DNA damage foci at dysfunctional telomeres.

By H. Takai, A. Smogorzewska, T. de Lange. Current Biology, 2003

1,466 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Physiology

View Paper: https://www.semanticscholar.org/paper/37a168534155a7bddf1d69b0866e10d8e499d3ae

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

In Oncology

In Physiology

Citations in the corpus

Telomeres and aging. (2008, background): “However, it has become clear that telomeres are directly responsible for sustained DNA damage signals in senescent cells (54, 203), and DNA damage foci originating from telomeres in senescent cells can readily be detected in vivo (104).”
Telomeres are favoured targets of a persistent DNA damage response in ageing and stress-induced senescence (2012, background): “Telomere-induced foci can be induced by experimental disruption of shelterin components such as TRF2 and POT”
Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors. (2005, background): “…that nuclear oci containing markers of DNA double strand breaks orm at critically short or dysfunctional telomeres d’Adda di Fagagna et al., 2003; Takai et al., 2003). oreover, dysfunctional telomeres activate many comonents of the p53-mediated damage response, and he senescence response to…”
Mitochondrial Dysfunction Accounts for the Stochastic Heterogeneity in Telomere-Dependent Senescence (2007, neutral): “signalling pathway leading to senescence [8,45–47].”
How shelterin solves the telomere end-protection problem. (2010, background): “Cytologically, these events are readily detectable as the occurrence of numerous DNA-damage foci that colocalize with telomeric markers (referred to as telomere dysfunction-induced foci [TIFs]; Takai et al. 2003).”
DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis (2005, background): “, can mimic DNA damage and activate the ATM/ATR-dependent checkpoints, thereby contributing to replicative senescence in cultured cell”
Living on a break: cellular senescence as a DNA-damage response (2008, background): “When telomeres shorten below a threshold length, an unrestrained DDR is activated that is manifested by the appearance of DDR foci in proximity to telomeric DNA and proteins and by the tight association of DDR factors with telomeric DNA in chromatin immunoprecipitation experiment”
Mammalian telomeres resemble fragile sites and require TRF1 for efficient replication (2009, positive): “Consistent with a DNA replication defect, cells lacking TRF1 showed a strong telomere damage response phenotype, as evidenced by 53BP1 and g -H2AX telomere dysfunction-induced foci (TIFs) (Takai et al., 2003) (Figures 3A, 3B, and S4).”
Senescence impairs successful reprogramming to pluripotent stem cells. (2009, background): “Accordingly DNA damage markers such as γH2AX (phosphorylated histone 2A variant X), are detected at the chromosomes ends of cells reaching replicative exhaustion and in stalk replication forks in cells suffering from oncogenic stress (Di Micco et al., 2006; Takai et al., 2003).”
Telomeres: protecting chromosomes against genome instability (2010, background): “These are almost identical to the foci detected at sites of breaks and repair following irradiation-induced DNA damag”
How shelterin protects mammalian telomeres. (2008, background): “The telomeric origin of the DNA damage signal is evident from cytological studies that showed the presence of 53BP1, MDC1, and γ-H2AX at chromosome ends (45, 52, 180).”