A novel role for high-mobility group a proteins in cellular senescence and heterochromatin formation.

By Masashi Narita, M. Narita, V. Krizhanovsky, S. Nũnez, A. Chicas, Stephen A Hearn, M. Myers, Scott W. Lowe. Cell, 2006

636 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/63e31686dfcfd69d3397aa67f50d787669787ced

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. J. Campisi
2. Jesús Gil
3. D. Peeper
4. T. Kuilman
5. F. Rodier
6. C. Michaloglou
7. W. Mooi
8. Masashi Narita

In Physiology

1. J. Campisi
2. Jesús Gil
3. F. Rodier
4. D. Peeper
5. T. Kuilman
6. Scott W. Lowe
7. V. Krizhanovsky
8. W. Mooi

Citations in the corpus

• Autophagy mediates the mitotic senescence transition. (2009, methodology): “Although it has been proposed that global and progressive epigenetic alterations play a crucial role in OIS ( Narita et al. 2006 ), the precise mechanism by which cells can achieve such a dramatic change is still unclear.”
• Cellular senescence and its effector programs (2014, background): “SAHFs are also characterized by alteration of chromatin architectural proteins, including accumulation of HMGA proteins and loss of linker histone H1 (Funayama et al. 2006; Narita et al. 2006).”
• Hmga2 promotes neural stem cell self-renewal in young, but not old, mice by reducing p16Ink4a and p19Arf expression (2008, background): “Another recent study found that HMGA1 and HMGA2 can promote cellular senescence by cooperating with p16 Ink4a to promote the formation of senescence-associated heterochromatin foci (SAHF) in cultured human fibroblasts (Narita et al., 2006).”
• Oncogenic BRAF induces senescence and apoptosis through pathways mediated by the secreted protein IGFBP7. (2008, neutral): “There have been several previous reports that loss of TP53 does not enable escape from oncogene-induced senescence (see, for example, Beausejour et al., 2003; Narita et al., 2006; Zhu et al., 1998).”
• DNA damage-induced alterations in chromatin contribute to genomic integrity and age-related changes in gene expression (2008, neutral): “Third, cells that senesce because of replicative aging in vitro or in aged tissues in vivo exhibit alterations in heterochromatin (Herbig et al., 2006; Narita et al., 2006) and secrete growth factors that can drive tumorigenesis (Campisi, 2005).”
• Senescence of activated stellate cells limits liver fibrosis (2008, background): “…liver sections from CCl4 and vehicle-treated (control) mice for a panel of senescence-associated markers, including SA-b-gal and proteins such as p16, p21, p53, and Hmga1, which have been causally linked to the senescence program (Collado et al., 2007; Narita et al., 2006; Serrano et al., 1997).”
• The essence of senescence. (2010, background): “RNAi depletion of either ASF1A or HMGA1 (a SAHF component) leads to a partial bypass of senescence (Zhang et al. 2005; Narita et al. 2006).”
• A Versatile Viral System for Expression and Depletion of Proteins in Mammalian Cells (2009, background): “Because chromo domains can bind methylated histones [76] and senescence-related growth arrest is often associated with formation of repressive chromatin structures [48,77,78], we tested whether the ARID4B chromo domain was required for the overexpression-associated growth arrest.”
• Senescence-messaging secretome: SMS-ing cellular stress (2009, background): “Induction of SAHF is linked to high mobility group A proteins and SUV39H1 (Ref”
• Directed elimination of senescent cells by inhibition of BCL-W and BCL-XL (2016, neutral): “To examine the resistance of senescent cells to intrinsic and extrinsic apoptotic pathways, we induced senescence in normal primary human fibroblasts (IMR-90), one of the most widely used cell models for the study of this program 5,22,23 .”
• Tumor suppressive functions of p53. (2009, background): “In this regard, it was found that RB directs the formation of SAHFs, senescence-associated heterochromatin foci that contain and are thought to stably silence E2F target genes (Narita et al. 2003; Narita et al. 2006).”
• Roles of HMGA proteins in cancer (2007, background): “How might HMGA proteins also act in tumour-suppressor networks? It has been shown that the HMGA proteins accumulate on chromatin in senescent fibroblasts and are essential structural components of senescence-associated heterochromatic foci (SAHFs”
• Control of the senescence-associated secretory phenotype by NF-κB promotes senescence and enhances chemosensitivity. (2011, background): “…that are associated with chromatin modifications that, in some cell types, lead to marked changes in the binding of transcription factors and other chromatin modifiers, including RB, p53, and the high-mobility group A proteins (HMGA1 and HMGA2) (Narita et al. 2003, 2006; Zhang et al. 2007).”
• Chemokine signaling via the CXCR2 receptor reinforces senescence. (2008, background): “Downregulation of CXCR2 Expression Extends Cellular Life Span Identifying genes that regulate senescence can reveal novel tumorigenic mechanisms, and several notable examples have been uncovered in different contexts (Gil et al., 2004; Narita et al., 2006; Rowland et al., 2005).”