HLA class I nucleotide sequences, 1991.
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Alleles↗
Biomedical subjects
J Zemmour
Publications and source records attributed to J Zemmour.
HLA class I nucleotide sequences, 1991.
The HLA Class I sequences included in this compilation are taken from publications listed in the papers: Nomenclature for factors of the HLA system, 1990 (1) and Nomenclature for factors of the HLA system, 1989 (2). Where discrepancies have arisen between reported sequences, the original authors have been contacted where possible, and necessary amendments to published sequences have been incorporated into this alignment. Future sequencing may identify errors in this list and we would welcome any evidence that helps to maintain the accuracy of this compilation. In the sequence alignments, identity between residues is indicated by a hyphen (-). An unavailable sequence is indicated by a period (.). Gaps in the sequence are inserted to maintain the alignment between different alleles showing variation in amino acid number.
Alleles↗
HLA class I nucleotide sequences, 1991.
The HLA class I sequences included in this compilation are taken from publications listed in the accompanying paper, Nomenclature for factors of the HLA system, 1990 (Bodmer et al., 1991), and also in Nomenclature for factors of the HLA system, 1989 (Bodmer et al., 1990). Where discrepancies have arisen between reported sequences the original authors have been contacted where possible, and necessary amendments to published sequences have been incorporated into this alignment. Future sequencing may identify errors in this list and we would welcome any evidence that helps to maintain the accuracy of this compilation. In the sequence alignments identity between residues is indicated by a hyphen (-). An unavailable sequence is indicated by a full point (.). Gaps in the sequence are inserted to maintain the alignment between different alleles showing variation in amino acid number.
Base Sequence↗
HLA class I nucleotide sequences, 1991.
The HLA Class I sequences included in this compilation are taken from publications listed in the accompanying paper, Nomenclature for factors of the HLA system, 1990 and Nomenclature for factors of the HLA system, 1989. Where discrepancies have arisen between reported sequences the original authors have been contacted where possible, and necessary amendments to published sequences have been incorporated into this alignment. Future sequencing may identify errors in this list and we would welcome any evidence that helps to maintain the accuracy of this compilation. In the sequence alignments identity between residues is indicated by a hyphen (-). Unavailable sequence is indicated by a period (.). Gaps in the sequence are inserted to maintain the alignment between different alleles showing variation in amino acid number.
Base Sequence↗
HLA-AR, an inactivated antigen-presenting locus related to HLA-A. Implications for the evolution of the MHC.
The MHC contains many class I genes other than those known to present peptides to T lymphocytes. These additional class I genes vary between species and their functions are unknown. Genes involved in Ag presentation, HLA-A,B,C in humans, are highly diverse whereas other class I genes are of much more limited diversity. We have studied alleles of a gene, HLA-AR, that is closely linked and structurally related to HLA-A; properties consistent with these two loci having been formed by a gene duplication. Compared to HLA-A the diversity in HLA-AR is much less, and does not focus on residues of a putative Ag recognition site. However, the structure of HLA-AR alleles closely resembles those encoding Ag-presenting molecules, although the presence of one or two deleterious mutations prevents these alleles being active in Ag presentation. These results suggest HLA-AR derives from an Ag-presenting locus that became inactivated, possibly as a result of positive natural selection due to changing demands on T cell immunity. Thus absence of diversity may sometimes correlate with loss rather than preservation of function in class I MHC genes.
Alleles↗
Rapid cloning of HLA-A,B cDNA by using the polymerase chain reaction: frequency and nature of errors produced in amplification.
A method for cloning full-length HLA-A,B cDNA (1.1 kilobases) by using the polymerase chain reaction (PCR) is described. Six HLA-A,B alleles (HLA-A2, -A25, -B7, -B37, -B51, and -B57) were cloned, and their structures were determined. Multiple PCR clones for each allele were sequenced to obtain both an accurate consensus sequence and an "authentic" clone having that sequence. Sequences from 50 clones encoding five different alleles permit assessment of the frequency and nature of PCR-produced errors. These include recombinations, deletions, and insertions in addition to point substitutions. Authentic clones were obtained at a frequency of between 30% and 70%, and analysis of three or four clones generally should be sufficient for characterization of an allele.
Alleles↗
Evolution of class-I MHC genes and proteins: from natural selection to thymic selection.
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Amino Acid Sequence↗
Comparison of the structure of HLA-Bw47 to HLA-B13 and its relationship to 21-hydroxylase deficiency.
Adrenal 21-hydroxylase deficiency is strongly associated with HLA-Bw47. This rare HLA allele and the HLA-B13 allele are both found in positive genetic linkage disequilibrium with HLA-A3, -Cw6, -DR7 and also display serological cross-reactivity. To investigate the relationship between these two alleles at the structural level, the nucleotide sequences of the HLA-B13 and HLA-Bw47 genes have been determined. They differ by 28 nucleotides, resulting in 14 amino acid substitutions: 5 in the alpha 1 domain, 8 in the alpha 2 domain, and 1 in the transmembrane region. Comparison of HLA-Bw47 nucleotide sequence with other HLA-B sequences shows a segment of 228 bp identical with B44 in the alpha 1 domain and a segment of 218 bp identical with B27 in the alpha 2 domain, but only a 91 bp segment of identity with B13 in the alpha 1 domain. The complex pattern of substitutions and their degree of divergence indicate that HLA-B13 and HLA-Bw47 alleles are not related by a simple mutational event.
Adrenal Hyperplasia, Congenital↗
Serological specificity of the liposome lysis test for measurement of anti-ganglioside antibodies. A comparison with hemagglutination inhibition.
A simple and reliable complement-dependent liposome lysis test for the detection of anti-ganglioside antibodies is described. For sera raised in rabbits against the monosialoganglioside NG-GM3, the sensitivity and specificity of antibody detection was compared with that of the HRBC hemagglutination-inhibition test: the liposome lysis test appears more sensitive. A difference in antigen presentation was also demonstrated.
Animals↗
Role of RNA in the induction of Thy-1+ phenotype on prothymocytes.
Differentiation of spleen prothymocytes into Thy-1.2+ cells under the influence of thymosin requires transcription of DNA and translation of RNA, as demonstrated by the effects of inhibitors of DNA, RNA and protein synthesis. The lifespan of the induction message for this T cell differentiation appeared to be relatively short (30 to 60 min) in the presence of a reversible inhibitor of protein synthesis. When anisomycin, a protein synthesis inhibitor, was first introduced into the cell suspension, induction was suppressed but it was restored when actinomycin D, a RNA synthesis inhibitor, was added following anisomycin. By flow cytometry, the RNA content was slightly increased in the presence of thymosin and this increase was enhanced by the simultaneous addition of RNA and protein synthesis inhibitors.
Animals↗