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The major histocompatibility complex class II-linked cim locus controls the kinetics of intracellular transport of a classical class I molecule

The dominant trans-acting major histocompatibility complex (MHC)-linked class I modifier (cim) locus, previously recognized through its ability to determine altered alloantigenicity of a rat class I molecule, RT1.A3, is shown here to influence class I intracellular transport. The MHC recombinant lab...

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Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1991
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2190796/
https://www.ncbi.nlm.nih.gov/pubmed/2007857
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collection PubMed
description The dominant trans-acting major histocompatibility complex (MHC)-linked class I modifier (cim) locus, previously recognized through its ability to determine altered alloantigenicity of a rat class I molecule, RT1.A3, is shown here to influence class I intracellular transport. The MHC recombinant laboratory rat strains PVG.R1 and PVG.R8 display unusually long retention of RT1.Aa within the endoplasmic reticulum or cis-Golgi. In appropriate F1 hybrid cells heterozygous for RT1.Aa and another class I MHC allele, RT1.Ac, only the RT1.Aa protein is subject to slow transport. The cim gene product therefore shows class I allele specificity in its action, cim appears to be a polymorphic locus whose product is directly involved in the processes of class I MHC assembly and/or intracellular transport.
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spelling pubmed-21907962008-04-17 The major histocompatibility complex class II-linked cim locus controls the kinetics of intracellular transport of a classical class I molecule J Exp Med Articles The dominant trans-acting major histocompatibility complex (MHC)-linked class I modifier (cim) locus, previously recognized through its ability to determine altered alloantigenicity of a rat class I molecule, RT1.A3, is shown here to influence class I intracellular transport. The MHC recombinant laboratory rat strains PVG.R1 and PVG.R8 display unusually long retention of RT1.Aa within the endoplasmic reticulum or cis-Golgi. In appropriate F1 hybrid cells heterozygous for RT1.Aa and another class I MHC allele, RT1.Ac, only the RT1.Aa protein is subject to slow transport. The cim gene product therefore shows class I allele specificity in its action, cim appears to be a polymorphic locus whose product is directly involved in the processes of class I MHC assembly and/or intracellular transport. The Rockefeller University Press 1991-04-01 /pmc/articles/PMC2190796/ /pubmed/2007857 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Articles
The major histocompatibility complex class II-linked cim locus controls the kinetics of intracellular transport of a classical class I molecule
title The major histocompatibility complex class II-linked cim locus controls the kinetics of intracellular transport of a classical class I molecule
title_full The major histocompatibility complex class II-linked cim locus controls the kinetics of intracellular transport of a classical class I molecule
title_fullStr The major histocompatibility complex class II-linked cim locus controls the kinetics of intracellular transport of a classical class I molecule
title_full_unstemmed The major histocompatibility complex class II-linked cim locus controls the kinetics of intracellular transport of a classical class I molecule
title_short The major histocompatibility complex class II-linked cim locus controls the kinetics of intracellular transport of a classical class I molecule
title_sort major histocompatibility complex class ii-linked cim locus controls the kinetics of intracellular transport of a classical class i molecule
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2190796/
https://www.ncbi.nlm.nih.gov/pubmed/2007857