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197 results on '"Su, Xin-zhuan"'

10. Size-dependent enhancement of gene expression by Plasmodium 5'UTR introns.

Author

Lin, Lirong, Liu, Yanjing, Liang, Rui, Guo, Yue, Xu, Ruixue, Fan, Ruoxi, Jiao, Zhiwei, Zhao, Wenting, Yue, Lixia, Lu, Mingke, Liu, Shengfa, Su, Xin-zhuan, and Li, Jian

Subjects
GENE expression, PLASMODIUM, INTRONS, PLASMODIUM yoelii, GENETIC regulation, NUCLEOTIDE sequence
Abstract

Background: Eukaryotic genes contain introns that are removed by the spliceosomal machinery during mRNA maturation. Introns impose a huge energetic burden on a cell; therefore, they must play an essential role in maintaining genome stability and/or regulating gene expression. Many genes (> 50%) in Plasmodium parasites contain predicted introns, including introns in 5′ and 3′ untranslated regions (UTR). However, the roles of UTR introns in the gene expression of malaria parasites remain unknown. Methods: In this study, an episomal dual-luciferase assay was developed to evaluate gene expression driven by promoters with or without a 5′UTR intron from four Plasmodium yoelii genes. To investigate the effect of the 5′UTR intron on endogenous gene expression, the pytctp gene was tagged with 3xHA at the N-terminal of the coding region, and parasites with or without the 5′UTR intron were generated using the CRISPR/Cas9 system. Results: We showed that promoters with 5′UTR introns had higher activities in driving gene expression than those without 5′UTR introns. The results were confirmed in recombinant parasites expressing an HA-tagged gene (pytctp) driven by promoter with or without 5′UTR intron. The enhancement of gene expression was intron size dependent, but not the DNA sequence, e.g. the longer the intron, the higher levels of expression. Similar results were observed when a promoter from one strain of P. yoelii was introduced into different parasite strains. Finally, the 5′UTR introns were alternatively spliced in different parasite development stages, suggesting an active mechanism employed by the parasites to regulate gene expression in various developmental stages. Conclusions: Plasmodium 5′UTR introns enhance gene expression in a size-dependent manner; the presence of alternatively spliced mRNAs in different parasite developmental stages suggests that alternative slicing of 5′UTR introns is one of the key mechanisms in regulating parasite gene expression and differentiation. [ABSTRACT FROM AUTHOR]

Published
2024
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12. Artemisinin resistance phenotypes and K13 inheritance in a Plasmodium falciparum cross and Aotus model

Author

Sá, Juliana M., Kaslow, Sarah R., Krause, Michael A., Melendez-Muniz, Viviana A., Salzman, Rebecca E., Kite, Whitney A., Zhang, Min, Barros, Roberto R. Moraes, Mu, Jianbing, Han, Paul K., Mershon, J. Patrick, Figan, Christine E., Caleon, Ramoncito L., Rahman, Rifat S., Gibson, Tyler J., Amaratunga, Chanaki, Nishiguchi, Erika P., Breglio, Kimberly F., Engels, Theresa M., Velmurugan, Soundarapandian, Ricklefs, Stacy, Straimer, Judith, Gnädig, Nina F., Deng, Bingbing, Liu, Anna, Diouf, Ababacar, Miura, Kazutoyo, Tullo, Gregory S., Eastman, Richard T., Chakravarty, Sumana, James, Eric R., Udenze, Kenneth, Li, Suzanne, Sturdevant, Daniel E., Gwadz, Robert W., Porcella, Stephen F., Long, Carole A., Fidock, David A., Thomas, Marvin L., Fay, Michael P., Sim, B. Kim Lee, Hoffman, Stephen L., Adams, John H., Fairhurst, Rick M., Su, Xin-zhuan, and Wellems, Thomas E.

Published
2018

13. Large-scale Artemisinin–Piperaquine Mass Drug Administration With or Without Primaquine Dramatically Reduces Malaria in a Highly Endemic Region of Africa

Author

Deng, Changsheng, Huang, Bo, Wang, Qi, Wu, Wanting, Zheng, Shaoqin, Zhang, Hongying, Li, Di, Feng, Danghong, Li, Guoming, Xue, Linlu, Yang, Tao, Tuo, Fei, Mohadji, Fouad, Su, Xin-zhuan, Xu, Qin, Wu, Zhibing, Lin, Li, Zhou, Jiuyao, Yan, Hong, Bacar, Affane, Abdallah, Kamal Said, Kéké, Rachadi A., Mliva, Ahamada Msa, Mohamed, Moussa, Wang, Xinhua, Huang, Shiguang, Oithik, Fatihou, Li, Xiao-bo, Lu, Fangli, Fay, Michael P., Liu, Xiao-hong, Wellems, Thomas E., and Song, Jianping

Published
2018

24. A Specific Inhibitor of PfCDPK4 Blocks Malaria Transmission: Chemical-genetic Validation

Author

Ojo, Kayode K., Eastman, Richard T., Vidadala, RamaSubbaRao, Zhang, Zhongsheng, Rivas, Kasey L., Choi, Ryan, Lutz, Justin D., Reid, Molly C., Fox, Anna M. W., Hulverson, Matthew A., Kennedy, Mark, Isoherranen, Nina, Kim, Laura M., Comess, Kenneth M., Kempf, Dale J., Verlinde, Christophe L. M. J., Su, Xin-zhuan, Kappe, Stefan H. I., Maly, Dustin J., Fan, Erkang, and Van Voorhis, Wesley C.

Published
2014

28. Genetic loci associated with delayed clearance of Plasmodium falciparum following artemisinin treatment in Southeast Asia

Author

Takala-Harrison, Shannon, Clark, Taane G., Jacob, Christopher G., Cummings, Michael P., Miotto, Olivo, Dondorp, Arjen M., Fukuda, Mark M., Nosten, Francois, Noedl, Harald, Imwong, Mallika, Bethell, Delia, Se, Youry, Lon, Chanthap, Tyner, Stuart D., Saunders, David L., Socheat, Duong, Ariey, Frederic, Phyo, Aung Pyae, Starzengruber, Peter, Fuehrer, Hans-Peter, Swoboda, Paul, Stepniewska, Kasia, Flegg, Jennifer, Arze, Cesar, Cerqueira, Gustavo C., Silva, Joana C., Ricklefs, Stacy M., Porcella, Stephen F., Stephens, Robert M., Adams, Matthew, Kenefic, Leo J., Campino, Susana, Auburn, Sarah, Maclnnis, Bronwyn, Kwiatkowski, Dominic P., Su, Xin-zhuan, White, Nicholas J., Ringwald, Pascal, and Plowe, Christopher V.

Published
2013

30. Artemisinin-resistant Plasmodium falciparum in Pursat province, western Cambodia: a parasite clearance rate study

Author

Amaratunga, Chanaki, Sreng, Sokunthea, Suon, Seila, Phelps, Erika S, Stepniewska, Kasia, Lim, Pharath, Zhou, Chongjun, Mao, Sivanna, Anderson, Jennifer M, Lindegardh, Niklas, Jiang, Hongying, Song, Jianping, Su, Xin-zhuan, White, Nicholas J, Dondorp, Arjen M, Anderson, Tim JC, Fay, Michael P, Mu, Jianbing, Duong, Socheat, and Fairhurst, Rick M

Published
2012
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42. Activation of cGAS‐STING by Lethal Malaria N67C Dictates Immunity and Mortality through Induction of CD11b+Ly6Chi Proinflammatory Monocytes.

Author

Du, Yang, Luo, Yien, Hu, Zhiqiang, Lu, Jiansen, Liu, Xin, Xing, Changsheng, Wu, Jian, Duan, Tianhao, Chu, Junjun, Wang, Helen Y., Su, Xin‐zhuan, Yu, Xiao, and Wang, Rong‐Fu

Subjects
MYELOID differentiation factor 88, MALARIA, MONOCYTES, IMMUNITY, NATURAL immunity, PLASMODIUM yoelii, IMMUNE response
Abstract

Cyclic GMP‐AMP synthase (cGAS) and stimulator of interferon genes (STING) play critical roles in the innate immunity against infectious diseases and are required to link pathogen DNA sensing to immune responses. However, the mechanisms by which cGAS‐STING‐induced cytokines suppress the adaptive immune response against malaria infections remain poorly understood. Here, cGAS‐STING signaling is identified to play a detrimental role in regulating anti‐malaria immunity. cGAS or STING deficiency in mice markedly prolongs mouse survival during lethal malaria Plasmodium yoelii nigeriensis N67C infections by reducing late interleukin (IL)‐6 production. Mechanistically, cGAS/STING recruits myeloid differentiation factor 88 (MyD88) and specifically induces the p38‐dependent signaling pathway for late IL‐6 production, which, in turn, expands CD11b+Ly6Chi proinflammatory monocytes to inhibit immunity. Moreover, the blockage or ablation of the cGAS‐STING‐MyD88‐p38‐IL‐6 signaling axis or the depletion of CD11b+Ly6Chi proinflammatory monocytes provides mice a significant survival benefit during N67C and other lethal malaria‐strain infections. Taken together, these findings identify a previously unrecognized detrimental role of cGAS‐STING‐MyD88‐p38 axis in infectious diseases through triggering the late IL‐6 production and proinflammatory monocyte expansion and provide insight into how targeting the DNA sensing pathway, dysregulated cytokines, and proinflammatory monocytes enhances immunity against infection. [ABSTRACT FROM AUTHOR]

Published
2022
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43. Malaria biology and disease pathogenesis: insights for new treatments

Author

Miller, Louis H., Ackerman, Hans C., Su, Xin-zhuan, and Wellems, Thomas E.

Subjects
Malaria, Biological sciences, Health
Abstract

Plasmodium falciparum malaria, an infectious disease caused by a parasitic protozoan, claims the lives of nearly a million children each year in Africa alone and is a top public health concern. Evidence is accumulating that resistance to artemisinin derivatives, the frontline therapy for the asexual blood stage of the infection, is developing in southeast Asia. Renewed initiatives to eliminate malaria will benefit from an expanded repertoire of antimalarials, including new drugs that kill circulating P. falciparum gametocytes, thereby preventing transmission. Our current understanding of the biology of asexual blood-stage parasites and gametocytes and the ability to culture them in vitro lends optimism that high-throughput screenings of large chemical libraries will produce a new generation of antimalarial drugs. There is also a need for new therapies to reduce the high mortality of severe malaria. An understanding of the pathophysiology of severe disease may identify rational targets for drugs that improve survival., Introduction Malaria is a devastating disease, killing nearly a million children each year in Africa alone. There exists a real and urgent need for new antimalarial drugs that can meet [...]

Published
2013
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45. Analysis of Plasmodium falciparum diversity in natural infections by deep sequencing

Author

Manske, Magnus, Miotto, Olivo, Campino, Susana, Auburn, Sarah, Almagro-Garcia, Jacob, Maslen, Gareth, O’Brien, Jack, Djimde, Abdoulaye, Doumbo, Ogobara, Zongo, Issaka, Ouedraogo, Jean-Bosco, Michon, Pascal, Mueller, Ivo, Siba, Peter, Nzila, Alexis, Borrmann, Steffen, Kiara, Steven M., Marsh, Kevin, Jiang, Hongying, Su, Xin-Zhuan, Amaratunga, Chanaki, Fairhurst, Rick, Socheat, Duong, Nosten, Francois, Imwong, Mallika, White, Nicholas J., Sanders, Mandy, Anastasi, Elisa, Alcock, Dan, Drury, Eleanor, Oyola, Samuel, Quail, Michael A., Turner, Daniel J., Ruano-Rubio, Valentin, Jyothi, Dushyanth, Amenga-Etego, Lucas, Hubbart, Christina, Jeffreys, Anna, Rowlands, Kate, Sutherland, Colin, Roper, Cally, Mangano, Valentina, Modiano, David, Tan, John C., Ferdig, Michael T., Amambua-Ngwa, Alfred, Conway, David J., Takala-Harrison, Shannon, Plowe, Christopher V., Rayner, Julian C., Rockett, Kirk A., Clark, Taane G., Newbold, Chris I., Berriman, Matthew, MacInnis, Bronwyn, and Kwiatkowski, Dominic P.

Published
2012
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50. Polymorphism in the Plasmodium falciparum erythrocyte-binding ligand JESEBL/EBA-181 alters its receptor specificity

Author

Mayer, D.C. Ghislaine, Mu, Jian-Bing, Kaneko, Osamu, Duan, Junhui, Su, Xin-zhuan, and Miller, Louis H.

Subjects
Erythrocytes -- Research, Malaria -- Research, Science and technology
Abstract

The malaria parasite lives within erythrocytes and depends on the binding of parasite ligands to host cell surface receptors for invasion. The most virulent human malaria parasite, Plasmodium falciparum, uses multiple ligands, including EBA-175, BAEBL, and JESEBL of the Duffy-binding-like (DBL) family of erythrocytebinding proteins, for invasion of human erythrocytes. Region II of these parasite ligands is the erythrocyte-binding domain. Previously, we had shown that polymorphism in region II of BAEBL leads to different erythrocyte-binding specificities. We have now identified and characterized the binding specificity of six JESEBL variants. We sequenced region II of JESEBL from 20 P. falciparum clones collected from various parts of the world where malaria is endemic. We observed eight JESEBL variants that contained amino acid polymorphisms at five positions among all clones. Seven of the eight variants could be connected by a single base change that led to an amino acid change. We investigated the functional significance of these polymorphisms by transiently expressing region II from six of JESEBL variants on the surface of Chinese hamster ovary cells. We observed four erythrocyte-binding patterns to enzyme-treated erythrocytes. Thus, P. falciparum DBL ligands JESEBL and BAEBL can recognize multiple receptors on the erythrocyte surface. In contrast to Plasmodium vivax, which has disappeared from West Africa because of the Duffy-negative blood group, P. falciparum may have been successful in endemic areas because it has mutated the ligands of the DBL family to create multiple pathways of invasion, thus making selection of refractory erythrocytes unlikely. parasite polymorphism

Published
2004

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