morinlab.bib
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+@article{masclePointMutationsBCL62003,
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+ title = {Point Mutations in {{BCL6 DNA-binding}} Domain Reveal Distinct Roles for the Six Zinc Fingers},
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+ author = {Mascle, Xavier and Albagli, Olivier and Lemercier, Claudie},
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+ date = {2003-01-10},
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+ journaltitle = {Biochemical and Biophysical Research Communications},
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+ shortjournal = {Biochem Biophys Res Commun},
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+ volume = {300},
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+ number = {2},
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+ eprint = {12504096},
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+ eprinttype = {pmid},
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+ pages = {391--396},
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+ issn = {0006-291X},
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+ doi = {10.1016/s0006-291x(02)02873-5},
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+ abstract = {The B-cell lymphoma 6 (BCL6) gene encodes a transcriptional repressor containing six C-terminal Krüppel-like zinc fingers. The zinc finger (ZF) cluster is necessary and sufficient for interaction with both DNA and several proteins and for nuclear targeting. However, the functional specificity of the six ZFs in these cellular roles is unknown. To characterize this domain, we mutated individually each ZF of BCL6. Our results reveal that mutation of the two N-terminal ZFs does not impair cognate DNA-binding, cellular localization of the protein nor the transcriptional repression capacity of BCL6. By contrast, mutation of any of the remaining ZFs abolishes the binding of BCL6 to DNA in vitro and the transrepressive function of the protein in vivo. Finally, none of the six mutations affect the interaction between BCL6 and class II histone deacetylases. Thus our experiments demonstrate that BCL6 uses each of the four C-terminus ZFs for binding to a target sequence while the two amino terminal fingers are likely engaged in other unknown function(s).},
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+ langid = {english},
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+ keywords = {Amino Acid Sequence,Binding Sites,DNA-Binding Proteins,Gene Expression Regulation,HeLa Cells,Histone Deacetylases,Humans,Molecular Sequence Data,Point Mutation,Protein Structure Tertiary,Proto-Oncogene Proteins,Proto-Oncogene Proteins c-bcl-6,Repressor Proteins,Sequence Alignment,Transcription Factors,Transcription Genetic,Zinc Fingers},
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+}
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@article{camachoATMGeneInactivation2002,
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title = {{{ATM}} Gene Inactivation in Mantle Cell Lymphoma Mainly Occurs by Truncating Mutations and Missense Mutations Involving the Phosphatidylinositol-3 Kinase Domain and Is Associated with Increasing Numbers of Chromosomal Imbalances},
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author = {Camacho, Emma and Hernández, Luis and Hernández, Silvia and Tort, Frederic and Bellosillo, Beatriz and Beà, Silvia and Bosch, Francesc and Montserrat, Emili and Cardesa, Antonio and Fernández, Pedro L. and Campo, Elias},
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abstract = {The ataxia-telangiectasia mutated (ATM) gene codifies for a protein critically involved in the cellular response to DNA damage. ATM alterations have been observed in some sporadic lymphoproliferative disorders. The recurrent 11q22-23 deletions found in mantle cell lymphoma (MCL) suggest that ATM could be inactivated in these lymphomas. In this study, ATM gene alterations and protein expression were examined in 20 and 17 MCL tumor specimens, respectively. Previously, these patients had been examined for p53 and p14(ARF) gene status and analyzed by comparative genomic hybridization. Nine patients had 11q22-23 losses. Eight ATM gene mutations were detected in 7 patients. These alterations were 3 missense mutations in the phosphatidylinositol-3 kinase (PI-3K) domain and 5 truncating mutations, including 3 frameshifts, a nonsense mutation, and a substitution of the initial methionine. All truncating mutations were associated with lack of protein expression. Somatic origin was demonstrated in 3 mutations, whereas one mutation was carried heterozygously in the patient germ line. Chromosomal imbalances were significantly higher in typical MCL with ATM inactivation (7.8 +/- 1.3) than in tumors with the wild-type gene (3 +/- 1.1) (P =.001). Moreover, tumors with bi-allelic ATM alteration were associated with 3q gains (P =.015) and frequent extranodal involvement (P =.049). ATM gene alterations were not related to the histologic variant of the tumors, p53/p14(ARF) gene status, survival, or other clinicopathologic features of the patients. These findings indicate that ATM gene mutations in MCL are mainly truncating or missense mutations involving the PI-3K domain, and that may play a role in the pathogenesis of a subset of these tumors with increased numbers of chromosomal imbalances.},
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langid = {english},
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keywords = {Alleles,Ataxia Telangiectasia Mutated Proteins,Blotting Western,Cell Cycle Proteins,Chromosome Aberrations,Chromosomes Human Pair 11,DNA Mutational Analysis,DNA-Binding Proteins,Gene Deletion,Gene Expression,Humans,Lymphoma Mantle-Cell,Mutation,Mutation Missense,Phosphatidylinositol 3-Kinases,Polymorphism Genetic,Protein Serine-Threonine Kinases,Tumor Suppressor Proteins},
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- file = {/Users/rmorin/Zotero/storage/NH2TDSEB/Camacho et al. - 2002 - ATM gene inactivation in mantle cell lymphoma main.pdf}
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}
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@article{yusufovaHistoneH1Loss2021,