ER Stress, Mitochondrial Dysfunction and Calpain/JNK Activation are Involved in Oligodendrocyte Precursor Cell Death by Unconjugated Bilirubin-Reference-Cited by-同舟云学术

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ER Stress, Mitochondrial Dysfunction and Calpain/JNK Activation are Involved in Oligodendrocyte Precursor Cell Death by Unconjugated Bilirubin

Published:2012-06-17 Issue:4 Volume:14 Page:285-302
ISSN:1535-1084
Container-title:NeuroMolecular Medicine
language:en
Short-container-title:Neuromol Med

Author:

Barateiro Andreia,Vaz Ana Rita,Silva Sandra Leitão,Fernandes Adelaide,Brites Dora

Publisher

Springer Science and Business Media LLC

Subject

Cellular and Molecular Neuroscience,Neurology,Molecular Medicine

Link

http://link.springer.com/content/pdf/10.1007/s12017-012-8187-9.pdf

Reference93 articles.

1. Ahdab-Barmada, M., & Moossy, J. (1984). The neuropathology of kernicterus in the premature neonate: Diagnostic problems. Journal of Neuropathology and Experimental Neurology, 43(1), 45–56.

2. Benarroch, E. E. (2009). Oligodendrocytes: Susceptibility to injury and involvement in neurologic disease. Neurology, 72(20), 1779–1785.

3. Benjamins, J. A., Nedelkoska, L., & George, E. B. (2003). Protection of mature oligodendrocytes by inhibitors of caspases and calpains. Neurochemical Research, 28(1), 143–152.

4. Bernales, S., Papa, F. R., & Walter, P. (2006). Intracellular signaling by the unfolded protein response. Annual Review of Cell and Developmental Biology, 22, 487–508.

5. Bogler, O., Wren, D., Barnett, S. C., Land, H., & Noble, M. (1990). Cooperation between two growth factors promotes extended self-renewal and inhibits differentiation of oligodendrocyte-type-2 astrocyte (O-2A) progenitor cells. Proc Natl Acad Sci USA, 87(16), 6368–6372.

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