This Human ALR overexpression lysate was created in HEK293 Cells and intented for use as a Western blot (WB) positive control. Purification of ALR protein (Cat: 15278-H08H) from the overexpression lysate was verified.
A DNA sequence encoding the human GFER (NP_005253.3) (Met1-Asp125) was expressed with a polyhistidine tag at the C-terminus.
The recombinant human GFER consists 136 amino acids and predicts a molecular mass of 16.5 kDa.
Human ALR HEK293 Overexpression Lysate: 使用指南
Cell lysate was prepared by homogenization of the over-expressed cells in ice-cold modified RIPA Lysis Buffer with cocktail of protease inhibitors (Sigma). Cell debris was removed by centrifugation. Protein concentration was determined by Bradford assay (Bio-Rad protein assay, Microplate Standard assay). The cell lysate was boiled for 5 min in 1 x SDS loading buffer (50 mM Tris-HCl pH 6.8, 12.5% glycerol, 1% sodium dodecylsulfate, 0.01% bromophenol blue) containing 5% b-mercaptoethanol, and lyophilized.
1. Centrifuge the tube for a few seconds and ensure the pellet at the bottom of the tube.
2. Re-dissolve the pellet using 200μL pure water and boil for 2-5 min.
1 X Sample Buffer (1 X modified RIPA buffer+1 X SDS loading buffer).
稳定性 & 储存条件
Store at 4℃ for up to twelve months from date of receipt. After re-dissolution, aliquot and store at -80℃ for up to twelve months. Avoid repeated freeze-thaw cycles.
Western Blot (WB) Optimal dilutions/concentrations should be determined by the end user.
Human ALR HEK293 Overexpression Lysate: 别称
Human ALR Overexpression Lysate; Human ERV1 Overexpression Lysate; Human HERV1 Overexpression Lysate; Human HPO Overexpression Lysate; Human HPO1 Overexpression Lysate; Human HPO2 Overexpression Lysate; Human HSS Overexpression Lysate
Alterations in GFER gene have been associated with progressive mitochondrial myopathy, congenital cataracts, hearing loss, developmental delay, lactic acidosis and respiratory chain deficiency in 3 siblings born to consanguineous Moroccan parents by homozygosity mapping and candidate gene approach. Using homozygosity mapping, we discovered that a mutation in the GFER gene causes an infantile mitochondrial disorder.