The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Use at an assay dependent concentration. PubMed: 24268659
Use at an assay dependent concentration.
Titre using peptide based assay: 1:1562500.
Use a concentration of 1.25 µg/ml. Detects a band of approximately 68 kDa (predicted molecular weight: 68 kDa). Good results were obtained when blocked with 5% non-fat dry milk in 0.05% PBS-T.
Required for pseudopod elongation in transformed cells. Substrate-specific adapter of an E3 ubiquitin-protein ligase complex which mediates the ubiquitination and subsequent proteasomal degradation of target proteins.
Ubiquitinated and probably targeted for proteasome-independent degradation.
Cytoplasm. Cytoplasm > cytoskeleton. Cell projection > pseudopodium. Cell projection > ruffle. Predominantly cytoplasmic but can co-localize with F-actin at the membrane ruffle-like structures at the tips of transformation-specific pseudopodia.
Kelch repeat and BTB domain-containing protein 10 antibody
Kelch-related protein 1 antibody
Immunohistochemistry (Frozen sections) - Anti-KBTBD10 antibody (ab66605)Image from Gupta VA et al., Am J Hum Genet. 2013;93(6):1108-17. Fig 2(C).; doi: 10.1016/j.ajhg.2013.10.020 with permission from Elsevier.
Immunohistochemistry (Frozen sections) analysis of human skeletal muscle tissue from control and nemaline myopathy affected individuals labelling KBTBD10 with ab66605. Costaining with sarcomeric markers in longitudinal planes showed that KLHL41 staining predominated over the I-bands of the sarcomere and at perinuclear regions. Scale bars represent 50 μm.
Western blot - KBTBD10 antibody (ab66605)
Anti-KBTBD10 antibody (ab66605) at 1.25 µg/ml (in 5% skim milk / PBS buffer) + fetal muscle lysate at 10 µg
Secondary HRP conjugated anti-Rabbit IgG at 1/50000 dilution
Predicted band size : 68 kDa Observed band size : 68 kDa gel concentration: 12%
Gupta VA et al. Identification of KLHL41 Mutations Implicates BTB-Kelch-Mediated Ubiquitination as an Alternate Pathway to Myofibrillar Disruption in Nemaline Myopathy. Am J Hum Genet93:1108-17 (2013).
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