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Times Cited: 1392
Times Cited: 1392
Times Cited
Times Co-cited
Similarity
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A biomarker that identifies senescent human cells in culture and in aging skin in vivo.
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Crucial role of p53-dependent cellular senescence in suppression of Pten-deficient tumorigenesis.
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A complex secretory program orchestrated by the inflammasome controls paracrine senescence.
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The Achilles' heel of senescent cells: from transcriptome to senolytic drugs.
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A DNA damage checkpoint response in telomere-initiated senescence.
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Senescence-associated reprogramming promotes cancer stemness.
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Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas.
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Senescence surveillance of pre-malignant hepatocytes limits liver cancer development.
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The senescence-associated secretory phenotype induces cellular plasticity and tissue regeneration.
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Cellular senescence: from physiology to pathology.
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Naturally occurring p16(Ink4a)-positive cells shorten healthy lifespan.
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Lamin B1 loss is a senescence-associated biomarker.
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Oncogene-induced senescence as an initial barrier in lymphoma development.
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An essential role for senescent cells in optimal wound healing through secretion of PDGF-AA.
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Clearance of senescent cells by ABT263 rejuvenates aged hematopoietic stem cells in mice.
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Hallmarks of Cellular Senescence.
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Persistent DNA damage signalling triggers senescence-associated inflammatory cytokine secretion.
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Chemokine signaling via the CXCR2 receptor reinforces senescence.
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Targeted Apoptosis of Senescent Cells Restores Tissue Homeostasis in Response to Chemotoxicity and Aging.
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Activation of the DNA damage checkpoint and genomic instability in human precancerous lesions.
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The role of nuclear lamin B1 in cell proliferation and senescence.
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Robust, universal biomarker assay to detect senescent cells in biological specimens.
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Cytoplasmic chromatin triggers inflammation in senescence and cancer.
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The hallmarks of aging.
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Redistribution of the Lamin B1 genomic binding profile affects rearrangement of heterochromatic domains and SAHF formation during senescence.
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Therapy-induced senescence in cancer.
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Senescence of activated stellate cells limits liver fibrosis.
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Mitochondrial Dysfunction Induces Senescence with a Distinct Secretory Phenotype.
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Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.