Apoptosis in the nervous system

By Junying Yuan, B. Yankner. Nature, 2000

1,934 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/4d50a737e30db442fc259fa43873ddcc5ecf51ec

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. L. Reichardt
2. Mark P. Mattson
3. Yigong Shi
4. R. Simerly
5. J. Ameisen
6. E. Huang
7. Ardem Patapoutian
8. S. Lipton

In Molecular Biology

1. Yigong Shi
2. L. Reichardt
3. Mark P. Mattson
4. S. Riedl
5. J. Ameisen
6. R. Simerly
7. John Calvin Reed
8. E. Huang

In Physiology

1. Mark P. Mattson
2. L. Reichardt
3. Yigong Shi
4. R. Simerly
5. J. Ameisen
6. E. Huang
7. Ardem Patapoutian
8. T. Franke

Citations in the corpus

• Neurotrophin-regulated signalling pathways (2006, background): “In collaboration with phosphoinositide-dependent kinases, they activate the protein kinase Akt, which in turn controls through phosphorylation the activities of several proteins important in promoting cell survival (Yuan & Yankner 2000; Brunet et al. 2001; Yuan et al. 2003a).”
• Cell death and endoplasmic reticulum stress: disease relevance and therapeutic opportunities (2008, background): “Chemical inhibitors of caspases might also be considered for stroke given that mice lacking CASP1, CASP2 and CASP11 (a candidate orthologue of human CASP4 or CASP5) display resistance to stroke injur”
• The neurodevelopmental hypothesis of schizophrenia, revisited. (2009, neutral): “Interestingly, caspase 3, the caspase molecule most associated with apoptosis in the CNS(215) is not upregulated in temporal cortex of subjects with schizophrenia,(216) suggesting that chronic apoptosis is not taking place, in contrast to classic neurodegenerative disorders.(216) The vulnerability o”
• FOXO transcription factors directly activate bim gene expression and promote apoptosis in sympathetic neurons (2003, background): “Programmed cell death (PCD) accounts for the death of approximately half of all neurons generated during embryogenesis and is essential for the correct innervation of target tissues and formation of neuronal networks during neural development (Oppenheim, 1991; Yuan and Yankner, 2000).”
• Role of neuroinflammation in neurodegenerative diseases (Review) (2016, neutral): “This phenomenon, which mainly affects elder individuals (3,4), occurs in neurodegenerative diseases such as Alzheimer's disease (AD), multiple sclerosis (MS), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS) following viral infections.”
• Trk receptors: mediators of neurotrophin action. (2001, background): “There is reduced apoptosis of neurons in murine mutants lacking Caspase-9 (a protease) or Bax (a Bcl-2 family member), while increased apoptosis is observed in animals lacking Bcl-x-L (reviewed in [34]).”
• On the origin, evolution, and nature of programmed cell death: a timeline of four billion years (2002, background): “Conversely, programmed cell death dysregulation has been proposed to participate in the pathogenesis of several diseases, ranging from cancer and autoimmunity to infectious diseases and neurodegenerative disorders,(9,14,29,35) ± 45 leading to the emergence of new concepts of therapeutic intervention”
• Neurotrophins: roles in neuronal development and function. (2001, background): “…kinases, phosphatidyl inositides generated by PI-3 kinase activate the protein kinase Akt/protein kinase B. Akt then phosphorylates and controls the biological functions of several proteins important in modulating cell survival (reviewed in Datta et al 1999, Yuan & Yankner 2000).”
• PI3K/Akt and apoptosis: size matters (2003, background): “…when considering the importance of Akt for homeostasis of the organism, it is likely that pharmacological inhibition of Akt will have severe side effects for the function of several organ systems, including cardiac cells (Matsui et al., 2003) and the nervous system (Yuan and Yankner, 2000).”
• Mechanisms of caspase activation and inhibition during apoptosis. (2002, background): “On the other hand, abnor- bonuclease), which degrades the chromosomes into mal upregulation of apoptosis contributes to neurologi- nucleosomal fragments during apoptosis (Enari et al., cal disorders (Yuan and Yankner, 2000).”