Parasites that cause malaria typically enter the body through the bite of a mosquito. Malaria is common in areas such as Africa, South America, and Southern Asia. Aralen patient teaching Plaquenil pregnancy complications Novus offers ready to use HeLa Chloroquine Treated / Untreated Cell Lysate and Neuro2a Chloroquine Treated / Untreated Cell Lysate which are highly recommended positive controls for WB assay of LC3. Overexpression lysates of LC3 such as NBP2-04906, or a total cell lysate from serum starved cells depicting excessive vacuolization are other. This antibody detects both the non-lipidated LC3-I non-autophagic and lipidated LC3-II autophagic under autophagy conditions. Immunogen Recombinant protein corresponding to Human LC3-I/II. Application Immunocytochemistry Analysis A 0 dilution of this antibody detected LC3 in serum-starved, chloroquine-treated HeLa cells. Chloroquine-induced autophagic vacuole accumulation and cell death in glioma cells is p53 independent. Chloroquine CQ, an antimalarial lysosomotropic agent, has been identified as a potential adjuvant in the treatment regimen of GBMs. However, the mechanism of CQ-induced tumor cell death is poorly defined. LC3-II is the cleaved and. Chloroquine is also used to treat amebiasis (infection caused by amoebae). Chloroquine is used to treat and to prevent malaria. Chloroquine and lc3 Chloroquine Sigma-Aldrich, Anti-LC3-I/II Antibody Sigma-Aldrich Plaquenil toll like endosomalPlaquenil drug classes P62 is a receptor for cargo destined to be degraded by autophagy, including ubiquitinated protein aggregates destined for clearance. The p62 protein is able to bind ubiquitin and also to LC3, thereby targeting the autophagosome and facilitating clearance of ubiquitinated proteins. Invitrogen Molecular Probes tools enable Tracking p62 in live cells Tracking Autophagy With LC3B & p62 Thermo Fisher.. Chloroquine-induced autophagic vacuole accumulation and.. CST - Chloroquine. Thus, it is important to measure the amount of LC3-II delivered to the lysosomes by comparing LC3-II amounts in the presence and absence of bafilomycin A 1 a vacuolar H +-ATPase inhibitor, lysosomal protease inhibitors e.g. E64d and pepstatin A, or lysosomotropic agents e.g. chloroquine to inhibit lysosomal degradation of LC3-II. Chloroquine prevented ductal carcinoma in situ xenografts’ outgrowth in athymic mice 37, 38 and inhibited N-methyl-N-nitrosurea-induced mammary carcinogenesis, suggesting chloroquine-based therapy as a possible agent in the prevention of initial premalignant lesions from progressing to breast cancer. Another problem with this method is that LC3-II tends to be much more sensitive to be detected by immunoblotting than LC3-I. Accordingly, simple comparison of LC3-I and LC3-II, or summation of LC3-I and LC3-II for ratio determinations, may not be appropriate, and rather, the amount of LC3-II can be compared between samples.