell injury or altered processing, but are usually markers of disease rather than direct drivers.
Annotation status
The present source text does not explicitly label MLYCD as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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