Applications
-
WB
-
IHC-P
-
FC
REACTIVITY
-
Human
-
Mouse
SPECIFICATIONS
Product Type
Rabbit polyclonal primary
Product Name
ACADL Antibody (ER1901-11)
Immunogen
Recombinant protein within n-terminal human acadl.
Host
Rabbit
Positive Control
SH-SY5Y cell lysates, MG-63, human kidney tissue, F9.
Conjugation
Unconjugated
Clonality
Polyclonal
PROPERTIES
Form
Liquid
Storage Condition
Store at +4C after thawing. Aliquot store at -20C. Avoid repeated freeze / thaw cycles.
Storage Buffer
1*PBS (pH7.4), 0.2% BSA, 50% Glycerol. Preservative: 0.05% Sodium Azide.
Concentration
1 ug/ul
PURIFICATION
Protein affinity purified.
MOLECULAR WEIGHT
48 kDa
Isotype
IgG
APPLICATION DILUTION
-
WB:1:500-1:2,000
-
IHC-P:1:50-1:200
-
FC:1:50-1:100
TARGET
UNIPROT #
PROTEIN NAME
ACADL
SYNONYMS
ACAD4 antibody; ACADL antibody; ACADL_HUMAN antibody; Acyl Coenzyme A dehydrogenase long chain antibody; Acyl-CoA dehydrogenase long chain antibody; FLJ94052 antibody; LCAD antibody; Long chain acyl CoA dehydrogenase antibody; Long-chain specific acyl-CoA dehydrogenase, mitochondrial antibody
SEQUENCE SIMILARITIES
Belongs to the acyl-CoA dehydrogenase family.
POST-TRANSLATIONAL MODIFICATION
Acetylation at Lys-318 and Lys-322 in proximity of the cofactor-binding sites strongly reduces catalytic activity. These sites are deacetylated by SIRT3.
SUBCELLULAR LOCATION
Mitochondrion matrix.
FUNCTION
ACADL is a gene that encodes LCAD - acyl-CoA dehydrogenase, long chain - which is a member of the acyl-CoA dehydrogenase family. The acyl-CoA dehydrogenase family is primarily responsible for beta-oxidation of fatty acids within the mitochondria. LCAD dysfunction is associated with lowered fatty acid oxidation capacity and decreased heat generation. As a result, LCAD deficiency has been correlated with increased cardiac hypertrophy, pulmonary disease, and overall insulin resistance. The LCAD enzyme catalyzes most of fatty acid beta-oxidation by forming a C2-C3 trans-double bond in the fatty acid. LCAD works on long-chain fatty acids, typically between C12 and C16-acylCoA. LCAD is essential for oxidizing unsaturated fatty acids such as oleic acid, but seems redundant in the oxidation of saturated fatty acids. Fatty acid oxidation has proven to spare glucose in fasting conditions, and is also required for amino acid metabolism, which is essential for the maintenance of adequate glucose production. LCAD is regulated by a reversible acetylation mechanism by SIRT3, in which the active form of the enzyme is deacetylated, and hyperacetylation reduces the enzymatic activity.