Protection of telomeres through independent control of ATM and ATR by TRF2 and POT1

By E. L. Denchi, T. de Lange. Nature, 2007

902 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Physiology

View Paper: https://www.semanticscholar.org/paper/c0ee5bcc6a11cf20840f15bdbbbab183906c6d3c

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. Karlseder
2. T. de Lange
3. Wilhelm Palm
4. D. Hockemeyer
5. Agnel Sfeir
6. Roderick J. O’Sullivan
7. Sheila L. MacRae
8. C. Schildkraut

In Oncology

1. J. Karlseder
2. Wilhelm Palm
3. D. Hockemeyer
4. Agnel Sfeir
5. Sheila L. MacRae
6. C. Schildkraut
7. Settapong T. Kosiyatrakul
8. T. Stracker

In Physiology

1. T. de Lange
2. J. Karlseder
3. Wilhelm Palm
4. D. Hockemeyer
5. Roderick J. O’Sullivan
6. Agnel Sfeir
7. Sheila L. MacRae
8. C. Schildkraut

Citations in the corpus

• Alternative lengthening of telomeres: models, mechanisms and implications (2010, background): “POT1-related telomere dysfunction in mammals is signalled through ataxia telangiectasia and Rad3-related (ATR), which is presumably still intact in these cell”
• Telomeres: protecting chromosomes against genome instability (2010, background): “and the suppression of ataxia telangiectasia mutated ( ATM )-dependent DDR and non-homologous end joining (NHEJ”
• How shelterin protects mammalian telomeres. (2008, background): “The DNA damage signal elicited by telomeres lacking TRF2 is completely abrogated when ATM is absent (105).”
• The MRE11 complex: starting from the ends (2011, background): “However, because the fusion of dysfunctional telomeres completely depends on AT”
• Mammalian telomeres resemble fragile sites and require TRF1 for efficient replication (2009, positive): “TRF2 and POT1 contribute to the protection of chromosome ends by repressing DNA damage signaling by the ATM and ATR kinases, respectively (Denchi and de Lange, 2007).”
• Advance Publication by J-STAGE Japanese Journal of Infectious Diseases Isolation of human coronaviruses OC43, HKU1, NL63, and 229E in Yamagata, Japan, using primary human airway epithelium cells cultured by employing an air-liquid interface culture (2020, positive): “Another member of the shelterin complex, TPP1, interacts with either TIN2 or POT1 and this event facilitates the interaction between telomere-binding proteins and the G-overhang which, in turn, prevents the activation of the DNA damage response [33].”
• ATM Activation by Oxidative Stress (2010, background): “However, in mammalian cells TRF2, a component of telomere shelterin complex, represses ATM-dependent nonhomologous end joining of dysfunctional telomeres [40].”