Identification of Minimal p53 Promoter Region Regulated by MALAT1 in Human Lung Adenocarcinoma Cells
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Title
Identification of Minimal p53 Promoter Region Regulated by MALAT1 in Human Lung Adenocarcinoma Cells
Authors
Keywords
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Journal
Frontiers in Genetics
Volume 8, Issue -, Pages -
Publisher
Frontiers Media SA
Online
2018-03-26
DOI
10.3389/fgene.2017.00208
References
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Note: Only part of the references are listed.- RNA-RNA Interactions Enable Specific Targeting of Noncoding RNAs to Nascent Pre-mRNAs and Chromatin Sites
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- MALAT1 — a paradigm for long noncoding RNA function in cancer
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- Long Noncoding RNA MALAT1 Controls Cell Cycle Progression by Regulating the Expression of Oncogenic Transcription Factor B-MYB
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- The Noncoding RNA MALAT1 Is a Critical Regulator of the Metastasis Phenotype of Lung Cancer Cells
- (2012) T. Gutschner et al. CANCER RESEARCH
- Genome-wide determination of RNA stability reveals hundreds of short-lived noncoding transcripts in mammals
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- Malat1 is not an essential component of nuclear speckles in mice
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- The lncRNA Malat1 Is Dispensable for Mouse Development but Its Transcription Plays a cis-Regulatory Role in the Adult
- (2012) Bin Zhang et al. Cell Reports
- Long non-coding RNAs in cancer progression
- (2012) Keiko Tano et al. Frontiers in Genetics
- ncRNA- and Pc2 Methylation-Dependent Gene Relocation between Nuclear Structures Mediates Gene Activation Programs
- (2011) Liuqing Yang et al. CELL
- MALAT-1 enhances cell motility of lung adenocarcinoma cells by influencing the expression of motility-related genes
- (2010) Keiko Tano et al. FEBS LETTERS
- The Nuclear-Retained Noncoding RNA MALAT1 Regulates Alternative Splicing by Modulating SR Splicing Factor Phosphorylation
- (2010) Vidisha Tripathi et al. MOLECULAR CELL
- Massively regulated genes: the example ofTP53
- (2009) Monica Hollstein et al. JOURNAL OF PATHOLOGY
- Long non-coding RNAs: insights into functions
- (2009) Tim R. Mercer et al. NATURE REVIEWS GENETICS
- Massive transcriptional start site analysis of human genes in hypoxia cells
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