Sequence of the pig major histocompatibility region containing the classical class I genes

2001 ◽  
Vol 53 (6) ◽  
pp. 490-500 ◽  
Author(s):  
Christine Renard ◽  
Marcel Vaiman ◽  
Nuchanard Chiannilkulchai ◽  
Laurence Cattolico ◽  
Catherine Robert ◽  
...  
1991 ◽  
Vol 173 (4) ◽  
pp. 913-921 ◽  
Author(s):  
S J Powis ◽  
J C Howard ◽  
G W Butcher

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.


2001 ◽  
Vol 75 (21) ◽  
pp. 10557-10562 ◽  
Author(s):  
Sayeh Vahdati Ben-Arieh ◽  
Baruch Zimerman ◽  
Nechama I. Smorodinsky ◽  
Margalit Yaacubovicz ◽  
Chana Schechter ◽  
...  

ABSTRACT HFE is a nonclassical class I major histocompatibility complex (MHC) molecule that is mutated in the autosomal recessive iron overload disease hereditary hemochromatosis. There is evidence linking HFE with reduced iron uptake by the transferrin receptor (TfR). Using a panel of HFE and TfR monoclonal antibodies to examine human HFE (hHFE)-expressing cell lines, we demonstrate the expression of stable and fully glycosylated TfR-free and TfR-associated hHFE/β2m complexes. We show that both the stability and assembly of hHFE complexes can be modified by the human cytomegalovirus (HCMV) viral protein US2, known to interfere with the expression of classical class I MHC molecules. HCMV US2, but not US11, targets HFE molecules for degradation by the proteasome. Whether this interference with the regulation of iron metabolism by a viral protein is a means of potentiating viral replication remains to be determined. The reduced expression of classical class I MHC and HFE complexes provides the virus with an efficient tool for altering cellular metabolism and escaping certain immune responses.


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