In summary, we generated specific mAbs directed against the human IRAS N-terminal. The mAb DA041 exhibited the best performance in a variety of assays including immunoblotting, immunoprecipitation, indirect immunofluorescence stainning, and flow cytometry. Specific mAbs may provide an ideal reagent for further investigation of the function of IRAS proteins. Molecular and physiologic basis of quinoline drug resistance in Plasmodium falciparum malaria 30 years before the discovery of the pfcrt gene, altered cellular drug accumulation in drug-resistant malarial parasites had been well documented. Heme released from catabolized hemoglobin was thought to be a key target for quinoline drugs, and additional modifications to quinoline drug structure in order to improve activity against chloroquine-resistant malaria were performed in a few laboratories. However, parasite cell culture methods were still in their infancy, assays for drug susceptibility were not well standardized, and the power of malarial genetics was decades away. The last 10 years have witnessed explosive progress in elucidation of the biochemistry of chloroquine resistance. This review briefly summarizes that progress, and discusses where additional work is needed. Human malarias are caused by infection with one of five malarial (Plasmodium) parasites (Plasmodium ovale, P. malariae, P. knowlesi, P. vivax and P. falciparum), which occurs during a female Anopheles mosquito blood meal (P. knowlesi is zoonotic, the others pass human to human). P. falciparum infections account for 95% of malaria mortality worldwide, so historically most malaria research has focused on this species. However, there is also a critical need for basic research on the others, particularly P. vivax. In P. falciparum malaria, sporozoites injected during the blood meal migrate through the skin via multiple routes, localize to the liver within hours, invade hepatocytes and are then released into the blood after approximately 2 weeks as large merosomes containing 5-10,000 new haploid merozoites. These then rapidly invade red blood cells (RBCs) [1] and proceed through an amazing differentiation and feeding cycle that is 45-50 h long. An initial 'ring' differentiates into a single trophozoite, which then differentiates to 8-36 new mero zoites. These are then released from lysed infected RBC (iRBC) and re-invade RBCs once again. The resulting increased parasitemia generates the well known symptoms of fever, anemia, and so on, which without treatment can ultimately progress to severe or cerebral malaria, coma and death. Sporadically, iRBCs commit to gametocyte differentiation via poorly understood pathways. Haploid gametocytes ingested by another mosquito feeding on an infected human, differentiate to male and female and combine in the mosquito to produce diploid stages that ultimately result in the injection of new sporozoites via mosquito saliva during another blood meal.