Sin3B expression is required for cellular senescence and is up-regulated upon oncogenic stress.

No abstract is available for this paper.

• Publication year

  2009

• Venue

  Cancer Research

• Publication date

  2009-08-15

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1158/0008-5472.CAN-09-0537PMID 19654306PMCID PMC2782780
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Notch and Kras reprogram pancreatic acinar cells to ductal intraepithelial neoplasia

  2008cited by this paper
• Sin3B: An essential regulator of chromatin modifications at E2F target promoters during cell cycle withdrawal

  2008cited by this paper
• Spontaneous induction of murine pancreatic intraepithelial neoplasia (mPanIN) by acinar cell targeting of oncogenic Kras in adult mice

  2008cited by this paper
• Specific requirement of the chromatin modifier mSin3B in cell cycle exit and cellular differentiation

  2008cited by this paper
• Molecular Dissection of Formation of Senescence-Associated Heterochromatin Foci

  2007cited by this paper
• Breaking news: high-speed race ends in arrest--how oncogenes induce senescence.

  2007cited by this paper
• Tumorigenesis and Neoplastic Progression Acinar Cells Contribute to the Molecular Heterogeneity of Pancreatic Intraepithelial Neoplasia

  2007cited by this paper
• Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas

  2007cited by this paper
• Delayed ageing through damage protection by the Arf/p53 pathway

  2007cited by this paper
• Cellular senescence in cancer and aging.

  2007cited by this paper
• RBP2 is an MRG15 complex component and down‐regulates intragenic histone H3 lysine 4 methylation

  2007cited by this paper
• Oncogene-induced senescence is a DNA damage response triggered by DNA hyper-replication

  2006cited by this paper
• The pathological response to DNA damage does not contribute to p53-mediated tumour suppression

  2006cited by this paper
• Stem-cell ageing modified by the cyclin-dependent kinase inhibitor p16INK4a

  2006cited by this paper
• Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints

  2006cited by this paper
• INK4a/ARF: a multifunctional tumor suppressor locus.

  2005cited by this paper
• BRAFE600-associated senescence-like cell cycle arrest of human naevi

  2005cited by this paper
• Oncogene-induced senescence as an initial barrier in lymphoma development

  2005cited by this paper
• Tumour biology: Senescence in premalignant tumours

  2005cited by this paper
• Pocket Protein Complexes Are Recruited to Distinct Targets in Quiescent and Proliferating Cells

  2005cited by this paper
• mSin3A corepressor regulates diverse transcriptional networks governing normal and neoplastic growth and survival.

  2005cited by this paper
• Crucial role of p53-dependent cellular senescence in suppression of Pten-deficient tumorigenesis

  2005cited by this paper
• Histone deacetylase inhibitors: development as cancer therapy.

  2004cited by this paper
• Repression of the Arf tumor suppressor by E2F3 is required for normal cell cycle kinetics.

  2004cited by this paper
• Hitting their targets: an emerging picture of E2F and cell cycle control.

  2004cited by this paper
• mSin3-associated protein, mSds3, is essential for pericentric heterochromatin formation and chromosome segregation in mammalian cells.

  2003cited by this paper
• Rb-mediated heterochromatin formation and silencing of E2F target genes during cellular senescence.

  2003cited by this paper
• Acute mutation of retinoblastoma gene function is sufficient for cell cycle re-entry

  2003cited by this paper
• Oxygen sensitivity severely limits the replicative lifespan of murine fibroblasts

  2003cited by this paper
• E2F transcriptional repressor complexes are critical downstream targets of p19(ARF)/p53-induced proliferative arrest.

  2002cited by this paper
• p53 mutant mice that display early ageing-associated phenotypes

  2002cited by this paper
• Loss of p16Ink4a confers susceptibility to metastatic melanoma in mice

  2001cited by this paper
• Escape from premature senescence is not sufficient for oncogenic transformation by Ras

  2001cited by this paper
• Loss of p16Ink4a with retention of p19Arf predisposes mice to tumorigenesis

  2001cited by this paper
• Sin meets NuRD and other tails of repression.

  1999cited by this paper
• c-Myc target gene specificity is determined by a post-DNAbinding mechanism.

  1998cited by this paper
• p19ARF links the tumour suppressor p53 to Ras

  1998cited by this paper
• The regulation of E2F by pRB-family proteins.

  1998cited by this paper
• Tumor Suppression at the Mouse INK4a Locus Mediated by the Alternative Reading Frame

  1997cited by this paper
• Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a.

  1997cited by this paper
• Tumor suppression at the mouse INK4a locus mediated by the alternative reading frame product p19ARF.

  1997cited by this paper
• A biomarker that identifies senescent human cells in culture and in aging skin in vivo.

  1995cited by this paper

• Loss of GATA2 promotes invasion and predicts cancer recurrence and survival in uterine serous carcinoma

  2025cites this paper
• Navigating the Paradox of Senescence and Chemoresistance in Pancreatic Cancer.

  2025cites this paper
• Interrogating the regulatory epigenome of cellular senescence

  2025cites this paper
• Knockout of SIN3B modulates transcriptional programs and cell survival in cutaneous melanoma.

  2025cites this paper
• miR-96-5p expression is sufficient to induce and maintain the senescent cell fate in the absence of stress

  2024cites this paper
• SIN3B Loss Heats up Cold Tumor Microenvironment to Boost Immunotherapy in Pancreatic Cancer

  2024cites this paper
• SDS3 regulates microglial inflammation by modulating the expression of the upstream kinase ASK1 in the p38 MAPK signaling pathway

  2024cites this paper
• Chromatin accessibility and cell cycle progression are controlled by the HDAC-associated Sin3B protein in murine hematopoietic stem cells

  2024cites this paper
• Senescence program and its reprogramming in pancreatic premalignancy

  2023cites this paper
• The Sin3B chromatin modifier restricts cell cycle progression to dictate hematopoietic stem cell differentiation

  2023cites this paper
• Mechanism of assembly, activation and lysine selection by the SIN3B histone deacetylase complex

  2023cites this paper
• Chromatin-associated SIN3B protects cancer cells from genotoxic stress-induced apoptosis and dictates DNA damage repair pathway choice.

  2023cites this paper
• Common Molecular Signatures Between Coronavirus Infection and Alzheimer’s Disease Reveal Targets for Drug Development

  2023cites this paper
• Common molecular signatures between coronavirus infection and Alzheimer’s disease reveal targets for drug development

  2023cites this paper
• Premalignant lesions and cellular senescence

  2022cites this paper
• The chromatin associated Sin3B is a critical regulator of DNA damage repair through the engagement of the Non-Homologous End Joining

  2022cites this paper
• Clinical significance of pancreatic ductal metaplasia

  2022cites this paper
• Invasive phenotype in triple negative breast cancer is inhibited by blocking SIN3A–PF1 interaction through KLF9 mediated repression of ITGA6 and ITGB1

  2021cites this paper
• Interphase Chromosomes in Replicative Senescence: Chromosome Positioning as a Senescence Biomarker and the Lack of Nuclear Motor-Driven Chromosome Repositioning in Senescent Cells

  2021cites this paper
• Co-repressor, co-activator and general transcription factor: the many faces of the Sin3 histone deacetylase (HDAC) complex

  2018cites this paper
• Cellular senescence in gastrointestinal diseases: from pathogenesis to therapeutics

  2018cites this paper
• The HDAC-Associated Sin3B Protein Represses DREAM Complex Targets and Cooperates with APC/C to Promote Quiescence

  2018cites this paper
• SIN3B promotes integrin αV subunit gene transcription and cell migration of hepatocellular carcinoma

  2018cites this paper
• The chromatin-associated Sin3B protein is required for hematopoietic stem cell functions in mice.

  2017influential citation
• MYC—Master Regulator of the Cancer Epigenome and Transcriptome

  2017cites this paper
• Oncogenic senescence: a multi-functional perspective

  2017cites this paper
• Chromatin-Associated Protein SIN3B Prevents Prostate Cancer Progression by Inducing Senescence.

  2017cites this paper
• Zebrafish sin3b mutants are viable but have size, skeletal, and locomotor defects

  2017cites this paper
• The potential of targeting Sin3B and its associated complexes for cancer therapy

  2017cites this paper
• Etude du rôle de facteurs génétiques et épigénétiques dans l'homéostasie et la fonction des cellules pancréatiques

  2017cites this paper
• The Chromatin-Associated Phf12 Protein Maintains Nucleolar Integrity and Prevents Premature Cellular Senescence

  2016cites this paper
• Emerging Roles of Epigenetic Regulator Sin3 in Cancer.

  2016cites this paper
• Implication of epigenetics in pancreas development and disease.

  2015cites this paper
• Stress-mediated Sin3B activation leads to negative regulation of subset of p53 target genes

  2015cites this paper
• Myc Levels Sin 3 b Interacts with Myc and Decreases Gene Regulation

  2014cites this paper
• Arrested development and the great escape--the role of cellular senescence in pancreatic cancer.

  2014cites this paper
• Transcriptional repression of Sin3B by Bmi-1 prevents cellular senescence and is relieved by oncogene activation

  2014influential citation
• SIN3B, the SASP, and pancreatic cancer

  2014cites this paper
• Sin3b Interacts with Myc and Decreases Myc Levels*

  2014cites this paper
• Senescence-associated SIN3B promotes inflammation and pancreatic cancer progression.

  2014influential citation
• MYC through miR-17-92 suppresses specific target genes to maintain survival, autonomous proliferation, and a neoplastic state.

  2014cites this paper
• Sin3: insight into its transcription regulatory functions.

  2013cites this paper
• Crosstalk between DNA repair and chromatin modifications

  2013cites this paper
• Small changes, big effects: chromatin goes aging.

  2013cites this paper
• Inactivate the two-faced HDAC-brake : Cell cycle regulation and tumor suppression by histone deacetylases HDAC 1 and HDAC 2

  2013influential citation
• Dissecting the complex regulation of Mad4 in glioblastoma multiforme cells

  2012cites this paper
• Role of histone deacetylase 2 in epigenetics and cellular senescence: implications in lung inflammaging and COPD.

  2012cites this paper
• Regulation of oncogene-induced cell cycle exit and senescence by chromatin modifiers

  2012cites this paper
• Tumor Suppressor Protein p53 Recruits Human Sin3B/HDAC1 Complex for Down-Regulation of Its Target Promoters in Response to Genotoxic Stress

  2011cites this paper
• A Novel Mammalian Complex Containing Sin3B Mitigates Histone Acetylation and RNA Polymerase II Progression within Transcribed Loci

  2010cites this paper
• Drosophila SIN3 Isoforms Interact with Distinct Proteins and Have Unique Biological Functions*

  2010cites this paper
• Ras-induced senescence and its physiological relevance in cancer.

  2010cites this paper
• Overlapping functions of Hdac1 and Hdac2 in cell cycle regulation and haematopoiesis

  2010cites this paper
• RNF220, an E3 ubiquitin ligase that targets Sin3B for ubiquitination.

  2010cites this paper
• Small molecule regulators of Rb-E2F pathway as modulators of transcription.

  2010cites this paper