Advances in research on the vacuolar membrane function and the associated proteins of plasmodium parasitophorous vacuole

doi:10.12140/j.issn.1000-7423.2022.03.019

Abstract

Abstract:

Malaria is one of the most important infectious diseases in the world and seriously threatens human health. It remains a critical problem to interrupt malaria transmission. Plasmodium parasites invade and multiply inside the host cells causing severe pathological damage to the host. As the interface between the host cells and Plasmodium parasites, PVM is of crucial importance for the survival of Plasmodium parasites. This manuscript briefly introduces the formation of PVM and its relationship with PPM and TVN. The PVM-associated proteins and their functions in blood-stage, liver-stage and sexual-stage parasites are summarized. This review also presents perspectives on malaria control strategies.

Key words: Plasmodium, PVM, Membrane protein, Malaria

CLC Number:

R382.31

GE Jie-yun, LIU Lei, SUN Yi-fan, CHENG Yang. Advances in research on the vacuolar membrane function and the associated proteins of plasmodium parasitophorous vacuole[J]. CHINESE JOURNAL OF PARASITOLOGY AND PARASITIC DISEASES, 2022, 40(3): 402-410.

Figures/Tables 3

蛋白	PlasmoDB_ID	功能	参考文献
PfETRAMP5	PF3D7_0532100	与载脂蛋白相互作用,维持脂质稳态;可能与营养渗透与蛋白输出有关。	[24-25]
PfETRAMP10.2	PF3D7_1033200	参与恶性疟原虫的蛋白输出。	[26]
PfHSP101	PF3D7_1116800	对输出蛋白起解折叠酶和解聚酶的作用。	[35-36]
PfEXP1	PF3D7_1121600	是EXP2发挥营养渗透通道功能所必须的,可能在维持PVM结构方面发挥重要功能;作为谷胱甘肽转移酶发挥作用,解毒血红蛋白副产物。	[48,52]
PfEXP2	PF3D7_1471100	作为PVM营养渗透通道;作为PTEX的转运通道。	[38,46]
PfPTEX150	PF3D7_1436300	与EXP2共同形成PTEX的转运通道。	[38]
PfPTEX88	PF3D7_1105600	可能作为一种受体将输出蛋白移交给HSP101。	[39]
PfTRX2	PF3D7_1345100	通过保守的CXXC活性位点减少底物蛋白质中的二硫键,从而促进输出蛋白的转运。	[42]
PfRON3	PF3D7_1252100	与葡萄糖的摄入与PTEX的转运蛋白功能有关。	[44]
PfPV1	PF3D7_1129100	作为PTEX辅助分子,在蛋白输出中起重要作用。	[45]
PfCG2	PF3D7_0709300	可能与血红蛋白摄入与消化过程有关。	[53]
PfCLAG3.1	PF3D7_0302500	与疟原虫表面阴离子通道（PSAC）活性相关联。	[61]
PfCLAG3.2	PF3D7_0302200	与疟原虫表面阴离子通道（PSAC）活性相关联。	[61]
PfRhopH2	PF3D7_0929400	可能对NPP活性以及与血浆交换营养和代谢产物以促进疟原虫的生长和增殖很重要。	[59]
PF3D7_0402000	PF3D7_0402000	可能在调节PVM与红细胞膜结构中起作用。	[62]
Pfs16	PF3D7_0531200	对性期疟原虫的发育是重要的,敲除后配子体数目显著较少。	[75]
PfPEG3/MDV1	PF3D7_1216500	对配子体感染红细胞正常膜结构的形成起关键作用,敲除导致雄性配子体细胞显著减少。	[78]
PvETRAMP4	PVX_090230	高免疫原性蛋白。	[22]
PvETRAMP11.2	PVP01_0422600	高免疫原性蛋白。	[22]
PvUIS4	PVX_001715	可用于区别肝细胞内休眠子与活跃发育的裂殖子。	[72]
PbSEP1	PBANKA_0524800	维持伯氏疟原虫红内期发育。	[28]
PbSEP2	PBANKA_0524200	维持伯氏疟原虫红内期发育。	[28]
PbSEP3	PBANKA_0501100	维持伯氏疟原虫红内期发育。	[28]
PbEXP1	PBANKA_0926700	将肝细胞ApoH募集到PVM,并介导ApoH和ApoH相关蛋白及脂质的摄取。	[11]
PbUIS3	PBANKA_1400800	与肝脏脂肪酸结合蛋白L-FABP相互作用,对肝内期疟原虫的生长必不可少;竞争结合宿主细胞LC3,充当自噬抑制剂。	[66-67]
PbUIS4	PBANKA_0501200	与肝细胞中疟原虫蛋白质的输出有关。	[6]
PbPL	PBANKA_1128100	与裂殖子从肝细胞中的释放有关。	[69]
PbIBIS1	PBANKA_1365500	与肝细胞中疟原虫蛋白质的输出有关。	[6]
PBANKA_1003900	PBANKA_1003900	影响按蚊中肠内动合子的生存能力或卵囊的早期发育。	[76]
Pbpeg3/mdv1	PBANKA_1432200	敲除导致疟原虫形成受精卵的能力大大下降。	[80]

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