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Validated All-in-One™ qPCR Primer for HADHA(NM_000182.4) Search again
Powered by BiozBy default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
This gene encodes the alpha subunit of the mitochondrial trifunctional protein, which catalyzes the last three steps of mitochondrial beta-oxidation of long chain fatty acids. The mitochondrial membrane-bound heterocomplex is composed of four alpha and four beta subunits, with the alpha subunit catalyzing the 3-hydroxyacyl-CoA dehydrogenase and enoyl-CoA hydratase activities.
Gene References into function
- The G1528C (E474Q) mutation in the alpha-subunit of the mitochondrial trifunctional protein was not found in 10 women with acute fatty liver of pregnancy.
- results of deficiency of (Long-chain L-3-hydroxyacyl-coenzyme a dehydrogenase)
- Plasma concentration varied more than erythrocyte levels. Postprandial period and fasting.
- Both alpha- and beta-subunit mutations result in TFP complex instability, demonstrating that the mechanism of disease is the same in alpha- or beta-mutation-derived disease and explaining the biochemical and clinical similarities.
- The retinal pigment epithelium rather than the choriocapillaris could be the critical affected cell layer in LCHAD retinopathy
- DNA analysis of patients 1 and 2 revealed homozygosity for a c.1689+2T>G mutation of the HADHA gene, resulting in the skipping of exon 16 with an in-frame 69-bp deletion.
- Neither maternal nor fetal heterozygosity for the E474Q mutation is a relevant factor of HELLP syndrome.
- There might be diverse etiological factors in China contributing to AFLP other than the frequently reported mutation in the LCHAD.
- The second of 220 SIDs cases was a compound heterozygous for the prevalent MTP G1528C mutation and a novel 1 bp deletion in exon 18 of the MTPalpha-subunit gene.
- Severe cardiac mitochondrial proliferation and TFP deficiency was observed in intrauterine cardiomyopathy.