Proteomics

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ER stress response in hepatocytes upon Plasmodium infection


ABSTRACT: Upon infection of a mammalian host, Plasmodium parasites first replicate inside hepato-cytes, generating thousands of new parasites. Although Plasmodium intra-hepatic devel-opment represents a substantial metabolic challenge to the host hepatocyte, how infected cells respond to and integrate this stress remains poorly understood. Here, we present proteomic and transcriptomic analysis revealing that the endoplasmic reticulum (ER)-resident unfolded protein response (UPR) is activated in host hepatocytes upon Plasmo-dium berghei infection. The expression of XBP1s -the active form of the UPR mediator XBP1- and the liver-specific UPR mediator CREBH is induced by P. berghei infection in vivo. Furthermore, this UPR induction increases parasite liver burden. Altogether, our data suggests that ER stress is a central feature of P. berghei intra-hepatic development, contributing to the success of infection.

INSTRUMENT(S): LTQ Orbitrap

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Nagarjuna Nagaraj  

LAB HEAD: Maria Manuel Dias Mota

PROVIDER: PXD002269 | Pride | 2016-04-20

REPOSITORIES: Pride

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Publications

Parasite-induced ER stress response in hepatocytes facilitates Plasmodium liver stage infection.

Inácio Patricia P   Zuzarte-Luís Vanessa V   Ruivo Margarida T G MT   Falkard Brie B   Nagaraj Nagarjuna N   Rooijers Koos K   Mann Matthias M   Mair Gunnar G   Fidock David A DA   Mota Maria M MM  

EMBO reports 20150625 8


Upon infection of a mammalian host, Plasmodium parasites first replicate inside hepatocytes, generating thousands of new parasites. Although Plasmodium intra-hepatic development represents a substantial metabolic challenge to the host hepatocyte, how infected cells respond to and integrate this stress remains poorly understood. Here, we present proteomic and transcriptomic analyses, revealing that the endoplasmic reticulum (ER)-resident unfolded protein response (UPR) is activated in host hepato  ...[more]

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