The cytosolic tail of class I MHC heavy chain is required for its dislocation by the human cytomegalovirus US2 and US11 gene products
about
A membrane protein required for dislocation of misfolded proteins from the ERA membrane protein complex mediates retro-translocation from the ER lumen into the cytosolDirect binding of human immunodeficiency virus type 1 Nef to the major histocompatibility complex class I (MHC-I) cytoplasmic tail disrupts MHC-I traffickingUbiquitination of serine, threonine, or lysine residues on the cytoplasmic tail can induce ERAD of MHC-I by viral E3 ligase mK3Presenilin/gamma-secretase and alpha-secretase-like peptidases cleave human MHC Class I proteinsUbiquitination is essential for human cytomegalovirus US11-mediated dislocation of MHC class I molecules from the endoplasmic reticulum to the cytosolFree major histocompatibility complex class I heavy chain is preferentially targeted for degradation by human T-cell leukemia/lymphotropic virus type 1 p12(I) proteinRequirements for the selective degradation of endoplasmic reticulum-resident major histocompatibility complex class I proteins by the viral immune evasion molecule mK3.Identification of a membrane targeting and degradation signal in the p42 protein of influenza C virus.Human cytomegalovirus US2 endoplasmic reticulum-lumenal domain dictates association with major histocompatibility complex class I in a locus-specific manner.Down-regulation of MHC class I antigen presentation by HCMV; lessons for tumor immunology.Polyubiquitination is required for US11-dependent movement of MHC class I heavy chain from endoplasmic reticulum into cytosolSite-directed mutagenesis study of yeast peptide:N-glycanase. Insight into the reaction mechanism of deglycosylation.The MHC class I antigen presentation pathway: strategies for viral immune evasion.The human cytomegalovirus US8 glycoprotein binds to major histocompatibility complex class I products.Kaposi's sarcoma-associated herpesvirus K3 utilizes the ubiquitin-proteasome system in routing class major histocompatibility complexes to late endocytic compartments.Human cytomegalovirus US3 chimeras containing US2 cytosolic residues acquire major histocompatibility class I and II protein degradation properties.Lessons from viral manipulation of protein disposal pathwaysThe C-terminal amino acid of the MHC-I heavy chain is critical for binding to Derlin-1 in human cytomegalovirus US11-induced MHC-I degradation.Binding of human cytomegalovirus US2 to major histocompatibility complex class I and II proteins is not sufficient for their degradation.HCMV infection: modulating the cell cycle and cell death.Dislocation of a type I membrane protein requires interactions between membrane-spanning segments within the lipid bilayerRegulation of ubiquitin-proteasome system mediated degradation by cytosolic stress.Viral modulation of antigen presentation: manipulation of cellular targets in the ER and beyond.The VCP/p97 and YOD1 Proteins Have Different Substrate-dependent Activities in Endoplasmic Reticulum-associated Degradation (ERAD)The pathway of US11-dependent degradation of MHC class I heavy chains involves a ubiquitin-conjugated intermediateDislocation and degradation from the ER are regulated by cytosolic stress.Endoplasmic reticulum chaperones participate in human cytomegalovirus US2-mediated degradation of class I major histocompatibility complex molecules.MHC class I molecules are preferentially ubiquitinated on endoplasmic reticulum luminal residues during HRD1 ubiquitin E3 ligase-mediated dislocation.Diverse immune evasion strategies by human cytomegalovirus.ERAD and how viruses exploit it.Classical and non-classical MHC I molecule manipulation by human cytomegalovirus: so many targets—but how many arrows in the quiver?Rad23 provides a link between the Png1 deglycosylating enzyme and the 26 S proteasome in yeast.Human NK Cell Subsets in Pregnancy and Disease: Toward a New Biological Complexity.Signal peptide cleavage of a type I membrane protein, HCMV US11, is dependent on its membrane anchor.The viral E3 ubiquitin ligase mK3 uses the Derlin/p97 endoplasmic reticulum-associated degradation pathway to mediate down-regulation of major histocompatibility complex class I proteins.Human cytomegalovirus protein US11 provokes an unfolded protein response that may facilitate the degradation of class I major histocompatibility complex productsMembrane-specific, host-derived factors are required for US2- and US11-mediated degradation of major histocompatibility complex class I molecules.Pivotal role of calnexin and mannose trimming in regulating the endoplasmic reticulum-associated degradation of major histocompatibility complex class I heavy chain.The glycoprotein gp48 of murine cytomegalovirusL proteasome-dependent cytosolic dislocation and degradation.
P2860
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P2860
The cytosolic tail of class I MHC heavy chain is required for its dislocation by the human cytomegalovirus US2 and US11 gene products
description
1999 nî lūn-bûn
@nan
1999 թուականի Յուլիսին հրատարակուած գիտական յօդուած
@hyw
1999 թվականի հուլիսին հրատարակված գիտական հոդված
@hy
1999年の論文
@ja
1999年論文
@yue
1999年論文
@zh-hant
1999年論文
@zh-hk
1999年論文
@zh-mo
1999年論文
@zh-tw
1999年论文
@wuu
name
The cytosolic tail of class I ...... rus US2 and US11 gene products
@ast
The cytosolic tail of class I ...... rus US2 and US11 gene products
@en
type
label
The cytosolic tail of class I ...... rus US2 and US11 gene products
@ast
The cytosolic tail of class I ...... rus US2 and US11 gene products
@en
prefLabel
The cytosolic tail of class I ...... rus US2 and US11 gene products
@ast
The cytosolic tail of class I ...... rus US2 and US11 gene products
@en
P2093
P2860
P356
P1476
The cytosolic tail of class I ...... rus US2 and US11 gene products
@en
P2093
P2860
P304
P356
10.1073/PNAS.96.15.8516
P407
P577
1999-07-01T00:00:00Z