Mouse MAP1LC3B (Microtubule-associated proteins 1A/1B light chain 3B) Microsample ELISA Kit

The test principle applied in this kit is Sandwich enzyme immunoassay. The microtiter plate provided in this kit has been pre-coated with an antibody specific to Mouse MAP1LC3B. Standards or samples are added to the appropriate microtiter plate wells then with a biotin-conjugated antibody specific to Mouse MAP1LC3B. Next, Avidin conjugated to Horseradish Peroxidase (HRP) is added to each microplate well and incubated. After TMB substrate solution is added, only those wells that contain Mouse MAP1LC3B, biotin-conjugated antibody and enzyme-conjugated Avidin will exhibit a change in color. The enzyme-substrate reaction is terminated by the addition of sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450nm ± 10nm. The concentration of Mouse MAP1LC3B in the samples is then determined by comparing the OD of the samples to the standard curve.Detection Range: 0.16-10 ng/mL. Sensitivity: 0.055 ng/mL. Assay Type: Sandwich. Standard: 10 ng/mL. Sample Type: sTissue homogenates, cell lysates and other biological fluids. Assay duration: 3.5h. Protein Function: Ubiquitin-like modifier involved in formation of autophagosomal vacuoles (autophagosomes). Plays a role in mitophagy which contributes to regulate mitochondrial quantity and quality by eliminating the mitochondria to a basal level to fulfill cellular energy requirements and preventing excess ROS production. In response to cellular stress and upon mitochondria fission, binds C-18 ceramides and anchors autophagolysosomes to outer mitochondrial membranes to eliminate damaged mitochondria. While LC3s are involved in elongation of the phagophore membrane, the GABARAP/GATE-16 subfamily is essential for a later stage in autophagosome maturation. Promotes primary ciliogenesis by removing OFD1 from centriolar satellites via the autophagic pathway. Through its interaction with the reticulophagy receptor TEX264, participates in the remodeling of subdomains of the endoplasmic reticulum into autophagosomes upon nutrient stress, which then fuse with lysosomes for endoplasmic reticulum turnover. Upon nutrient stress, directly recruits cofactor JMY to the phagophore membrane surfaces and promotes JMY's actin nucleation activity and autophagosome biogenesis during autophagy [The Uniprot Consortium]