Scholarlink

<p>The viral infection and subsequent accumulation of viral proteins in the infected cells leads to endoplasmic reticulum (ER) stress. Japanese encephalitis virus (JEV) infection in the Central Nervous System (CNS) has been shown to induce unfolded protein response (UPR). The ER stress is resolved by the UPR which comprises certain signals that are transduced from the ER either to both the cytoplasm or nucleus, resulting in the adaptation for survival or may even lead to apoptosis. Here, we demonstrate that Poly ADP-ribose polymerase-16 (PARP-16) expression is regulating the ER stress response following JEV infection of Neural Stem/Progenitor cells (NSPCs) in the BALB/c mouse model. Activation of the key sensors of UPR, namely, protein kinase R (PKR)-like ER kinase (PERK) and Inositol-requiring enzyme-1α (IRE-1α) by PARP-16 upon JEV infection, led to the activation of their downstream signalling cascade. The siRNA-mediated in vitro downregulation of PARP-16 in NSPCs alleviated the overall UPR, as the abundance of UPR markers and their downstream modulators of signalling cascade was found to be downregulated. These results highlight an important role of PARP-16 during JEV infection of NSPCs.</p> Graphical Abstract <p>Schematic diagram illustrating the molecular signalling pathway for JEV-induced increased PARP-16 expression and initiation of UPR in NSPCs.</p> <p></p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

PARP-16 regulates the PERK and IRE-1α Mediated Unfolded Protein Response in Japanese Encephalitis Virus–Infected Neural Stem/Progenitor Cells

  • 期刊论文

  • 发表日期：

    2025年2月20日

查看全文
  • Shivangi Sharma,
  • Anirudh Satheesan,
  • Atreye Majumdar,
  • Sriparna Mukherjee,
  • Anirban Basu

摘要

The viral infection and subsequent accumulation of viral proteins in the infected cells leads to endoplasmic reticulum (ER) stress. Japanese encephalitis virus (JEV) infection in the Central Nervous System (CNS) has been shown to induce unfolded protein response (UPR). The ER stress is resolved by the UPR which comprises certain signals that are transduced from the ER either to both the cytoplasm or nucleus, resulting in the adaptation for survival or may even lead to apoptosis. Here, we demonstrate that Poly ADP-ribose polymerase-16 (PARP-16) expression is regulating the ER stress response following JEV infection of Neural Stem/Progenitor cells (NSPCs) in the BALB/c mouse model. Activation of the key sensors of UPR, namely, protein kinase R (PKR)-like ER kinase (PERK) and Inositol-requiring enzyme-1α (IRE-1α) by PARP-16 upon JEV infection, led to the activation of their downstream signalling cascade. The siRNA-mediated in vitro downregulation of PARP-16 in NSPCs alleviated the overall UPR, as the abundance of UPR markers and their downstream modulators of signalling cascade was found to be downregulated. These results highlight an important role of PARP-16 during JEV infection of NSPCs.

Graphical Abstract

Schematic diagram illustrating the molecular signalling pathway for JEV-induced increased PARP-16 expression and initiation of UPR in NSPCs.