Oxidative DNA damage is concurrently repaired by base excision repair (BER) and apyrimidinic endonuclease 1 (APE1)‐initiated nonhomologous end joining (NHEJ) in cortical neurons-Reference-Cited by-同舟云学术

Oxidative DNA damage is concurrently repaired by base excision repair (BER) and apyrimidinic endonuclease 1 (APE1)‐initiated nonhomologous end joining (NHEJ) in cortical neurons

Published:2019-11-06 Issue:4 Volume:46 Page:375-390
ISSN:0305-1846
Container-title:Neuropathology and Applied Neurobiology
language:en
Short-container-title:Neuropathol Appl Neurobiol

Author:

Yang J.‐L.¹^ORCID,Chen W.‐Y.¹,Mukda S.¹²,Yang Y.‐R.¹,Sun S.‐F.¹,Chen S.‐D.¹³⁴

Affiliation:

1. Institute for Translation Research in Biomedicine Kaohsiung Chang Gung Memorial Hospital Kaohsiung Taiwan

2. Research Center for Neuroscience Institute of Molecular Biosciences Mahidol University Nakhon Pathom Thailand

3. Department of Neurology Kaohsiung Chang Gung Memorial Hospital Kaohsiung Taiwan

4. College of Medicine Chang Gung University Taoyuan Taiwan

Funder

Ministry of Science and Technology, Taiwan

Chang Gung Medical Foundation

Publisher

Wiley

Subject

Physiology (medical),Neurology (clinical),Neurology,Histology,Pathology and Forensic Medicine

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1111/nan.12584

Reference57 articles.

1. Genome instability and DNA repair in brain, ageing and neurological disease

2. Accumulation of DNA Damage in Aging Neurons Occurs Through a Mechanism Other than Apoptosis

3. DNA Damage and Repair

4. Molecular Regulation of DNA Damage-Induced Apoptosis in Neurons of Cerebral Cortex

5. Oxidative genome damage and its repair: Implications in aging and neurodegenerative diseases

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