Modulation of DNA base excision repair during neuronal differentiation

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Modulation of DNA base excision repair during neuronal differentiation. / Sykora, Peter; Yang, Jenq-Lin; Ferrarelli, Leslie K; Tian, Jingyan; Tadokoro, Takashi; Kulkarni, Avanti; Weissman, Lior; Keijzers, Guido; Wilson, David M; Mattson, Mark P; Bohr, Vilhelm A.

In: Neurobiology of Aging, Vol. 34, No. 7, 07.2013, p. 1717-27.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Sykora, P, Yang, J-L, Ferrarelli, LK, Tian, J, Tadokoro, T, Kulkarni, A, Weissman, L, Keijzers, G, Wilson, DM, Mattson, MP & Bohr, VA 2013, 'Modulation of DNA base excision repair during neuronal differentiation', Neurobiology of Aging, vol. 34, no. 7, pp. 1717-27. https://doi.org/10.1016/j.neurobiolaging.2012.12.016

APA

Sykora, P., Yang, J-L., Ferrarelli, L. K., Tian, J., Tadokoro, T., Kulkarni, A., Weissman, L., Keijzers, G., Wilson, D. M., Mattson, M. P., & Bohr, V. A. (2013). Modulation of DNA base excision repair during neuronal differentiation. Neurobiology of Aging, 34(7), 1717-27. https://doi.org/10.1016/j.neurobiolaging.2012.12.016

Vancouver

Sykora P, Yang J-L, Ferrarelli LK, Tian J, Tadokoro T, Kulkarni A et al. Modulation of DNA base excision repair during neuronal differentiation. Neurobiology of Aging. 2013 Jul;34(7):1717-27. https://doi.org/10.1016/j.neurobiolaging.2012.12.016

Author

Sykora, Peter ; Yang, Jenq-Lin ; Ferrarelli, Leslie K ; Tian, Jingyan ; Tadokoro, Takashi ; Kulkarni, Avanti ; Weissman, Lior ; Keijzers, Guido ; Wilson, David M ; Mattson, Mark P ; Bohr, Vilhelm A. / Modulation of DNA base excision repair during neuronal differentiation. In: Neurobiology of Aging. 2013 ; Vol. 34, No. 7. pp. 1717-27.

Bibtex

@article{2846390fd3e247a3b61f0ffc42e343c8,
title = "Modulation of DNA base excision repair during neuronal differentiation",
abstract = "Neurons are terminally differentiated cells with a high rate of metabolism and multiple biological properties distinct from their undifferentiated precursors. Previous studies showed that nucleotide excision DNA repair is downregulated in postmitotic muscle cells and neurons. Here, we characterize DNA damage susceptibility and base excision DNA repair (BER) capacity in undifferentiated and differentiated human neural cells. The results show that undifferentiated human SH-SY5Y neuroblastoma cells are less sensitive to oxidative damage than their differentiated counterparts, in part because they have robust BER capacity, which is heavily attenuated in postmitotic neurons. The reduction in BER activity in differentiated cells correlates with diminished protein levels of key long patch BER components, flap endonuclease-1, proliferating cell nuclear antigen, and ligase I. Thus, because of their higher BER capacity, proliferative neural progenitor cells are more efficient at repairing DNA damage compared with their neuronally differentiated progeny.",
author = "Peter Sykora and Jenq-Lin Yang and Ferrarelli, {Leslie K} and Jingyan Tian and Takashi Tadokoro and Avanti Kulkarni and Lior Weissman and Guido Keijzers and Wilson, {David M} and Mattson, {Mark P} and Bohr, {Vilhelm A}",
note = "Published by Elsevier Inc.",
year = "2013",
month = jul,
doi = "10.1016/j.neurobiolaging.2012.12.016",
language = "English",
volume = "34",
pages = "1717--27",
journal = "Neurobiology of Aging",
issn = "0197-4580",
publisher = "Elsevier",
number = "7",

}

RIS

TY - JOUR

T1 - Modulation of DNA base excision repair during neuronal differentiation

AU - Sykora, Peter

AU - Yang, Jenq-Lin

AU - Ferrarelli, Leslie K

AU - Tian, Jingyan

AU - Tadokoro, Takashi

AU - Kulkarni, Avanti

AU - Weissman, Lior

AU - Keijzers, Guido

AU - Wilson, David M

AU - Mattson, Mark P

AU - Bohr, Vilhelm A

N1 - Published by Elsevier Inc.

PY - 2013/7

Y1 - 2013/7

N2 - Neurons are terminally differentiated cells with a high rate of metabolism and multiple biological properties distinct from their undifferentiated precursors. Previous studies showed that nucleotide excision DNA repair is downregulated in postmitotic muscle cells and neurons. Here, we characterize DNA damage susceptibility and base excision DNA repair (BER) capacity in undifferentiated and differentiated human neural cells. The results show that undifferentiated human SH-SY5Y neuroblastoma cells are less sensitive to oxidative damage than their differentiated counterparts, in part because they have robust BER capacity, which is heavily attenuated in postmitotic neurons. The reduction in BER activity in differentiated cells correlates with diminished protein levels of key long patch BER components, flap endonuclease-1, proliferating cell nuclear antigen, and ligase I. Thus, because of their higher BER capacity, proliferative neural progenitor cells are more efficient at repairing DNA damage compared with their neuronally differentiated progeny.

AB - Neurons are terminally differentiated cells with a high rate of metabolism and multiple biological properties distinct from their undifferentiated precursors. Previous studies showed that nucleotide excision DNA repair is downregulated in postmitotic muscle cells and neurons. Here, we characterize DNA damage susceptibility and base excision DNA repair (BER) capacity in undifferentiated and differentiated human neural cells. The results show that undifferentiated human SH-SY5Y neuroblastoma cells are less sensitive to oxidative damage than their differentiated counterparts, in part because they have robust BER capacity, which is heavily attenuated in postmitotic neurons. The reduction in BER activity in differentiated cells correlates with diminished protein levels of key long patch BER components, flap endonuclease-1, proliferating cell nuclear antigen, and ligase I. Thus, because of their higher BER capacity, proliferative neural progenitor cells are more efficient at repairing DNA damage compared with their neuronally differentiated progeny.

U2 - 10.1016/j.neurobiolaging.2012.12.016

DO - 10.1016/j.neurobiolaging.2012.12.016

M3 - Journal article

C2 - 23375654

VL - 34

SP - 1717

EP - 1727

JO - Neurobiology of Aging

JF - Neurobiology of Aging

SN - 0197-4580

IS - 7

ER -

ID: 47451185