A Tandem Array of Sp-1 Sites and a Reverse Initiator Element Are Both Required for Synergistic Transcriptional Activation of the T-Cell-Specific MAL Gene
Author:
Publisher
Mary Ann Liebert Inc
Subject
Cell Biology,Genetics,Molecular Biology,General Medicine
Link
http://www.liebertpub.com/doi/pdf/10.1089/dna.1997.16.245
Reference57 articles.
1. cDNA cloning and sequence of MAL, a hydrophobic protein associated with human T-cell differentiation.
2. Assignment of the T-cell differentiation gene MAL to human chromosome 2, region cen?q13
3. Synergistic activation of a human promoter in vivo by transcription factor Sp1.
4. Gene regulation by steroid hormones
5. Three clustered Sp1 sites are required for efficient transcription of the TATA-less promoter of the gene for insulin-like growth factor-binding protein-2 from the rat.
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1. Hypermethylation-Mediated Silencing of CIDEA, MAL and PCDH17 Tumour Suppressor Genes in Canine DLBCL: From Multi-Omics Analyses to Mechanistic Studies;International Journal of Molecular Sciences;2022-04-05
2. The MAL Protein, an Integral Component of Specialized Membranes, in Normal Cells and Cancer;Cells;2021-04-30
3. Inactivation of theMALGene in Breast Cancer Is a Common Event That Predicts Benefit from Adjuvant Chemotherapy;Molecular Cancer Research;2009-02
4. Hypermethylated MAL gene – a silent marker of early colon tumorigenesis;Journal of Translational Medicine;2008-03-17
5. Characterization of the Mouse Myeloid-associated Differentiation Marker (Myadm) Gene: Promoter Analysis and Protein Localization;Molecular Biology Reports;2005-09
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