Literature DB >> 12022953

Mitochondrial involvement in the point of no return in neuronal apoptosis.

L K Chang1, G V Putcha, M Deshmukh, E M Johnson.   

Abstract

Programmed cell death (PCD) contributes to development, maintenance, and pathology in various tissues, including the nervous system. Many molecular, biochemical, and genetic events occur within cells undergoing PCD. Some of these events are incompatible with long-term cell survival because they have irreversible, catastrophic consequences. The onset of such changes marks the point of no return, a decisive regulatory event termed 'the commitment-to-die.' In this review, we discuss events that underlie the commitment-to-die in nerve growth factor-deprivation-induced death of sympathetic neurons. Findings in this model system implicate the mitochondrion as an important site of regulation for the commitment-to-die in the presence or absence of caspase inhibition.

Entities:  

Mesh:

Substances:

Year:  2002        PMID: 12022953     DOI: 10.1016/s0300-9084(02)01372-x

Source DB:  PubMed          Journal:  Biochimie        ISSN: 0300-9084            Impact factor:   4.079


  35 in total

1.  Serum or target deprivation-induced neuronal death causes oxidative neuronal accumulation of Zn2+ and loss of NAD+.

Authors:  Christian T Sheline; Ai-Li Cai; Julia Zhu; Chunxiao Shi
Journal:  Eur J Neurosci       Date:  2010-08-16       Impact factor: 3.386

Review 2.  Programmed cell death 50 (and beyond).

Authors:  R A Lockshin
Journal:  Cell Death Differ       Date:  2015-11-13       Impact factor: 15.828

Review 3.  Apoptotic cell death regulation in neurons.

Authors:  Emilie Hollville; Selena E Romero; Mohanish Deshmukh
Journal:  FEBS J       Date:  2019-07-12       Impact factor: 5.542

Review 4.  BAX to basics: How the BCL2 gene family controls the death of retinal ganglion cells.

Authors:  Margaret E Maes; Cassandra L Schlamp; Robert W Nickells
Journal:  Prog Retin Eye Res       Date:  2017-01-04       Impact factor: 21.198

5.  Methazolamide and melatonin inhibit mitochondrial cytochrome C release and are neuroprotective in experimental models of ischemic injury.

Authors:  Xin Wang; Bryan E Figueroa; Irina G Stavrovskaya; Yi Zhang; Ana C Sirianni; Shan Zhu; Arthur L Day; Bruce S Kristal; Robert M Friedlander
Journal:  Stroke       Date:  2009-03-19       Impact factor: 7.914

6.  Bax induces cytochrome c release by multiple mechanisms in mitochondria from MCF7 cells.

Authors:  Nancy P Gómez-Crisóstomo; Rebeca López-Marure; Estrella Zapata; Cecilia Zazueta; Eduardo Martínez-Abundis
Journal:  J Bioenerg Biomembr       Date:  2013-03-28       Impact factor: 2.945

7.  Cyclosporin A enhances colchicine-induced apoptosis in rat cerebellar granule neurons.

Authors:  Anna Maria Canudas; Elvira G Jordà; Ester Verdaguer; Andrés Jiménez; Francesc Xavier Sureda; Víctor Rimbau; Antoni Camins; Mercè Pallàs
Journal:  Br J Pharmacol       Date:  2004-02       Impact factor: 8.739

8.  Histone H4 deacetylation plays a critical role in early gene silencing during neuronal apoptosis.

Authors:  Heather R Pelzel; Cassandra L Schlamp; Robert W Nickells
Journal:  BMC Neurosci       Date:  2010-05-26       Impact factor: 3.288

9.  The apoptotic response in HCT116BAX-/- cancer cells becomes rapidly saturated with increasing expression of a GFP-BAX fusion protein.

Authors:  Sheila J Semaan; Robert W Nickells
Journal:  BMC Cancer       Date:  2010-10-13       Impact factor: 4.430

10.  Abeta oligomers and fibrillar aggregates induce different apoptotic pathways in LAN5 neuroblastoma cell cultures.

Authors:  Pasquale Picone; Rita Carrotta; Giovanna Montana; Maria Rita Nobile; Pier Luigi San Biagio; Marta Di Carlo
Journal:  Biophys J       Date:  2009-05-20       Impact factor: 4.033

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.