| Chapter title |
Probing the Telomere Damage Response
|
|---|---|
| Chapter number | 13 |
| Book title |
Telomeres and Telomerase
|
| Published in |
Methods in molecular biology, March 2017
|
| DOI | 10.1007/978-1-4939-6892-3_13 |
| Pubmed ID | |
| Book ISBNs |
978-1-4939-6891-6, 978-1-4939-6892-3
|
| Authors |
Rekha Rai, Sandy Chang |
| Editors |
Zhou Songyang |
| Abstract |
Telomere dysfunctions, rendered through replicative attrition of telomeric DNA or due to the removal of shelterin components, are recognized as DNA double-stranded breaks (DSBs) by the DNA damage repair (DDR) pathway. This leads to the activation of DNA damage checkpoint sensors, including the Mre11-Rad50-Nbs1 (MRN) complex, γ-H2AX and 53BP1, the ATM and ATR signal-transducing kinases, and downstream effectors, including Chk1, Chk2, and p53. Robust DNA damage response signals at dysfunctional telomeres, achieved by the complete deletion of TRF2 or by expressing dominant-negative mutant TPP1ΔRD, can be detected by their association with γ-H2AX and 53BP1 forming "telomere dysfunction induced foci (TIFs)." Induction of TIFs at telomeres provides an opportunity to quantify the extent of telomere dysfunction and monitor downstream signaling pathways. |
Mendeley readers
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|---|---|---|
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Demographic breakdown
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|---|---|---|
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| Professor | 1 | 11% |
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| Researcher | 1 | 11% |
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