Drug resistance. Population transcriptomics of human malaria parasites reveals the mechanism of artemisinin resistance

Artemisinin resistance in Plasmodium falciparum threatens global efforts to control and eliminate malaria. Polymorphisms in the kelch domain-carrying protein K13 are associated with artemisinin resistance, but the underlying molecular mechanisms are unknown. We analyzed the in vivo transcriptomes of...
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Autor*in:	Mok, Sachel [verfasserIn] Ashley, Elizabeth A Ferreira, Pedro E Zhu, Lei Lin, Zhaoting Yeo, Tomas Chotivanich, Kesinee Imwong, Mallika Pukrittayakamee, Sasithon Dhorda, Mehul Nguon, Chea Lim, Pharath Amaratunga, Chanaki Suon, Seila Hien, Tran Tinh Htut, Ye Faiz, M Abul Onyamboko, Marie A Mayxay, Mayfong Newton, Paul N Tripura, Rupam Woodrow, Charles J Miotto, Olivo Kwiatkowski, Dominic P Nosten, François Day, Nicholas P J Preiser, Peter R White, Nicholas J Dondorp, Arjen M Fairhurst, Rick M Bozdech, Zbynek

Format:	Artikel
Sprache:	Englisch

Erschienen:	2015

Rechteinformationen:	Nutzungsrecht: Copyright © 2015, American Association for the Advancement of Science.

Schlagwörter:	Malaria - parasitology Malaria, Falciparum - drug therapy Malaria, Falciparum - parasitology Plasmodium falciparum - drug effects Malaria - drug therapy Antimalarials - pharmacology Chaperonin Containing TCP-1 - metabolism Unfolded Protein Response - genetics Chaperonin Containing TCP-1 - genetics Plasmodium falciparum - genetics Artemisinins - pharmacology Drug Resistance - genetics

Übergeordnetes Werk:	Enthalten in: Science - Washington, DC : AAAS, American Assoc. for the Advancement of Science, 1883, 347(2015), 6220, Seite 431
Übergeordnetes Werk:	volume:347 ; year:2015 ; number:6220 ; pages:431

Links:	Link aufrufen Link aufrufen

Katalog-ID:	OLC1966820771

Internformat


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520			\|a Artemisinin resistance in Plasmodium falciparum threatens global efforts to control and eliminate malaria. Polymorphisms in the kelch domain-carrying protein K13 are associated with artemisinin resistance, but the underlying molecular mechanisms are unknown. We analyzed the in vivo transcriptomes of 1043 P. falciparum isolates from patients with acute malaria and found that artemisinin resistance is associated with increased expression of unfolded protein response (UPR) pathways involving the major PROSC and TRiC chaperone complexes. Artemisinin-resistant parasites also exhibit decelerated progression through the first part of the asexual intraerythrocytic development cycle. These findings suggest that artemisinin-resistant parasites remain in a state of decelerated development at the young ring stage, whereas their up-regulated UPR pathways mitigate protein damage caused by artemisinin. The expression profiles of UPR-related genes also associate with the geographical origin of parasite isolates, further suggesting their role in emerging artemisinin resistance in the Greater Mekong Subregion.
540			\|a Nutzungsrecht: Copyright © 2015, American Association for the Advancement of Science.
650		4	\|a Malaria - parasitology
650		4	\|a Malaria, Falciparum - drug therapy
650		4	\|a Malaria, Falciparum - parasitology
650		4	\|a Plasmodium falciparum - drug effects
650		4	\|a Malaria - drug therapy
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650		4	\|a Chaperonin Containing TCP-1 - metabolism
650		4	\|a Unfolded Protein Response - genetics
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allfields	PQ20160617 (DE-627)OLC1966820771 (DE-599)GBVOLC1966820771 (PRQ)p614-b78eec4e5e987f588376b95778db5f000b9a3f9b94cd21eca584c60c050bebcc0 (KEY)0063888920150000347622000431drugresistancepopulationtranscriptomicsofhumanmala DE-627 ger DE-627 rakwb eng 500 DNB LING fid Mok, Sachel verfasserin aut Drug resistance. Population transcriptomics of human malaria parasites reveals the mechanism of artemisinin resistance 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Artemisinin resistance in Plasmodium falciparum threatens global efforts to control and eliminate malaria. Polymorphisms in the kelch domain-carrying protein K13 are associated with artemisinin resistance, but the underlying molecular mechanisms are unknown. We analyzed the in vivo transcriptomes of 1043 P. falciparum isolates from patients with acute malaria and found that artemisinin resistance is associated with increased expression of unfolded protein response (UPR) pathways involving the major PROSC and TRiC chaperone complexes. Artemisinin-resistant parasites also exhibit decelerated progression through the first part of the asexual intraerythrocytic development cycle. These findings suggest that artemisinin-resistant parasites remain in a state of decelerated development at the young ring stage, whereas their up-regulated UPR pathways mitigate protein damage caused by artemisinin. The expression profiles of UPR-related genes also associate with the geographical origin of parasite isolates, further suggesting their role in emerging artemisinin resistance in the Greater Mekong Subregion. Nutzungsrecht: Copyright © 2015, American Association for the Advancement of Science. Malaria - parasitology Malaria, Falciparum - drug therapy Malaria, Falciparum - parasitology Plasmodium falciparum - drug effects Malaria - drug therapy Antimalarials - pharmacology Chaperonin Containing TCP-1 - metabolism Unfolded Protein Response - genetics Chaperonin Containing TCP-1 - genetics Plasmodium falciparum - genetics Artemisinins - pharmacology Drug Resistance - genetics Ashley, Elizabeth A oth Ferreira, Pedro E oth Zhu, Lei oth Lin, Zhaoting oth Yeo, Tomas oth Chotivanich, Kesinee oth Imwong, Mallika oth Pukrittayakamee, Sasithon oth Dhorda, Mehul oth Nguon, Chea oth Lim, Pharath oth Amaratunga, Chanaki oth Suon, Seila oth Hien, Tran Tinh oth Htut, Ye oth Faiz, M Abul oth Onyamboko, Marie A oth Mayxay, Mayfong oth Newton, Paul N oth Tripura, Rupam oth Woodrow, Charles J oth Miotto, Olivo oth Kwiatkowski, Dominic P oth Nosten, François oth Day, Nicholas P J oth Preiser, Peter R oth White, Nicholas J oth Dondorp, Arjen M oth Fairhurst, Rick M oth Bozdech, Zbynek oth Enthalten in Science Washington, DC : AAAS, American Assoc. for the Advancement of Science, 1883 347(2015), 6220, Seite 431 (DE-627)12931482X (DE-600)128410-1 (DE-576)014533189 0036-8075 nnns volume:347 year:2015 number:6220 pages:431 http://www.ncbi.nlm.nih.gov/pubmed/25502316 http://kipublications.ki.se/Default.aspx?queryparsed=id:130644534 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-SPO SSG-OLC-IBL SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-FOR GBV_ILN_11 GBV_ILN_20 GBV_ILN_21 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_30 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_47 GBV_ILN_55 GBV_ILN_59 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_92 GBV_ILN_101 GBV_ILN_110 GBV_ILN_120 GBV_ILN_131 GBV_ILN_170 GBV_ILN_171 GBV_ILN_179 GBV_ILN_181 GBV_ILN_211 GBV_ILN_252 GBV_ILN_259 GBV_ILN_290 GBV_ILN_600 GBV_ILN_601 GBV_ILN_647 GBV_ILN_754 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2012 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2116 GBV_ILN_2120 GBV_ILN_2121 GBV_ILN_2173 GBV_ILN_2185 GBV_ILN_2219 GBV_ILN_2221 GBV_ILN_2279 GBV_ILN_2286 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4036 GBV_ILN_4046 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4302 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4310 GBV_ILN_4314 GBV_ILN_4317 GBV_ILN_4318 GBV_ILN_4320 GBV_ILN_4324 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4700 AR 347 2015 6220 431
spelling	PQ20160617 (DE-627)OLC1966820771 (DE-599)GBVOLC1966820771 (PRQ)p614-b78eec4e5e987f588376b95778db5f000b9a3f9b94cd21eca584c60c050bebcc0 (KEY)0063888920150000347622000431drugresistancepopulationtranscriptomicsofhumanmala DE-627 ger DE-627 rakwb eng 500 DNB LING fid Mok, Sachel verfasserin aut Drug resistance. Population transcriptomics of human malaria parasites reveals the mechanism of artemisinin resistance 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Artemisinin resistance in Plasmodium falciparum threatens global efforts to control and eliminate malaria. Polymorphisms in the kelch domain-carrying protein K13 are associated with artemisinin resistance, but the underlying molecular mechanisms are unknown. We analyzed the in vivo transcriptomes of 1043 P. falciparum isolates from patients with acute malaria and found that artemisinin resistance is associated with increased expression of unfolded protein response (UPR) pathways involving the major PROSC and TRiC chaperone complexes. Artemisinin-resistant parasites also exhibit decelerated progression through the first part of the asexual intraerythrocytic development cycle. These findings suggest that artemisinin-resistant parasites remain in a state of decelerated development at the young ring stage, whereas their up-regulated UPR pathways mitigate protein damage caused by artemisinin. The expression profiles of UPR-related genes also associate with the geographical origin of parasite isolates, further suggesting their role in emerging artemisinin resistance in the Greater Mekong Subregion. Nutzungsrecht: Copyright © 2015, American Association for the Advancement of Science. Malaria - parasitology Malaria, Falciparum - drug therapy Malaria, Falciparum - parasitology Plasmodium falciparum - drug effects Malaria - drug therapy Antimalarials - pharmacology Chaperonin Containing TCP-1 - metabolism Unfolded Protein Response - genetics Chaperonin Containing TCP-1 - genetics Plasmodium falciparum - genetics Artemisinins - pharmacology Drug Resistance - genetics Ashley, Elizabeth A oth Ferreira, Pedro E oth Zhu, Lei oth Lin, Zhaoting oth Yeo, Tomas oth Chotivanich, Kesinee oth Imwong, Mallika oth Pukrittayakamee, Sasithon oth Dhorda, Mehul oth Nguon, Chea oth Lim, Pharath oth Amaratunga, Chanaki oth Suon, Seila oth Hien, Tran Tinh oth Htut, Ye oth Faiz, M Abul oth Onyamboko, Marie A oth Mayxay, Mayfong oth Newton, Paul N oth Tripura, Rupam oth Woodrow, Charles J oth Miotto, Olivo oth Kwiatkowski, Dominic P oth Nosten, François oth Day, Nicholas P J oth Preiser, Peter R oth White, Nicholas J oth Dondorp, Arjen M oth Fairhurst, Rick M oth Bozdech, Zbynek oth Enthalten in Science Washington, DC : AAAS, American Assoc. for the Advancement of Science, 1883 347(2015), 6220, Seite 431 (DE-627)12931482X (DE-600)128410-1 (DE-576)014533189 0036-8075 nnns volume:347 year:2015 number:6220 pages:431 http://www.ncbi.nlm.nih.gov/pubmed/25502316 http://kipublications.ki.se/Default.aspx?queryparsed=id:130644534 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-SPO SSG-OLC-IBL SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-FOR GBV_ILN_11 GBV_ILN_20 GBV_ILN_21 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_30 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_47 GBV_ILN_55 GBV_ILN_59 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_92 GBV_ILN_101 GBV_ILN_110 GBV_ILN_120 GBV_ILN_131 GBV_ILN_170 GBV_ILN_171 GBV_ILN_179 GBV_ILN_181 GBV_ILN_211 GBV_ILN_252 GBV_ILN_259 GBV_ILN_290 GBV_ILN_600 GBV_ILN_601 GBV_ILN_647 GBV_ILN_754 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2012 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2116 GBV_ILN_2120 GBV_ILN_2121 GBV_ILN_2173 GBV_ILN_2185 GBV_ILN_2219 GBV_ILN_2221 GBV_ILN_2279 GBV_ILN_2286 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4036 GBV_ILN_4046 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4302 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4310 GBV_ILN_4314 GBV_ILN_4317 GBV_ILN_4318 GBV_ILN_4320 GBV_ILN_4324 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4700 AR 347 2015 6220 431
allfields_unstemmed	PQ20160617 (DE-627)OLC1966820771 (DE-599)GBVOLC1966820771 (PRQ)p614-b78eec4e5e987f588376b95778db5f000b9a3f9b94cd21eca584c60c050bebcc0 (KEY)0063888920150000347622000431drugresistancepopulationtranscriptomicsofhumanmala DE-627 ger DE-627 rakwb eng 500 DNB LING fid Mok, Sachel verfasserin aut Drug resistance. Population transcriptomics of human malaria parasites reveals the mechanism of artemisinin resistance 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Artemisinin resistance in Plasmodium falciparum threatens global efforts to control and eliminate malaria. Polymorphisms in the kelch domain-carrying protein K13 are associated with artemisinin resistance, but the underlying molecular mechanisms are unknown. We analyzed the in vivo transcriptomes of 1043 P. falciparum isolates from patients with acute malaria and found that artemisinin resistance is associated with increased expression of unfolded protein response (UPR) pathways involving the major PROSC and TRiC chaperone complexes. Artemisinin-resistant parasites also exhibit decelerated progression through the first part of the asexual intraerythrocytic development cycle. These findings suggest that artemisinin-resistant parasites remain in a state of decelerated development at the young ring stage, whereas their up-regulated UPR pathways mitigate protein damage caused by artemisinin. The expression profiles of UPR-related genes also associate with the geographical origin of parasite isolates, further suggesting their role in emerging artemisinin resistance in the Greater Mekong Subregion. Nutzungsrecht: Copyright © 2015, American Association for the Advancement of Science. Malaria - parasitology Malaria, Falciparum - drug therapy Malaria, Falciparum - parasitology Plasmodium falciparum - drug effects Malaria - drug therapy Antimalarials - pharmacology Chaperonin Containing TCP-1 - metabolism Unfolded Protein Response - genetics Chaperonin Containing TCP-1 - genetics Plasmodium falciparum - genetics Artemisinins - pharmacology Drug Resistance - genetics Ashley, Elizabeth A oth Ferreira, Pedro E oth Zhu, Lei oth Lin, Zhaoting oth Yeo, Tomas oth Chotivanich, Kesinee oth Imwong, Mallika oth Pukrittayakamee, Sasithon oth Dhorda, Mehul oth Nguon, Chea oth Lim, Pharath oth Amaratunga, Chanaki oth Suon, Seila oth Hien, Tran Tinh oth Htut, Ye oth Faiz, M Abul oth Onyamboko, Marie A oth Mayxay, Mayfong oth Newton, Paul N oth Tripura, Rupam oth Woodrow, Charles J oth Miotto, Olivo oth Kwiatkowski, Dominic P oth Nosten, François oth Day, Nicholas P J oth Preiser, Peter R oth White, Nicholas J oth Dondorp, Arjen M oth Fairhurst, Rick M oth Bozdech, Zbynek oth Enthalten in Science Washington, DC : AAAS, American Assoc. for the Advancement of Science, 1883 347(2015), 6220, Seite 431 (DE-627)12931482X (DE-600)128410-1 (DE-576)014533189 0036-8075 nnns volume:347 year:2015 number:6220 pages:431 http://www.ncbi.nlm.nih.gov/pubmed/25502316 http://kipublications.ki.se/Default.aspx?queryparsed=id:130644534 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-SPO SSG-OLC-IBL SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-FOR GBV_ILN_11 GBV_ILN_20 GBV_ILN_21 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_30 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_47 GBV_ILN_55 GBV_ILN_59 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_92 GBV_ILN_101 GBV_ILN_110 GBV_ILN_120 GBV_ILN_131 GBV_ILN_170 GBV_ILN_171 GBV_ILN_179 GBV_ILN_181 GBV_ILN_211 GBV_ILN_252 GBV_ILN_259 GBV_ILN_290 GBV_ILN_600 GBV_ILN_601 GBV_ILN_647 GBV_ILN_754 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2012 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2116 GBV_ILN_2120 GBV_ILN_2121 GBV_ILN_2173 GBV_ILN_2185 GBV_ILN_2219 GBV_ILN_2221 GBV_ILN_2279 GBV_ILN_2286 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4036 GBV_ILN_4046 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4302 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4310 GBV_ILN_4314 GBV_ILN_4317 GBV_ILN_4318 GBV_ILN_4320 GBV_ILN_4324 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4700 AR 347 2015 6220 431
allfieldsGer	PQ20160617 (DE-627)OLC1966820771 (DE-599)GBVOLC1966820771 (PRQ)p614-b78eec4e5e987f588376b95778db5f000b9a3f9b94cd21eca584c60c050bebcc0 (KEY)0063888920150000347622000431drugresistancepopulationtranscriptomicsofhumanmala DE-627 ger DE-627 rakwb eng 500 DNB LING fid Mok, Sachel verfasserin aut Drug resistance. Population transcriptomics of human malaria parasites reveals the mechanism of artemisinin resistance 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Artemisinin resistance in Plasmodium falciparum threatens global efforts to control and eliminate malaria. Polymorphisms in the kelch domain-carrying protein K13 are associated with artemisinin resistance, but the underlying molecular mechanisms are unknown. We analyzed the in vivo transcriptomes of 1043 P. falciparum isolates from patients with acute malaria and found that artemisinin resistance is associated with increased expression of unfolded protein response (UPR) pathways involving the major PROSC and TRiC chaperone complexes. Artemisinin-resistant parasites also exhibit decelerated progression through the first part of the asexual intraerythrocytic development cycle. These findings suggest that artemisinin-resistant parasites remain in a state of decelerated development at the young ring stage, whereas their up-regulated UPR pathways mitigate protein damage caused by artemisinin. The expression profiles of UPR-related genes also associate with the geographical origin of parasite isolates, further suggesting their role in emerging artemisinin resistance in the Greater Mekong Subregion. Nutzungsrecht: Copyright © 2015, American Association for the Advancement of Science. Malaria - parasitology Malaria, Falciparum - drug therapy Malaria, Falciparum - parasitology Plasmodium falciparum - drug effects Malaria - drug therapy Antimalarials - pharmacology Chaperonin Containing TCP-1 - metabolism Unfolded Protein Response - genetics Chaperonin Containing TCP-1 - genetics Plasmodium falciparum - genetics Artemisinins - pharmacology Drug Resistance - genetics Ashley, Elizabeth A oth Ferreira, Pedro E oth Zhu, Lei oth Lin, Zhaoting oth Yeo, Tomas oth Chotivanich, Kesinee oth Imwong, Mallika oth Pukrittayakamee, Sasithon oth Dhorda, Mehul oth Nguon, Chea oth Lim, Pharath oth Amaratunga, Chanaki oth Suon, Seila oth Hien, Tran Tinh oth Htut, Ye oth Faiz, M Abul oth Onyamboko, Marie A oth Mayxay, Mayfong oth Newton, Paul N oth Tripura, Rupam oth Woodrow, Charles J oth Miotto, Olivo oth Kwiatkowski, Dominic P oth Nosten, François oth Day, Nicholas P J oth Preiser, Peter R oth White, Nicholas J oth Dondorp, Arjen M oth Fairhurst, Rick M oth Bozdech, Zbynek oth Enthalten in Science Washington, DC : AAAS, American Assoc. for the Advancement of Science, 1883 347(2015), 6220, Seite 431 (DE-627)12931482X (DE-600)128410-1 (DE-576)014533189 0036-8075 nnns volume:347 year:2015 number:6220 pages:431 http://www.ncbi.nlm.nih.gov/pubmed/25502316 http://kipublications.ki.se/Default.aspx?queryparsed=id:130644534 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-SPO SSG-OLC-IBL SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-FOR GBV_ILN_11 GBV_ILN_20 GBV_ILN_21 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_30 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_47 GBV_ILN_55 GBV_ILN_59 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_92 GBV_ILN_101 GBV_ILN_110 GBV_ILN_120 GBV_ILN_131 GBV_ILN_170 GBV_ILN_171 GBV_ILN_179 GBV_ILN_181 GBV_ILN_211 GBV_ILN_252 GBV_ILN_259 GBV_ILN_290 GBV_ILN_600 GBV_ILN_601 GBV_ILN_647 GBV_ILN_754 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2012 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2116 GBV_ILN_2120 GBV_ILN_2121 GBV_ILN_2173 GBV_ILN_2185 GBV_ILN_2219 GBV_ILN_2221 GBV_ILN_2279 GBV_ILN_2286 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4036 GBV_ILN_4046 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4302 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4310 GBV_ILN_4314 GBV_ILN_4317 GBV_ILN_4318 GBV_ILN_4320 GBV_ILN_4324 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4700 AR 347 2015 6220 431
allfieldsSound	PQ20160617 (DE-627)OLC1966820771 (DE-599)GBVOLC1966820771 (PRQ)p614-b78eec4e5e987f588376b95778db5f000b9a3f9b94cd21eca584c60c050bebcc0 (KEY)0063888920150000347622000431drugresistancepopulationtranscriptomicsofhumanmala DE-627 ger DE-627 rakwb eng 500 DNB LING fid Mok, Sachel verfasserin aut Drug resistance. Population transcriptomics of human malaria parasites reveals the mechanism of artemisinin resistance 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Artemisinin resistance in Plasmodium falciparum threatens global efforts to control and eliminate malaria. Polymorphisms in the kelch domain-carrying protein K13 are associated with artemisinin resistance, but the underlying molecular mechanisms are unknown. We analyzed the in vivo transcriptomes of 1043 P. falciparum isolates from patients with acute malaria and found that artemisinin resistance is associated with increased expression of unfolded protein response (UPR) pathways involving the major PROSC and TRiC chaperone complexes. Artemisinin-resistant parasites also exhibit decelerated progression through the first part of the asexual intraerythrocytic development cycle. These findings suggest that artemisinin-resistant parasites remain in a state of decelerated development at the young ring stage, whereas their up-regulated UPR pathways mitigate protein damage caused by artemisinin. The expression profiles of UPR-related genes also associate with the geographical origin of parasite isolates, further suggesting their role in emerging artemisinin resistance in the Greater Mekong Subregion. Nutzungsrecht: Copyright © 2015, American Association for the Advancement of Science. Malaria - parasitology Malaria, Falciparum - drug therapy Malaria, Falciparum - parasitology Plasmodium falciparum - drug effects Malaria - drug therapy Antimalarials - pharmacology Chaperonin Containing TCP-1 - metabolism Unfolded Protein Response - genetics Chaperonin Containing TCP-1 - genetics Plasmodium falciparum - genetics Artemisinins - pharmacology Drug Resistance - genetics Ashley, Elizabeth A oth Ferreira, Pedro E oth Zhu, Lei oth Lin, Zhaoting oth Yeo, Tomas oth Chotivanich, Kesinee oth Imwong, Mallika oth Pukrittayakamee, Sasithon oth Dhorda, Mehul oth Nguon, Chea oth Lim, Pharath oth Amaratunga, Chanaki oth Suon, Seila oth Hien, Tran Tinh oth Htut, Ye oth Faiz, M Abul oth Onyamboko, Marie A oth Mayxay, Mayfong oth Newton, Paul N oth Tripura, Rupam oth Woodrow, Charles J oth Miotto, Olivo oth Kwiatkowski, Dominic P oth Nosten, François oth Day, Nicholas P J oth Preiser, Peter R oth White, Nicholas J oth Dondorp, Arjen M oth Fairhurst, Rick M oth Bozdech, Zbynek oth Enthalten in Science Washington, DC : AAAS, American Assoc. for the Advancement of Science, 1883 347(2015), 6220, Seite 431 (DE-627)12931482X (DE-600)128410-1 (DE-576)014533189 0036-8075 nnns volume:347 year:2015 number:6220 pages:431 http://www.ncbi.nlm.nih.gov/pubmed/25502316 http://kipublications.ki.se/Default.aspx?queryparsed=id:130644534 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-SPO SSG-OLC-IBL SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-FOR GBV_ILN_11 GBV_ILN_20 GBV_ILN_21 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_30 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_47 GBV_ILN_55 GBV_ILN_59 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_92 GBV_ILN_101 GBV_ILN_110 GBV_ILN_120 GBV_ILN_131 GBV_ILN_170 GBV_ILN_171 GBV_ILN_179 GBV_ILN_181 GBV_ILN_211 GBV_ILN_252 GBV_ILN_259 GBV_ILN_290 GBV_ILN_600 GBV_ILN_601 GBV_ILN_647 GBV_ILN_754 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2012 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2116 GBV_ILN_2120 GBV_ILN_2121 GBV_ILN_2173 GBV_ILN_2185 GBV_ILN_2219 GBV_ILN_2221 GBV_ILN_2279 GBV_ILN_2286 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4036 GBV_ILN_4046 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4302 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4310 GBV_ILN_4314 GBV_ILN_4317 GBV_ILN_4318 GBV_ILN_4320 GBV_ILN_4324 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4700 AR 347 2015 6220 431
language	English
source	Enthalten in Science 347(2015), 6220, Seite 431 volume:347 year:2015 number:6220 pages:431
sourceStr	Enthalten in Science 347(2015), 6220, Seite 431 volume:347 year:2015 number:6220 pages:431
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Malaria - parasitology Malaria, Falciparum - drug therapy Malaria, Falciparum - parasitology Plasmodium falciparum - drug effects Malaria - drug therapy Antimalarials - pharmacology Chaperonin Containing TCP-1 - metabolism Unfolded Protein Response - genetics Chaperonin Containing TCP-1 - genetics Plasmodium falciparum - genetics Artemisinins - pharmacology Drug Resistance - genetics
dewey-raw	500
isfreeaccess_bool	false
container_title	Science
authorswithroles_txt_mv	Mok, Sachel @@aut@@ Ashley, Elizabeth A @@oth@@ Ferreira, Pedro E @@oth@@ Zhu, Lei @@oth@@ Lin, Zhaoting @@oth@@ Yeo, Tomas @@oth@@ Chotivanich, Kesinee @@oth@@ Imwong, Mallika @@oth@@ Pukrittayakamee, Sasithon @@oth@@ Dhorda, Mehul @@oth@@ Nguon, Chea @@oth@@ Lim, Pharath @@oth@@ Amaratunga, Chanaki @@oth@@ Suon, Seila @@oth@@ Hien, Tran Tinh @@oth@@ Htut, Ye @@oth@@ Faiz, M Abul @@oth@@ Onyamboko, Marie A @@oth@@ Mayxay, Mayfong @@oth@@ Newton, Paul N @@oth@@ Tripura, Rupam @@oth@@ Woodrow, Charles J @@oth@@ Miotto, Olivo @@oth@@ Kwiatkowski, Dominic P @@oth@@ Nosten, François @@oth@@ Day, Nicholas P J @@oth@@ Preiser, Peter R @@oth@@ White, Nicholas J @@oth@@ Dondorp, Arjen M @@oth@@ Fairhurst, Rick M @@oth@@ Bozdech, Zbynek @@oth@@
publishDateDaySort_date	2015-01-01T00:00:00Z
hierarchy_top_id	12931482X
dewey-sort	3500
id	OLC1966820771
language_de	englisch
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Polymorphisms in the kelch domain-carrying protein K13 are associated with artemisinin resistance, but the underlying molecular mechanisms are unknown. We analyzed the in vivo transcriptomes of 1043 P. falciparum isolates from patients with acute malaria and found that artemisinin resistance is associated with increased expression of unfolded protein response (UPR) pathways involving the major PROSC and TRiC chaperone complexes. Artemisinin-resistant parasites also exhibit decelerated progression through the first part of the asexual intraerythrocytic development cycle. These findings suggest that artemisinin-resistant parasites remain in a state of decelerated development at the young ring stage, whereas their up-regulated UPR pathways mitigate protein damage caused by artemisinin. 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author	Mok, Sachel
spellingShingle	Mok, Sachel ddc 500 fid LING misc Malaria - parasitology misc Malaria, Falciparum - drug therapy misc Malaria, Falciparum - parasitology misc Plasmodium falciparum - drug effects misc Malaria - drug therapy misc Antimalarials - pharmacology misc Chaperonin Containing TCP-1 - metabolism misc Unfolded Protein Response - genetics misc Chaperonin Containing TCP-1 - genetics misc Plasmodium falciparum - genetics misc Artemisinins - pharmacology misc Drug Resistance - genetics Drug resistance. Population transcriptomics of human malaria parasites reveals the mechanism of artemisinin resistance
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topic_title	500 DNB LING fid Drug resistance. Population transcriptomics of human malaria parasites reveals the mechanism of artemisinin resistance Malaria - parasitology Malaria, Falciparum - drug therapy Malaria, Falciparum - parasitology Plasmodium falciparum - drug effects Malaria - drug therapy Antimalarials - pharmacology Chaperonin Containing TCP-1 - metabolism Unfolded Protein Response - genetics Chaperonin Containing TCP-1 - genetics Plasmodium falciparum - genetics Artemisinins - pharmacology Drug Resistance - genetics
topic	ddc 500 fid LING misc Malaria - parasitology misc Malaria, Falciparum - drug therapy misc Malaria, Falciparum - parasitology misc Plasmodium falciparum - drug effects misc Malaria - drug therapy misc Antimalarials - pharmacology misc Chaperonin Containing TCP-1 - metabolism misc Unfolded Protein Response - genetics misc Chaperonin Containing TCP-1 - genetics misc Plasmodium falciparum - genetics misc Artemisinins - pharmacology misc Drug Resistance - genetics
topic_unstemmed	ddc 500 fid LING misc Malaria - parasitology misc Malaria, Falciparum - drug therapy misc Malaria, Falciparum - parasitology misc Plasmodium falciparum - drug effects misc Malaria - drug therapy misc Antimalarials - pharmacology misc Chaperonin Containing TCP-1 - metabolism misc Unfolded Protein Response - genetics misc Chaperonin Containing TCP-1 - genetics misc Plasmodium falciparum - genetics misc Artemisinins - pharmacology misc Drug Resistance - genetics
topic_browse	ddc 500 fid LING misc Malaria - parasitology misc Malaria, Falciparum - drug therapy misc Malaria, Falciparum - parasitology misc Plasmodium falciparum - drug effects misc Malaria - drug therapy misc Antimalarials - pharmacology misc Chaperonin Containing TCP-1 - metabolism misc Unfolded Protein Response - genetics misc Chaperonin Containing TCP-1 - genetics misc Plasmodium falciparum - genetics misc Artemisinins - pharmacology misc Drug Resistance - genetics
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title	Drug resistance. Population transcriptomics of human malaria parasites reveals the mechanism of artemisinin resistance
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title_full	Drug resistance. Population transcriptomics of human malaria parasites reveals the mechanism of artemisinin resistance
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title_sort	drug resistance. population transcriptomics of human malaria parasites reveals the mechanism of artemisinin resistance
title_auth	Drug resistance. Population transcriptomics of human malaria parasites reveals the mechanism of artemisinin resistance
abstract	Artemisinin resistance in Plasmodium falciparum threatens global efforts to control and eliminate malaria. Polymorphisms in the kelch domain-carrying protein K13 are associated with artemisinin resistance, but the underlying molecular mechanisms are unknown. We analyzed the in vivo transcriptomes of 1043 P. falciparum isolates from patients with acute malaria and found that artemisinin resistance is associated with increased expression of unfolded protein response (UPR) pathways involving the major PROSC and TRiC chaperone complexes. Artemisinin-resistant parasites also exhibit decelerated progression through the first part of the asexual intraerythrocytic development cycle. These findings suggest that artemisinin-resistant parasites remain in a state of decelerated development at the young ring stage, whereas their up-regulated UPR pathways mitigate protein damage caused by artemisinin. The expression profiles of UPR-related genes also associate with the geographical origin of parasite isolates, further suggesting their role in emerging artemisinin resistance in the Greater Mekong Subregion.
abstractGer	Artemisinin resistance in Plasmodium falciparum threatens global efforts to control and eliminate malaria. Polymorphisms in the kelch domain-carrying protein K13 are associated with artemisinin resistance, but the underlying molecular mechanisms are unknown. We analyzed the in vivo transcriptomes of 1043 P. falciparum isolates from patients with acute malaria and found that artemisinin resistance is associated with increased expression of unfolded protein response (UPR) pathways involving the major PROSC and TRiC chaperone complexes. Artemisinin-resistant parasites also exhibit decelerated progression through the first part of the asexual intraerythrocytic development cycle. These findings suggest that artemisinin-resistant parasites remain in a state of decelerated development at the young ring stage, whereas their up-regulated UPR pathways mitigate protein damage caused by artemisinin. The expression profiles of UPR-related genes also associate with the geographical origin of parasite isolates, further suggesting their role in emerging artemisinin resistance in the Greater Mekong Subregion.
abstract_unstemmed	Artemisinin resistance in Plasmodium falciparum threatens global efforts to control and eliminate malaria. Polymorphisms in the kelch domain-carrying protein K13 are associated with artemisinin resistance, but the underlying molecular mechanisms are unknown. We analyzed the in vivo transcriptomes of 1043 P. falciparum isolates from patients with acute malaria and found that artemisinin resistance is associated with increased expression of unfolded protein response (UPR) pathways involving the major PROSC and TRiC chaperone complexes. Artemisinin-resistant parasites also exhibit decelerated progression through the first part of the asexual intraerythrocytic development cycle. These findings suggest that artemisinin-resistant parasites remain in a state of decelerated development at the young ring stage, whereas their up-regulated UPR pathways mitigate protein damage caused by artemisinin. The expression profiles of UPR-related genes also associate with the geographical origin of parasite isolates, further suggesting their role in emerging artemisinin resistance in the Greater Mekong Subregion.
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container_issue	6220
title_short	Drug resistance. Population transcriptomics of human malaria parasites reveals the mechanism of artemisinin resistance
url	http://www.ncbi.nlm.nih.gov/pubmed/25502316 http://kipublications.ki.se/Default.aspx?queryparsed=id:130644534
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author2	Ashley, Elizabeth A Ferreira, Pedro E Zhu, Lei Lin, Zhaoting Yeo, Tomas Chotivanich, Kesinee Imwong, Mallika Pukrittayakamee, Sasithon Dhorda, Mehul Nguon, Chea Lim, Pharath Amaratunga, Chanaki Suon, Seila Hien, Tran Tinh Htut, Ye Faiz, M Abul Onyamboko, Marie A Mayxay, Mayfong Newton, Paul N Tripura, Rupam Woodrow, Charles J Miotto, Olivo Kwiatkowski, Dominic P Nosten, François Day, Nicholas P J Preiser, Peter R White, Nicholas J Dondorp, Arjen M Fairhurst, Rick M Bozdech, Zbynek
author2Str	Ashley, Elizabeth A Ferreira, Pedro E Zhu, Lei Lin, Zhaoting Yeo, Tomas Chotivanich, Kesinee Imwong, Mallika Pukrittayakamee, Sasithon Dhorda, Mehul Nguon, Chea Lim, Pharath Amaratunga, Chanaki Suon, Seila Hien, Tran Tinh Htut, Ye Faiz, M Abul Onyamboko, Marie A Mayxay, Mayfong Newton, Paul N Tripura, Rupam Woodrow, Charles J Miotto, Olivo Kwiatkowski, Dominic P Nosten, François Day, Nicholas P J Preiser, Peter R White, Nicholas J Dondorp, Arjen M Fairhurst, Rick M Bozdech, Zbynek
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author2_role	oth oth oth oth oth oth oth oth oth oth oth oth oth oth oth oth oth oth oth oth oth oth oth oth oth oth oth oth oth oth
up_date	2024-07-03T23:01:01.017Z
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