Lamin B1 loss is a senescence-associated biomarker

By Adam Freund, Rémi-Martin Laberge, M. Demaria, J. Campisi. Molecular Biology of the Cell, 2012

933 citations recorded by the source corpus.

This study rigorously defines lamin B1 loss as a marker of senescence in response to all classic signals of senescence, including DNA damage, oncogene activation, and replicative exhaustion. This decline is induced by activation of either the p53 or the pRb pathway and occurs in vivo in response to a senescence-inducing dose of radiation.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/ab67425e2a1cc09cc28636c4038021efbb8e7414

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Citations in the corpus

Cellular senescence and its effector programs (2014, background): “Since then, several studies have confirmed the reduction of LMNB1 in various senescent cell types (Barascu et al. 2012; Freund et al. 2012; Dreesen et al. 2013; Sadaie et al. 2013; Shah et al. 2013).”
Cellular Senescence: Defining a Path Forward. (2019, positive): “Downregulation of lamin B1, a major component of the nuclear lamina, is another key feature of senescence (Dou et al., 2015; Freund et al., 2012; Shah et al., 2013; Shimi et al., 2011).”
The hallmarks of aging. (2013, background): “In addition to these age-associated changes in A-type lamins, lamin B1 levels decline during cell senescence, pointing to its utility as a biomarker of this process (Freund et al., 2012; Shimi et al., 2011).”
Cellular senescence promotes adverse effects of chemotherapy and cancer relapse (2016, methodology): “and elevated levels of p21 and reduced levels of LaminB1 and intracellular HMGB1 proteins (5, 18, 19) using western analyses (Fig.”
Innate immune sensing of cytosolic chromatin fragments through cGAS promotes senescence (2017, positive): “Degradation of the nuclear envelope component lamin B1 and the occurrence of cytosolic chromatin fragments (CCFs) are well-described features of senescent cells 43 31.”
Long Noncoding RNA MALAT1 Controls Cell Cycle Progression by Regulating the Expression of Oncogenic Transcription Factor B-MYB (2013, background): “Recent studies have demonstrated specific loss of nuclear lamina associated lamin B1 in senescent cells [55,56].”
Mitochondrial Dysfunction Induces Senescence with a Distinct Secretory Phenotype (2015, background): “Nonetheless, SIRT3 depletion induced three senescence markers: reduced lamin B1 (LMNB1) levels (Freund et al., 2012), decreased nuclear localization of high mobility group protein B1 (HMGB1) (Davalos et al.”
Targeted Apoptosis of Senescent Cells Restores Tissue Homeostasis in Response to Chemotoxicity and Aging (2017, methodology): “For stable transduction of HRASG12V, we used pLENTI-Puro (670-1)-HRASG12V(Freund et al., 2012).”
Aging, Cellular Senescence, and Cancer (2012, background): “Senescent cells also markedly downregulate expression of the nuclear lamina protein lamin B1 (LMNB1) (89, 90).”
An Essential Role for Senescent Cells in Optimal Wound Healing through Secretion of PDGF-AA. (2026, methodology): “We conﬁrmed senescence by decreased DNA synthesis, increased SA-b -gal activity (Figure S1B), increased levels of mRNAs encoding p16 INK4a , p21, and the SASP factors interleukin-6 (IL-6) and MMP-3, and decreased levels of the mRNA encoding laminB1 (Freund et al., 2012) (Figure 1B).”
Hallmarks of Cellular Senescence. (2018, positive): “Reactive oxygen species (ROS): by-products of mitochondrial respiration [143].”