ACAD9 Antibody

Code CSB-PA887999ESR1HU
Size US$166
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  • Western blot
    All lanes: ACAD9 antibody at 6μg/ml
    Lane 1: MCF-7 whole cell lysate
    Lane 2: 293T whole cell lysate
    Lane 3: K562 whole cell lysate
    Secondary
    Goat polyclonal to rabbit IgG at 1/10000 dilution
    Predicted band size: 69 kDa
    Observed band size: 69 kDa

  • Immunohistochemistry of paraffin-embedded human small intestine tissue using CSB-PA887999ESR1HU at dilution of 1:100

  • Immunohistochemistry of paraffin-embedded human colon cancer using CSB-PA887999ESR1HU at dilution of 1:100

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Product Details

Full Product Name
Rabbit anti-Homo sapiens (Human) ACAD9 Polyclonal antibody
Uniprot No.
Target Names
Alternative Names
ACAD9Complex I assembly factor ACAD9 antibody; mitochondrial antibody; Acyl-CoA dehydrogenase family member 9 antibody; ACAD-9 antibody; EC 1.3.8.- antibody
Raised in
Rabbit
Species Reactivity
Human
Immunogen
Recombinant Human Acyl-CoA dehydrogenase family member 9, mitochondrial protein (1-270AA)
Immunogen Species
Homo sapiens (Human)
Conjugate
Non-conjugated
Clonality
Polyclonal
Isotype
IgG
Purification Method
Antigen Affinity Purified
Concentration
It differs from different batches. Please contact us to confirm it.
Buffer
PBS with 0.02% sodium azide, 50% glycerol, pH7.3.
Form
Liquid
Tested Applications
ELISA, WB, IHC
Recommended Dilution
Application Recommended Dilution
WB 1:200-1:1000
IHC 1:20-1:200
Troubleshooting and FAQs
Storage
Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
Lead Time
Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.

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Target Background

Function
As part of the MCIA complex, primarily participates in the assembly of the mitochondrial complex I and therefore plays a role in oxidative phosphorylation. This moonlighting protein has also a dehydrogenase activity toward a broad range of substrates with greater specificity for long-chain unsaturated acyl-CoAs. However, in vivo, it does not seem to play a primary role in fatty acid oxidation. In addition, the function in complex I assembly is independent of the dehydrogenase activity of the protein.
Gene References into Functions
  1. Mutations in the ND6, NDUFV1 or ACAD9 genes are responsible for the mitochondrial complex I deficiency. PMID: 29348607
  2. Study identified new mutations in ACAD9 responsible for a wide spectrum of heart diseases in the presence of elevated serum lactate levels. PMID: 27233227
  3. ACAD9 mutation is the most frequent cause of cardiac hypertrophy and isolated complex I deficiency. PMID: 26669660
  4. Case Report: neonatal multiorgan failure due to ACAD9 mutation and complex I deficiency with mitochondrial hyperplasia in liver, cardiac myocytes, skeletal muscle, and renal tubules. PMID: 26826406
  5. In cells where it is strongly expressed, ACAD9 plays a physiological role in fatty acid oxidation. PMID: 25721401
  6. Our results underscore the importance of the ACAD9 protein in complex I assembly and suggest that the enzymatic activity is a rudiment of the duplication event. PMID: 24158852
  7. Our data support a new function for ACAD9 in complex I function, making this gene an important new candidate for patients with complex I deficiency, which could be improved by riboflavin treatment. PMID: 20929961
  8. ACAD9 screening of 120 additional complex I-defective index cases led us to identify two additional unrelated cases and a total of five pathogenic ACAD9 alleles. PMID: 21057504
  9. Data show that two closely related metabolic enzymes, ACAD9 and VLCAD, diverged at the root of the vertebrate lineage to function in two separate mitochondrial metabolic pathways and have clinical implications for the diagnosis of complex I deficiency. PMID: 20816094
  10. Very high activity of CPT2 and VCLAD, involved in the metabolism of long-chain fatty acids. Fatty acid oxidation may play role in energy generation in placenta, and deficiency in may result in placental dysfunction and gestational complications. PMID: 12971426
  11. ACAD9 may play a role in the turnover of lipid membrane unsaturated fatty acids that are essential for membrane integrity and structure PMID: 16020546
  12. acyl-CoA dehydrogenase 9 (ACAD 9)was identified as the long-chain ACAD in human embryonic and fetal brain and central nervous tissue, using in situ hybridization as well as enzymatic studies PMID: 16750164
  13. We now report three cases of ACAD9 deficiency. PMID: 17564966
  14. Accumulation of 3-hydroxylated intermediates of long-chain fatty acids may contribute to the pathogenesis of retinopathy in MTP deficiencies. PMID: 18385088
  15. Validated occurrence of an unusual TG 3' splice site in intron 10. PMID: 17672918

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Involvement in disease
Acyl-CoA dehydrogenase family, member 9, deficiency (ACAD9 deficiency)
Subcellular Location
Mitochondrion inner membrane; Peripheral membrane protein; Matrix side.
Protein Families
Acyl-CoA dehydrogenase family
Tissue Specificity
Ubiquitously expressed in most normal human tissues and cancer cell lines with high level of expression in heart, skeletal muscles, brain, kidney and liver. In the cerebellum uniquely expressed in the granular layer (at protein level).
Database Links

HGNC: 21497

OMIM: 611103

KEGG: hsa:28976

STRING: 9606.ENSP00000312618

UniGene: Hs.567482

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