The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Use a concentration of 1 µg/ml. Predicted molecular weight: 85 kDa. Good results were obtained when blocked with 5% non-fat dry milk in 0.05% PBS-T.
Forms hydroxylysine residues in -Xaa-Lys-Gly- sequences in collagens. These hydroxylysines serve as sites of attachment for carbohydrate units and are essential for the stability of the intermolecular collagen cross-links.
Highly expressed in pancreas and muscle. Isoform 1 and isoform 2 are expressed in the majority of the examined cell types. Isoform 2 is specifically expressed in skin, lung, dura and aorta.
Defects in PLOD2 are the cause of Bruck syndrome type 2 (BRKS2) [MIM:609220]. Bruck syndrome, also known as osteogenesis imperfecta with congenital joint contractures, is an autosomal recessive disease characterized by generalized osteopenia, joint contractures at birth, fragile bones and short stature. It can be distinguished from osteogenesis imperfecta by the absence of hearing loss and dentinogenesis imperfecta, and by the presence of clubfoot and congenital joint limitations. The molecular defect is an aberrant cross-linking of bone collagen, due to underhydroxylation of lysine residues within the telopeptides of type I collagen, whereas the lysine residues in the triple helix are normal.
Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) analysis of human bronchial epithelial tissue labelling PLOD2 with ab90088 at 1/100. A Cy3-conjugated donkey anti-rabbit IgG (1/200) was used as the secondary antibody. Positive staining shown in the cytoplasm. Magnification: 20X. Exposure time: 0.5 - 2.0 seconds. Left - DAPI. Middle - PLOD2. Right - Merge.
Western blot - Anti-PLOD2 antibody (ab90088)
Anti-PLOD2 antibody (ab90088) at 1 µg/ml (in 5% skim milk / PBS buffer) + DU145 cell lysate at 10 µg
Secondary HRP conjugated anti-Rabbit IgG at 1/50000 dilution