REVISION JVI 00281 - 11 1 Autophagosome formation during varicella - zoster virus infection following endoplasmic 2 reticulum stress and the unfolded protein

نویسندگان

  • John E. Carpenter
  • Luca Benetti
  • Charles Grose
چکیده

1 Autophagosome formation during varicella-zoster virus infection following endoplasmic 2 reticulum stress and the unfolded protein response. 3 John E. Carpenter 1 , Wallen Jackson 1 , Luca Benetti 2 and Charles Grose 1 4 1. Children’s Hospital, University of Iowa, Iowa City, IA 5 2. Vaccine Manufacturing Sciences and Commercialization, Merck Manufacturing Division, 6 Merck, Sharp & Dohme Corp., West Point, PA 7 8 Short Title: VZV induces ER stress and UPR 9 10 Correspondent: Dr Charles Grose 11 University of Iowa Hospital/2501 JCP 12 200 Hawkins Drive 13 Iowa City IA 52242 14 Tel: 319-356-2270; Fax: 319-356-4855 15 Email: [email protected] 16 Copyright © 2011, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved. J. Virol. doi:10.1128/JVI.00281-11 JVI Accepts, published online ahead of print on 13 July 2011

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Varicella-Zoster Virus Infectious Cycle: ER Stress, Autophagic Flux, and Amphisome-Mediated Trafficking

Varicella-zoster virus (VZV) induces abundant autophagy. Of the nine human herpesviruses, the VZV genome is the smallest (~124 kbp), lacking any known inhibitors of autophagy, such as the herpes simplex virus ICP34.5 neurovirulence gene. Therefore, this review assesses the evidence for VZV-induced cellular stress, endoplasmic-reticulum-associated degradation (ERAD), and autophagic flux during t...

متن کامل

Varicella-zoster virus glycoprotein expression differentially induces the unfolded protein response in infected cells

Varicella-zoster virus (VZV) is a human herpesvirus that spreads to children as varicella or chicken pox. The virus then establishes latency in the nervous system and re-emerges, typically decades later, as zoster or shingles. We have reported previously that VZV induces autophagy in infected cells as well as exhibiting evidence of the Unfolded Protein Response (UPR): XBP1 splicing, a greatly e...

متن کامل

Insulin-degrading enzyme binds to the nonglycosylated precursor of varicella-zoster virus gE protein found in the endoplasmic reticulum.

Insulin degradation enzyme (IDE) is a 110-kDa zinc metalloprotease found in the cytosol of all cells. IDE degrades insulin and a variety of small proteins including amyloid-beta. Recently, IDE has been proposed as the receptor for varicella-zoster virus (VZV) attachment. During our reassessment, some of the original studies were repeated and expanded in scope. We first confirmed that IDE antibo...

متن کامل

Venezuelan Equine Encephalitis Virus Induces Apoptosis through the Unfolded Protein Response Activation of EGR1.

UNLABELLED Venezuelan equine encephalitis virus (VEEV) is a previously weaponized arthropod-borne virus responsible for causing acute and fatal encephalitis in animal and human hosts. The increased circulation and spread in the Americas of VEEV and other encephalitic arboviruses, such as eastern equine encephalitis virus and West Nile virus, underscore the need for research aimed at characteriz...

متن کامل

Rotavirus infection induces the unfolded protein response of the cell and controls it through the nonstructural protein NSP3.

The unfolded protein response (UPR) is a cellular mechanism that is triggered in order to cope with the stress caused by the accumulation of misfolded proteins in the endoplasmic reticulum (ER). This response is initiated by the endoribonuclease inositol-requiring enzyme 1 (IRE1), activating transcription factor 6 (ATF6), and PKR-like ER kinase, which increase the expression of the genes involv...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2011