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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Genomic EMBL 3 DNA clones representing part of the human Fc gamma receptor II and the beta Fc gamma receptor II genes were characterized. One of them contains the first five exons including the 5' flanking region of the beta FcRII gene. The signal peptide, the extracellular domains, the putative membrane spanning region, and the first amino acids of the cytoplasmic region encoded by these five exons are spread over approximately 11 kb. Another genomic DNA clone comprises four exons encoding the second extracellular domain and the transmembrane and cytoplasmic regions of the FcRII. Alignment of the genomic DNA clones reveals that these FcR genes are identically organized. Comparison of the corresponding regions of these clones shows that not only the exons are strikingly homologous but also the splice junctions and parts of the intervening sequences are conserved. Furthermore, the genomic organization of FcRII and HLA-class I resemble each other.
Mol Immunol 1990 Apr
PMID:Organization of human FcRII and FcRII-like (beta FcRII) genes: structural homology to HLA class I and class II genes. 214 67

The cellular responses to alpha and beta interferons (IFN-alpha and -beta) are mediated through the IFN-alpha/beta (type I) receptor, while the response to IFN-gamma is mediated through the IFN-gamma (type II) receptor. The receptors for IFN-alpha/beta and IFN-gamma are encoded by genes on human chromosomes 21 and 6q, respectively. The presence of chromosome 21q confers both ligand binding and responsiveness to human IFN-alpha/beta, whereas chromosome 6q confers binding of Hu-IFN-gamma, but not cellular responsiveness on somatic cell hybrids. Chromosome 6q (i.e., the Hu-IFN-gamma receptor gene) and chromosome 21q are both necessary for the cellular response of somatic cell hybrids (from fibroblasts) to Hu-IFN-gamma. It is conceivable that the factor mediating activity through the IFN-gamma receptor is, in fact, the IFN-alpha receptor, or that the two genes are distinct but part of an "interferon response" region. Here we more precisely localize on human chromosome 21 the genes for the IFN-alpha receptor and for the factor(s) mediating the action of IFN-gamma through the chromosome 6-encoded receptor. Hamster-human somatic cell hybrids containing various fragments of human chromosome 21 were used. The presence of the human IFN-alpha/beta receptor was determined by binding 32P-labeled human IFN-alpha to cells, covalently cross-linking the [32P]IFN-alpha-receptor complex, and analyzing it by SDS-polyacrylamide gel electrophoresis. The presence of the IFN-gamma receptor-related factor mediating cellular responsiveness was determined by HLA induction in hybrid cells containing the IFN-gamma receptor (chromosome 6q), a transfected copy of the human HLA-B7 gene, and various portions of chromosome 21. In all hybrids examined, the two genes cosegregate. Specifically, both genes are localized to the region of chromosome 21 containing the markers D21S58, D21S65, and GART and appear to be proximal to D21S58. The implications for IFN action are discussed.
Somat Cell Mol Genet 1990 May
PMID:Sublocalization on chromosome 21 of human interferon-alpha receptor gene and the gene for an interferon-gamma response protein. 214 27

A review of reproductive biology and oncologic immunology reveals striking similarities between the tolerance of neoantigen as demonstrated in pregnancy and cancer. The author discusses the phylogeny of sexual reproduction and the oncologic condition, and suggests that an evolved mechanism of acquired tolerance to HLA-incompatible tissue necessitated by sexual reproduction consequently provides a mechanism for the tolerance of cancer.
Mol Biother 1990 Sep
PMID:The phylogeny of oncology. 222 97

The authors have used the modified method of the direct gene cloning suggested by Nichols et al to isolate HLA-B27 gene from a patient suffering from ankylosing spondylitis. Five restriction enzymes (ClaI, HindIII, SnaBI, PvuI, SalGI) which had no recognition sites within the 6.0 kb EcoRI-BamHI-DNA fragment supposedly containing the HLA-B27 gene have been chosen by blotting-hybridization of the restriction fragments of the patients DNA with HLA-B27-specific probe. The 6.0 +/- 0.5 kb DNA fragments were isolated and cloned after the DNA treatment by 300 micrograms of all of these restriction enzymes. The obtained mini-library containing 280 recombinants has been screened with the use of HLA-B27 specific oligonucleotide probe. The clone PB27-2 has been isolated the restriction map of which is identical to HLA-B27k. The authors are planning to determine the sequence of the isolated gene in order to find a possible structural defect in it.
Mol Gen Mikrobiol Virusol 1990 Aug
PMID:[Directed cloning of the HLA-B27 gene isolated from a patient with ankylosing spondylitis (Bechterew's disease)]. 223 90

The human major histocompatibility complex contains approximately 20 class I genes, pseudogenes, and gene fragments. These include the genes for the three major transplantation antigens, HLA-A, HLA-B, and HLA-C, as well as a number of other genes or pseudogenes of unknown biological significance. Most of the latter have C + G-rich sequences in their 5' ends that are unmethylated in the B-lymphoblastoid cell line 3.1.0. We investigated one of these genes, HLA-H, in more detail. The gene is, overall, strongly homologous in sequence to HLA-A but differs in several potentially significant ways, including changes in conserved promoter sequences, a single-base deletion producing a translation termination codon in exon 4, and a region of sequence divergence downstream of the transcribed portion of the gene. Nevertheless, mouse L cells transfected with the gene accumulated small amounts of apparently full-length polyadenylated RNA. A portion of this RNA begins at the transcription site predicted by analogy to certain class I cDNA clones, while another portion appears to begin shortly upstream. L cells transfected with a hybrid gene containing the first three exons of HLA-H and the last five exons of HLA-B27 accumulated full-length HLA transcripts at the same level as cells transfected with an HLA-B27 gene; both levels are at least 15- to 20-fold higher than that directed by HLA-H alone. In addition, we isolated a cDNA clone for HLA-H that contains a portion of intron 3 attached to a normally spliced sequence comprising exons 4 through 8. These results suggest that low levels of translatable mRNA for the truncated class I heavy chain encoded by HLA-H are produced under physiologic circumstances and that sequences 3' of intron 3 decrease the levels of stable transcripts.
Mol Cell Biol 1990 Jan
PMID:Transcription analysis, physical mapping, and molecular characterization of a nonclassical human leukocyte antigen class I gene. 229 3

Exon 2 nucleotide sequence of the DRB1 gene encoding the HLA-DRw13b allele defined by DNA-RFLP (Restriction Fragment Length Polymorphism) typing, has been obtained by using five heterozygous individuals genomic DNA and a non isotopic automated "dideoxi" methodology. Its comparison with other known homologous DRB1 sequences suggests that two different mechanisms which generate HLA allele variability may have occurred in this particular exon 2: a gene conversion between DRw11 or DRw13 as acceptors and DR4-Dw15 or DRw8.1 as donors and in addition, a non-conservative point mutation at base 221. The relationship between this HLA sequence characteristics and certain diseases susceptibility is discussed.
Mol Immunol 1990 Mar
PMID:Exon 2 DNA sequence of the HLA-DRw13b allele obtained from genomes of five different individuals. 234 92

Persistent polyclonal lymphocytosis has been described in a group of female patients who all have the HLA-DR7 antigen in common and who are all heavy cigarette smokers. Immunoglobulin heavy chain gene rearrangement was analyzed by hybridization with specific immunoglobulin heavy chain genes to restriction enzyme-digested genomic DNA samples. The results in two of these patients showed that the lymphocytosis was associated with an expanded subpopulation of B-lineage cells represented by the presence of an unusual immunoglobulin gene rearrangement pattern. Expansion of this subpopulation of B cells appeared to be linked to cigarette smoking since the intensity of the cell population harboring the rearranged gene was much stronger in patients who were smoking heavily compared with the same patients who were temporarily not smoking.
Am J Respir Cell Mol Biol 1990 Jun
PMID:Expansion of B lymphocytes with an unusual immunoglobulin rearrangement associated with atypical lymphocytosis and cigarette smoking. 234 60

This paper presents the initial characterization of a mouse monoclonal antibody (RH1-38) which blocks, in the absence of complement, three different systems of cell-mediated cytotoxicity. This monoclonal antibody markedly inhibits cytotoxicity mediated by human natural killer cells, a monocyte-like cell [phorbol myristate acetate (PMA) stimulated HL-60], and cytotoxic T-lymphocytes generated in a mixed leukocyte reaction. RH1-38 is not nonspecifically toxic to cells since antibody-dependent cellular cytotoxicity was not inhibited and viability as assessed by trypan blue exclusion was not affected. Inhibition is specific since control hybridoma culture supernatants, parent (NS-1) ascites supernatant, monoclonal anti-HLA and normal mouse IgG were not significantly inhibitory. In the NK system, the inhibitory effect appears to be due to binding of monoclonal antibody to effector cell surface since exposure of targets to antibody followed by washing yielded no inhibition of killing. Inhibition requires the antigen-binding portion of the antibody molecule and thus appears to be related to steric hindrance of an effector cell surface molecule which is important in the expression of cell-mediated cytotoxicity. Immunoprecipitation of surface-radioiodinated membranes from PMA-stimulated HL-60 cells and analysis on sodium dodecyl sulfate-polyacrylamide gels revealed a bimolecular complex (195,000 and 125,000 daltons) without significant change under reducing conditions. Control immunoprecipitates yielded no peaks of activity. This monoclonal antibody should serve as a useful probe of the function and biochemistry of a killer cell surface antigen important in the expression of cell-mediated cytotoxicity. Since RH1-38 inhibits cytotoxicity mediated by at least three apparently unrelated effector cells, the relevant antigen may be part of a common mechanistic step. As the companion paper demonstrates, this monoclonal antibody does not affect the conjugation step, but appears to block a late step in the NK cytolytic mechanism. Thus, RH1-38 recognizes either an epitope district from previously-described anti-LFA-1 antibodies or alternatively recognizes a distinct functional killer cell surface molecule.
Mol Immunol 1985 Jul
PMID:A monoclonal antibody (RH1-38) which inhibits multiple systems of cell-mediated cytotoxicity--I. Identification of a novel epitope on a killer cell surface bimolecular complex important in the cytotoxic response. 241 10

We describe the isolation and characterization of a human X-chromosomal gene that is subject to both single-active-X control and tissue-specific control. The A-11 gene was identified by a cDNA that hydridizes to a 3.2-kb EcoR1 fragment of genomic DNA on the long arm of the human X chromosome. A-11 transcripts are normally present in fibroblasts but not in B- or T-lymphoblasts. However, A-11 transcription was activated in four of 11 independent, gamma ray-induced B-lymphoblastoid HLA antigen-loss mutants. Cell hybrids with a human fibroblast-derived active X contained A-11 transcripts but hybrids carrying the human inactive X did not. Azacytidine, a potent inhibitor of DNA methylation, readily reactivated the A-11 locus on the inactive X in hybrid cells, indicating that differential methylation is likely to be involved in the single-active-X control of A-11 transcription in fibroblasts. Failure of cells to remethylate DNA synthesized to repair gamma ray-induced damage may also have resulted in the activation of A-11 transcription among the lymphoblastoid mutants. The A-11 locus provides an opportunity to study the relationship between two types of transcriptional regulation of a gene.
Somat Cell Mol Genet 1988 Nov
PMID:A-11: cell type-specific and single-active-X transcription controls of newly found gene in cultured human cells. 246 99

Potential antigenic regions of the various external domains of the HLA-B27 antigen were expressed as fusion proteins in bacterial hosts and analyzed for their ability to induce humoral and cellular responses. Monoclonal antibodies directed against the proteins recognized monomorphic determinants of denatured HLA-antigens, but not B27-antigens expressed by intact lymphocytes. T-cell proliferation and IL-2 secretion were induced with a fusion protein representing regions of the first and second domains around amino acid residue 114. None of the fusion proteins stimulated cytotoxic T-lymphocytes (CTL) in an HLA-specific manner, although several included those amino acid sequences thought to be important for CTL recognition.
Mol Immunol 1989 Jan
PMID:The use of fusion proteins to study HLA-B27-specific allorecognition. 246 95


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