Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.79 (granzyme B)
 3,301 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have isolated cDNA clones from a human NK cell cDNA library that encode the serine protease granzyme B. Although the sequence of the entire coding region for the mature protein and the 3' untranslated region of the clone are identical to other cDNA isolates of this gene obtained from human T cell cDNA libraries, the 5' end of two clones is 103 bp longer than the previously described sequences and would encode a protein with a 54-amino-acid-long signal sequence. Experiments characterizing granzyme B mRNA suggest that transcripts that initiate at or before the 5' end of these clones comprise a detectable but infrequent class of granzyme B transcripts in NK and T cells. We have mapped this gene to human chromosome 14 in the region 14q11----14q32, distal to the T cell receptor alpha locus and proximal to the immunoglobulin heavy chain locus. The chromosomal location of this gene, together with the previously described high sequence homology between this gene and the mouse CTLA 1/ccp1 gene, make it likely that this is the human equivalent of the mouse CTLA1/ccp1.
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PMID:Isolation of a cDNA clone encoding a novel form of granzyme B from human NK cells and mapping to chromosome 14. 232 80

Two human serine protease genes have been cloned. One corresponds to CTLA1, the human equivalent of the mouse cytotoxic cell protease gene Ctla-1, and the other is novel. Both genes were localized to 14q11.2----q12 by in situ hybridization. This result confirms the assignment of human CTLA1 to 14q11.2----q12 and provides new mapping data for another human serine protease gene located in the same chromosome region.
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PMID:Chromosome localization of two human serine protease genes to region 14q11.2----q12 by in situ hybridization. 236 46

Seven monoclonal antibodies (mAb) were used to characterize antigens present on chicken T lymphocytes and on natural killer cells by flow cytometry, radioimmunoprecipitation and by effects on cell-mediated cytotoxicity and mitogen-induced proliferation. mAb CTLA8 and 5 stained 73% of thymus, 44% of spleen and 51% of peripheral blood lymphocytes (PBL), respectively, and immunoprecipitated 65- and 45-kDa proteins from detergent extracts of 125I surface-labeled thymocytes. Pretreatment of splenic lymphocytes with mAb CTLA5 and 8 in the presence of rabbit complement (C) eliminated the concanavalin A (Con A)-induced T cell proliferative responses. mAb CTLA3, 4 and 9 stained 43% of thymus, 36% of spleen and 18% of PBL, and immunoprecipitated 33-35-kDa proteins. Pretreatment of spleen cells with mAb 4 or 9 plus C reduced, but did not eliminate, the Con A-induced proliferative response and significantly reduced both major histocompatibility complex (MHC)-restricted and non-MHC-restricted cellular cytotoxicity. mAb CTLA1 and 6 stained 58% of thymus, 13% of spleen and 19% of PBL. mAb CTLA1 and 6 immunoprecipitated a 65-kDa protein. mAb CTLA1 and 6 had no effect on the Con A-induced blastogenesis and CTLA6 caused no decrease in virus-specific cytotoxic T lymphocyte and natural killer activity. These results indicate that (a) mAb CTLA5 and 8 identify antigens on mature T lymphocytes that are similar in tissue distribution, molecular mass and function to the mammalian CD5 antigen; (b) mAb CTLA3, 4 and 9 detect the avian homologue of CD8 antigen; and (c) mAb CTLA1 and 6 identify the avian homologue of CD4 antigen.
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PMID:Functional and biochemical characterizations of avian T lymphocyte antigens identified by monoclonal antibodies. 297 3

Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare haematological malignancy derived from the precursors of plamacytoid dendritic cells, with an aggressive clinical course and high frequency of cutaneous and bone marrow involvement. Neoplastic cells express CD4, CD43 (also termed SPN), CD45RA and CD56 (also termed NCAM1), as well as the plasmacytoid dendritic cell-associated antigens CD123 (also termed IL3RA), BDCA-2 (also termed CD303, CLEC4E) TCL1 and CTLA1 (also termed GZMB). The median survival is only a few months as the tumour exhibits a progressive course despite initial response to chemotherapy. The best modality of treatment remains to be defined. Generally, patients receive acute leukaemia-like induction, according to acute myeloid leukaemia (AML)-type or acute lymphoid leukaemia (ALL)-type regimens. The frequent neuromeningeal involvement indicates systematic pre-emptive intrathecal chemotherapy in addition to intensive chemotherapy. Allogeneic haematopoietic stem cell transplantation (HSCT), particularly when performed in first remission, may improve the survival. Preliminary data suggest a potential role for immunomodulatory agents and novel targeted drugs. Herein epidemiology, clinical manifestations, diagnosis and management of BPDCN will be presented. In detail, this review focuses on the therapeutic aspects of BPDCN, proposing a treatment algorithm for the management of the disease, including induction chemotherapy, allogeneic HSCT and intrathecal prophylaxis at different steps of treatment, according to compliance, biological and clinical characteristics of patients.
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PMID:Blastic plasmacytoid dendritic cell neoplasm: diagnostic criteria and therapeutical approaches. 2726 21