NP_004449.1
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NCBI GenBank Nucleotide #
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UniProt Primary Accession #
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UniProt Secondary Accession #
UniProt Related Accession #
Molecular Weight
79,188 Da
NCBI Official Full Name
long-chain-fatty-acid--CoA ligase 4 isoform 1
NCBI Official Synonym Full Names
acyl-CoA synthetase long-chain family member 4
NCBI Official Synonym Symbols
ACS4; FACL4; LACS4; MRX63; MRX68 [Similar Products]
NCBI Protein Information
long-chain-fatty-acid--CoA ligase 4; LACS 4; acyl-CoA synthetase 4; lignoceroyl-CoA synthase; long-chain acyl-CoA synthetase 4; long-chain fatty-acid-Coenzyme A ligase 4; fatty-acid-Coenzyme A ligase, long-chain 4
UniProt Protein Name
Long-chain-fatty-acid--CoA ligase 4
UniProt Synonym Protein Names
Long-chain acyl-CoA synthetase 4; LACS 4
UniProt Synonym Gene Names
UniProt Entry Name
ACSL4_HUMAN
NCBI Summary for ACSL4
The protein encoded by this gene is an isozyme of the long-chain fatty-acid-coenzyme A ligase family. Although differing in substrate specificity, subcellular localization, and tissue distribution, all isozymes of this family convert free long-chain fatty acids into fatty acyl-CoA esters, and thereby play a key role in lipid biosynthesis and fatty acid degradation. This isozyme preferentially utilizes arachidonate as substrate. The absence of this enzyme may contribute to the mental retardation or Alport syndrome. Alternative splicing of this gene generates 2 transcript variants. [provided by RefSeq, Jul 2008]
UniProt Comments for ACSL4
ACSL4: Activation of long-chain fatty acids for both synthesis of cellular lipids, and degradation via beta-oxidation. Preferentially uses arachidonate and eicosapentaenoate as substrates. Defects in ACSL4 are the cause of mental retardation X- linked type 63 (MRX63). Mental retardation is a mental disorder characterized by significantly sub-average general intellectual functioning associated with impairments in adaptative behavior and manifested during the developmental period. Non- syndromic mental retardation patients do not manifest other clinical signs. Defects in ACSL4 are involved in Alport syndrome with mental retardation midface hypoplasia and elliptocytosis (ATS-MR). A X-linked contiguous gene deletion syndrome characterized by glomerulonephritis, deafness, mental retardation, midface hypoplasia and elliptocytosis. Belongs to the ATP-dependent AMP-binding enzyme family. 2 isoforms of the human protein are produced by alternative splicing.
Protein type: EC 6.2.1.3; Ligase; Membrane protein, integral; Lipid Metabolism - fatty acid
Chromosomal Location of Human Ortholog: Xq22.3-q23
Cellular Component: peroxisomal membrane; mitochondrial outer membrane; endoplasmic reticulum membrane; cell soma; membrane; cytoplasm; integral to membrane; lipid particle
Molecular Function: arachidonate-CoA ligase activity; very-long-chain-fatty-acid-CoA ligase activity; ATP binding; long-chain-fatty-acid-CoA ligase activity
Biological Process: lipid biosynthetic process; embryonic process involved in female pregnancy; triacylglycerol biosynthetic process; lipid metabolic process; cellular lipid metabolic process; long-chain fatty acid metabolic process; negative regulation of prostaglandin secretion; positive regulation of cell growth; fatty acid transport; response to nutrient
Disease: Mental Retardation, X-linked 63
Research Articles on ACSL4
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Pathways associated with ACSL4 elisa kit
Diseases associated with ACSL4 elisa kit
Organs/Tissues associated with ACSL4 elisa kit
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