Cited by 434Cancer-related Molecular PathwaysDNA Repair MechanismsCell death mechanisms and regulation

Identification of BTG2, an antiproliferative p53–dependent component of the DNA damage cellular response pathway

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Rouault, Jean-Pierre, Falette, Nicole, Guéhenneux, Fabienne, Guillot, Céline, Rimokh, Ruth, Wang, Qing, Berthet, Cyril, Moyret-Lalle, Caroline +9 more·1996·Nature Genetics

Abstract

Cell cycle regulation is critical for maintenance of genome integrity. A prominent factor that guarantees genomic stability of cells is p53 (ref. 1). The P53 gene encodes a transcription factor that has a role as a tumour suppressor. Identification of p53-target genes should provide greater insight into the molecular mechanisms that mediate the tumour suppressor activities of p53. The rodent Pc3/Tis21 gene was initially described as an immediate early gene induced by tumour promoters and growth factors in PC12 and Swiss 3T3 cells. It is expressed in a variety of cell and tissue types and encodes a remarkably labile protein. Pc3/Tis21 has a strong sequence similarity to the human antiproliferative BTG1 gene cloned from a chromosomal translocation of a B-cell chronic lymphocytic leukaemia. This similarity led us to speculate that BTG1 and the putative human homologue of Pc3/Tis21 (named BTG2) were members of a new family of genes involved in growth control and/or differentiation. This hypothesis was recently strengthened by the identification of a new antiproliferative protein, named TOB, which shares sequence similarity with BTG1 and PC3/TIS21 (ref. 7). Here, we cloned and localized the human BTG2 gene. We show that BTG2 expression is induced through a p53-dependent mechanism and that BTG2 function may be relevant to cell cycle control and cellular response to DNA damage.

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  • BTG2 can induce G1/S cell cycle arrest.

    “The p53 target genes BTG236, 154, 155 and GADD45A13, 156 can also induce G1/S and G2/M cell cycle arrest, respectively.”

    From Census and evaluation of p53 target genes (2017) · cites this paper as [155]

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Authors
Rouault, J.-P., Falette, N., Guéhenneux, F., Guillot, C., Rimokh, R., Wang, Q., Berthet, C., Moyret-Lalle, C., Savatier, P., Pain, B., Shaw, P., Berger, R., Samarut, J., Magaud, J.-P., Ozturk, M., Samarut, C., & Puisieux, A.
Affiliations
  • Centre National de la Recherche Scientifique (FR)
  • Centre Léon Bérard (FR)
  • École Normale Supérieure de Lyon (FR)
  • Inserm (FR)
Venue
Nature Genetics
Published
1996-12
Volume
14
Issue
4
Pages
482-486
ISSN
  • 1061-4036 (ISSN-L)
  • 1546-1718
OpenAlex
W2028468783
Cited by
434
References
46
Citations by year
2026: 8 · 2025: 10 · 2024: 18 · 2023: 9 · 2022: 19 · 2021: 9 · 2020: 12 · 2019: 8 · 2018: 15 · 2017: 12 · 2016: 8 · 2015: 20 · 2014: 25 · 2013: 23 · 2012: 21
FWCI
3.90
Type
journal article
Language
en
Open access
Locations
  • Nature Genetics (publishedVersion)
  • PubMed (publishedVersion)
  • Bilkent University Institutional Repository (Bilkent University) (submittedVersion)
  • HAL (submittedVersion)
  • IRIS (submittedVersion)
  • SERVAL (Université de Lausanne) (submittedVersion)
Topics
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
BTG2, BTG1, p53, p53 target genes, DNA damage response, cell cycle regulation, tumour suppressor, gene cloning, genome stability
MeSH terms
Amino Acid Sequence, Animals, Cell Cycle, Cell Division, Cell Line, Chromosome Mapping, Chromosomes, Human, Pair 1, Cloning, Molecular, DNA Damage, Gene Expression Regulation, Humans, Hybrid Cells, Molecular Sequence Data, Neoplasm Proteins, Proteins, Genes, Tumor Suppressor, Tumor Suppressor Protein p53, 3T3 Cells, Sequence Homology, Amino Acid, Immediate-Early Proteins, Tumor Suppressor Proteins, Mice

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