|Positive WB detected in||HEK-293T cells, HEK-293 cells, MCF-7 cells|
|Positive IHC detected in||human liver cancer tissue|
Note: suggested antigen retrieval with TE buffer pH 9.0; (*) Alternatively, antigen retrieval may be performed with citrate buffer pH 6.0
|Western Blot (WB)||WB : 1:500-1:1000|
|Immunohistochemistry (IHC)||IHC : 1:50-1:500|
|Sample-dependent, check data in validation data gallery|
15770-1-AP targets ACAD9 in WB, IHC, ELISA applications and shows reactivity with human, mouse, rat samples.
|Tested Reactivity||human, mouse, rat|
|Cited Reactivity||human, mouse|
|Host / Isotype||Rabbit / IgG|
|Immunogen||ACAD9 fusion protein Ag8414|
|Full Name||acyl-Coenzyme A dehydrogenase family, member 9|
|Calculated molecular weight||69 kDa|
|Observed molecular weight||65 kDa|
|GenBank accession number||BC007970|
|Gene ID (NCBI)||28976|
|Purification Method||Antigen affinity purification|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage.|
Acyl-CoA dehydrogenases (ACADs) are a family of mitochondrial enzymes catalyzing the initial rate-limiting step in the β-oxidation of fatty acyl-CoA. ACAD9 belongs to the group of ACADs. The deduced 621-amino acid protein has a calculated molecular mass of 68.8 kD. It has an N-terminal leader sequence, 2 conserved motifs shared by all ACAD family members, and a potential N-glycosylation site(PMID:12359260). Defects in ACAD9 are a cause of acyl-CoA dehydrogenase family member type 9 deficiency (ACAD9 deficiency).
Integrative analyses of translatome and transcriptome reveal important translational controls in brown and white adipose regulated by microRNAs.
MITRAC15/COA1 promotes mitochondrial translation in a ND2 ribosome-nascent chain complex.