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PubMed:7592598 JSONTXT 29 Projects

Annnotations TAB TSV DIC JSON TextAE Lectin_function IAV-Glycan

Id Subject Object Predicate Lexical cue
T1 0-118 Sentence denotes Mutually exclusive interaction of a novel matrix attachment region binding protein and the NF-muNR enhancer repressor.
T1 0-118 Sentence denotes Mutually exclusive interaction of a novel matrix attachment region binding protein and the NF-muNR enhancer repressor.
T2 119-188 Sentence denotes Implications for regulation of immunoglobulin heavy chain expression.
T2 119-188 Sentence denotes Implications for regulation of immunoglobulin heavy chain expression.
T3 189-337 Sentence denotes The immunoglobulin heavy chain (IgH) intronic enhancer stimulates transcription from functional promoters in B lymphocytes but not other cell types.
T3 189-337 Sentence denotes The immunoglobulin heavy chain (IgH) intronic enhancer stimulates transcription from functional promoters in B lymphocytes but not other cell types.
T4 338-663 Sentence denotes The observation that binding sites for the nuclear factor-mu negative regulator (NF-muNR) enhancer repressor overlap nuclear matrix attachment regions (MARs) in this enhancer has lead to the hypothesis that the cell type specificity of the enhancer might be controlled by regulating nuclear matrix attachment (Scheuermann, R.
T4 338-663 Sentence denotes The observation that binding sites for the nuclear factor-mu negative regulator (NF-muNR) enhancer repressor overlap nuclear matrix attachment regions (MARs) in this enhancer has lead to the hypothesis that the cell type specificity of the enhancer might be controlled by regulating nuclear matrix attachment (Scheuermann, R.
T5 664-700 Sentence denotes H., and Chen, U. (1989) Genes & Dev.
T5 664-700 Sentence denotes H., and Chen, U. (1989) Genes & Dev.
T6 701-715 Sentence denotes 3, 1255-1266).
T6 701-715 Sentence denotes 3, 1255-1266).
T7 716-947 Sentence denotes To understand the role of MARs in IgH enhancer regulation, we have identified a novel MAR-binding protein, MAR-BP1, from soluble nuclear matrix preparations based on its ability to bind to the MARs associated with the IgH enhancer.
T7 716-947 Sentence denotes To understand the role of MARs in IgH enhancer regulation, we have identified a novel MAR-binding protein, MAR-BP1, from soluble nuclear matrix preparations based on its ability to bind to the MARs associated with the IgH enhancer.
T8 948-1102 Sentence denotes Purified MAR-BP1 migrates as a 33-kDa protein, and it can be found in nuclear matrix preparations from a number of different types of lymphoid cell lines.
T8 948-1102 Sentence denotes Purified MAR-BP1 migrates as a 33-kDa protein, and it can be found in nuclear matrix preparations from a number of different types of lymphoid cell lines.
T9 1103-1282 Sentence denotes Although specific binding sites have been difficult to localize by chemical or enzymatic footprinting procedures, NF-muNR binding sites are critical for efficient MAR-BP1 binding.
T9 1103-1282 Sentence denotes Although specific binding sites have been difficult to localize by chemical or enzymatic footprinting procedures, NF-muNR binding sites are critical for efficient MAR-BP1 binding.
T10 1283-1419 Sentence denotes Indeed, binding of the IgH enhancer to either intact nuclear matrix preparations or to MAR-BP1 is mutually exclusive to NF-muNR binding.
T10 1283-1419 Sentence denotes Indeed, binding of the IgH enhancer to either intact nuclear matrix preparations or to MAR-BP1 is mutually exclusive to NF-muNR binding.
T11 1420-1665 Sentence denotes These results are consistent with a model for cell-type specific regulation in which binding of the NF-muNR repressor to the IgH enhancer prevents nuclear matrix attachment in inappropriate cells by interfering with MAR-BP1/enhancer interaction.
T11 1420-1665 Sentence denotes These results are consistent with a model for cell-type specific regulation in which binding of the NF-muNR repressor to the IgH enhancer prevents nuclear matrix attachment in inappropriate cells by interfering with MAR-BP1/enhancer interaction.