The Plasmodium falciparum parasitophorous vacuole protein P113 interacts with the parasite protein export machinery and maintains normal vacuole architecture.
The Plasmodium falciparum parasitophorous vacuole protein P113 interacts with the parasite protein export machinery and maintains normal vacuole architecture.
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DOI：
10.1111/mmi.14904
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发表时间：
2022-05
影响因子：
3.6
通讯作者：
Crabb, Brendan S.
中科院分区：
文献类型：
--
作者：
Bullen, Hayley E.;Sanders, Paul R.;Dans, Madeline G.;Jonsdottir, Thorey K.;Riglar, David T.;Looker, Oliver;Palmer, Catherine S.;Kouskousis, Betty;Charnaud, Sarah C.;Triglia, Tony;Gabriela, Mikha;Schneider, Molly Parkyn;Chan, Jo-Anne;de Koning-Ward, Tania F.;Baum, Jake;Kazura, James W.;Beeson, James G.;Cowman, Alan F.;Gilson, Paul R.;Crabb, Brendan S.
感染恶性疟原虫每年导致约62.7万人死于疟疾。寄生虫成功的关键是它们能够侵入并随后在人红细胞内生长。因此，参与寄生虫入侵和增殖的寄生虫蛋白本质上是非常有趣的，因为靶向这些蛋白质可以提供新的治疗干预手段。其中一种蛋白质是P113，据报道，它既是一种入侵蛋白，也是一种位于寄生液泡（PV）内的细胞内蛋白。PV由一层膜（PVM）分隔，大量寄生虫特异性蛋白通过输出蛋白的疟原虫转位子（PTEX）进入红细胞，以实现各种免疫逃避功能。为了更好地了解P113的作用，我们从体外培养的恶性疟原虫中分离出它的结合伙伴。我们检测了与蛋白质输出机制（PTEX和输出蛋白相互作用复合物）的相互作用，以及多种通过PV转运或驻留在寄生虫质膜上的蛋白质。基因敲低或部分缺失P113不会显著减少寄生虫的生长或蛋白质输出，但会破坏PVM的形态，这表明P113可能在维持正常的PVM结构中发挥作用。P113是恶性疟原虫的寄生液泡驻留蛋白。它与寄生物液泡空间中的蛋白质相互作用，以帮助维持正常的液泡结构。
Infection with Plasmodium falciparum parasites results in approximately 627,000 deaths from malaria annually. Key to the parasite’s success is their ability to invade and subsequently grow within human erythrocytes. Parasite proteins involved in parasite invasion and proliferation are therefore intrinsically of great interest, as targeting these proteins could provide novel means of therapeutic intervention. One such protein is P113 which has been reported to be both an invasion protein and an intracellular protein located within the parasitophorous vacuole (PV). The PV is delimited by a membrane (PVM) across which a plethora of parasite‐specific proteins are exported via the Plasmodium Translocon of Exported proteins (PTEX) into the erythrocyte to enact various immune evasion functions. To better understand the role of P113 we isolated its binding partners from in vitro cultures of P. falciparum. We detected interactions with the protein export machinery (PTEX and exported protein‐interacting complex) and a variety of proteins that either transit through the PV or reside on the parasite plasma membrane. Genetic knockdown or partial deletion of P113 did not significantly reduce parasite growth or protein export but did disrupt the morphology of the PVM, suggesting that P113 may play a role in maintaining normal PVM architecture. P113 is a parasitophorous vacuole‐resident protein in Plasmodium falciparum. It interacts with proteins in the parasitophorous vacuole space to assist in maintaining normal vacuole architecture.
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影响因子：
64.8
作者：
Ho CM;Beck JR;Lai M;Cui Y;Goldberg DE;Egea PF;Zhou ZH
通讯作者：
Zhou ZH
影响因子：
16.6
作者：
Batinovic S;McHugh E;Chisholm SA;Matthews K;Liu B;Dumont L;Charnaud SC;Schneider MP;Gilson PR;de Koning-Ward TF;Dixon MWA;Tilley L
通讯作者：
Tilley L
影响因子：
64.8
作者：
de Koning-Ward, Tania F.;Gilson, Paul R.;Boddey, Justin A.;Rug, Melanie;Smith, Brian J.;Papenfuss, Anthony T.;Sanders, Paul R.;Lundie, Rachel J.;Maier, Alexander G.;Cowman, Alan F.;Crabb, Brendan S.
通讯作者：
Crabb, Brendan S.
影响因子：
15.9
作者：
Chan, Jo-Anne;Howell, Katherine B.;Beeson, James G.
通讯作者：
Beeson, James G.
影响因子：
64.8
作者：
Beck, Josh R.;Muralidharan, Vasant;Oksman, Anna;Goldberg, Daniel E.
通讯作者：
Goldberg, Daniel E.