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An antigen of high molecular weight (CA-3) was isolated from the cytosol fraction of GW-39 human colon tumor cells by antibody affinity chromatography. CA-3 was characterized by an acidic pI value of 4.5-4.9, a molecular weight of 700 kilodaltons and a sedimentation coefficient of 13S. It contained all of the commonly occurring amino acids and had an acidic to basic amino acid ratio of 1.4. CA-3 was resistant to dissociation by reducing agents as well as by sodium dodecylsulfate. Quantitation of CA-3 by a radioimmunoassay employing rabbit anti-CA-3 antiserum revealed a marked elevation of CA-3 in the cytosol extracts of human primary colon carcinoma in comparison to normal colon. The molecular properties of CA-3 are compared to those of carcinoembryonic antigen, high molecular weight colon specific antigen CSAp and two other high molecular weight proteins, fibronectin and conglutinin. Colon antigen CA-3 appears to be different from these other molecules in terms of its molecular weight, sedimentation value, isoelectric point and amino acid composition. 相似文献
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On the basis of correlative data on the global distribution of leprosy, its bacteria metabolizing fossil fuels (FF), and the FF themselves, the origin of leprosy in the world as a whole, and in the leprosy-free countries, in particular, as indigenous cases, appeared to be primarily due to a soil-to-man, and secondarily due to a man-to-man infection. These findings helped to elucidate similar problems of animal leprosies and nocardial diseases. 相似文献
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Nabamita Roy Sunanda Bhattacharyya Swati Chakrabarty Shyamasree Laskar Somepalli Mastan Babu Mrinal Kanti Bhattacharyya 《Molecular microbiology》2014,94(2):353-366
Malaria parasites survive through repairing a plethora of DNA double‐stranded breaks (DSBs) experienced during their asexual growth. In Plasmodium Rad51 mediated homologous recombination (HR) mechanism and homology‐independent alternative end‐joining mechanism have been identified. Here we address whether loss of HR activity can be compensated by other DSB repair mechanisms. Creating a transgenic Plasmodium line defective in HR function, we demonstrate that HR is the most important DSB repair pathway in malarial parasite. Using mouse malaria model we have characterized the dominant negative effect of PfRad51K143R mutant on Plasmodium DSB repair and host–parasite interaction. Our work illustrates that Plasmodium berghei harbouring the mutant protein (PfRad51K143R) failed to repair DSBs as evidenced by hypersensitivity to DNA‐damaging agent. Mice infected with mutant parasites lived significantly longer with markedly reduced parasite burden. To better understand the effect of mutant PfRad51K143R on HR, we used yeast as a surrogate model and established that the presence of PfRad51K143R completely inhibited DNA repair, gene conversion and gene targeting. Biochemical experiment confirmed that very low level of mutant protein was sufficient for complete disruption of wild‐type PfRad51 activity. Hence our work provides evidence that HR pathway of Plasmodium could be efficiently targeted to curb malaria. 相似文献
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