The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Blocking - Blocking peptide for Anti-SDHA antibody (ab66484)
70 - 90% by HPLC.
- First try to dissolve a small amount of peptide in either water or buffer. The more charged residues on a peptide, the more soluble it is in aqueous solutions. - If the peptide doesn’t dissolve try an organic solvent e.g. DMSO, then dilute using water or buffer. - Consider that any solvent used must be compatible with your assay. If a peptide does not dissolve and you need to recover it, lyophilise to remove the solvent. - Gentle warming and sonication can effectively aid peptide solubilisation. If the solution is cloudy or has gelled the peptide may be in suspension rather than solubilised. - Peptides containing cysteine are easily oxidised, so should be prepared in solution just prior to use.
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Preparation and Storage
Stability and Storage
Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.
Succinate dehydrogenase complex subunit A flavoprotein
Succinate dehydrogenase complex subunit A flavoprotein (Fp)
Flavoprotein (FP) subunit of succinate dehydrogenase (SDH) that is involved in complex II of the mitochondrial electron transport chain and is responsible for transferring electrons from succinate to ubiquinone (coenzyme Q).
Defects in SDHA are a cause of mitochondrial complex II deficiency (MT-C2D) [MIM:252011]. A disorder of the mitochondrial respiratory chain with heterogeneous clinical manifestations. Clinical features include psychomotor regression in infants, poor growth with lack of speech development, severe spastic quadriplegia, dystonia, progressive leukoencephalopathy, muscle weakness, exercise intolerance, cardiomyopathy. Some patients manifest Leigh syndrome or Kearns-Sayre syndrome. Defects in SDHA are a cause of Leigh syndrome (LS) [MIM:256000]. LS is a severe disorder characterized by bilaterally symmetrical necrotic lesions in subcortical brain regions. Defects in SDHA are the cause of cardiomyopathy dilated type 1GG (CMD1GG) [MIM:613642]. CMD1GG is a disorder characterized by ventricular dilation and impaired systolic function, resulting in congestive heart failure and arrhythmia. Patients are at risk of premature death.
Belongs to the FAD-dependent oxidoreductase 2 family. FRD/SDH subfamily.