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Presentation of cytoplasmic antigens to class I-restricted cytotoxic T cells implied the existence of a specialized peptide transporter. For most class I heavy chains, association with peptides of the appropriate length is required for stable assembly with beta 2-microglobulin. Mutant cells RMA-S and .174/T2 neither assemble stable class I molecules nor present intracellular antigens, and we have suggested that they have lost a function required for the transport of short peptides from the cytosol to the endoplasmic reticulum. The genetic defect in .174 has been localized to a large deletion in the class II region of the major histocompatibility complex, within which two genes (RING4 and RING11) have been identified that code for 'ABC' (ATP-binding cassette) transporters. We report here that the protein products of these two genes assemble to form a complex. Defects in either protein result in the formation of unstable class I molecules and loss of presentation of intracellular antigens. The molecular defect in a new mutant, BM36.1, is shown to be in the ATP-binding domain of the RING11/PSF2 protein. This is in contrast to the mutant .134, which lacks the RING4/PSF1 protein.

Original publication

DOI

10.1038/355641a0

Type

Journal article

Journal

Nature

Publication Date

13/02/1992

Volume

355

Pages

641 - 644

Keywords

ATP-Binding Cassette Sub-Family B Member 2, ATP-Binding Cassette Transporters, Amino Acid Sequence, Base Sequence, Blotting, Southern, Carrier Proteins, Electrophoresis, Polyacrylamide Gel, Gene Expression, Genotype, Histocompatibility Antigens Class I, Humans, Major Histocompatibility Complex, Membrane Proteins, Molecular Sequence Data, Mutation, Precipitin Tests, Protein Biosynthesis, Transformation, Genetic