Application DetailsWestern Blotting (1:500-1:2,000), Immunohistochemistry (1:200-1:1,000, use at 1:200 for paraffin-embedded tissues), Immunocytochemistry (1:200-1:1,000) and ELISA (1:10,000). Other applications have not been tested. Biosensis recommends optimal dilutions/concentrations should be determined by the end user.
TargetSortilin-related receptor (SorLA/SORL1)
SpecificityAnti-SorLA SORL1 Monoclonal Antibody validated for WB, IHC, IF, ELISA. Reactive to human, other species not yet tested
Target Host SpeciesHuman
Immunogen DescriptionPurified recombinant fragment of human SorLA expressed in E. Coli
Purity DescriptionAsciteis Fluid, 0.45 m filtered
FormatAscitic fluid containing 0.03% sodium azide
Storage InstructionsSpin vial briefly before opening. Divide into aliquots and store at -20°C for long-term storage. Store at 2-8°C short-term (up to 4 weeks). Avoid repetitive freeze/thaw cycles.
Batch NumberPlease see item label.
Expiration Date12 months after date of receipt (unopened vial).
Alternative NamesSortilin-related receptor; Low-density lipoprotein receptor relative with 11 ligand-binding repeats; LDLR relative with 11 ligand-binding repeats; LR11; SorLA-11; Sorting protein-related receptor containing LDLR class A repeats; SorLA
Scientific BackgroundThe sortilin-related receptor SORLA is an endocytic receptor that belongs to the vacuolar protein sorting 10 (VPS10) domain receptor family. SORLA binds to the amyloid precursor protein (APP). It functions as an intracellular sorting receptor as APP is being trafficked between the secretory pathway, the cell surface, and, subsequently, endosomes. SORLA is localized primarily to the trans-Golgi network and early endosomes, shuttling between these two membrane compartments. SORLA's interaction with APP in endosomal compartments limits the amyloidogenic proteolysis of APP. Reduced brain levels of SORLA are thought to alter the transport and processing of APP to increase generation of Aβ peptides in early or late endosomes. SORLA is highly expressed in the brain. Expression is reported to be normal in familial Alzheimer's disease caused by mutations in presenilin or APP genes, but decreased in some cases of sporadic late-onset AD. In these cases, loss of SORLA activity has been hypothesized to be a proximal cause of amyloidosis. In addition, several private nonsense and missense mutations in SORLA that decrease SORLA levels in the brain were found in rare cases of familial AD. A genetic association of SORLA with AD is well established. Population-based studies initially linked nearly 30 SNPs in SORLA to increased risk of AD, and subsequent studies, meta-analyses, and GWAS have confirmed some of these associations. The genetic data on SORLA and LOAD is complex, with at least six different polymorphisms pointing toward the existence of several causative variants in distinct regions of the gene. Ref: alzforum.org
A. Western blotting detection of truncated SorLA recombinant protein (lane 1). B. Analysis of SorLA expression (green) in PANC-1 cells by Immunocytochemistry. Red: Actin filaments. Blue: Cell nucleus. C. SorLA expression in paraffin-embedded human cerebrum tissue by Immunohistochemistry