Anamorsin, a Novel Caspase-3 Substrate in Neurodegeneration

Yun, Nuri; Lee, Young Mook; Kim, Chiho; Shibayama, Hirohiko; Tanimura, Akira; Hamanaka, Yuri; Park, Il Seon; Jo, Areum; Shin, Joo‐Ho; Ju, Chung; Kim, Won Ki; Oh, Young J.

doi:10.1074/jbc.m114.552679

Cited by 10 publications

(9 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Caspase-3 activation is involved in most pathways of neuronal apoptosis (Yun et al 2014;Zhang et al 2014). Active caspase-3 and Bcl-2 have been shown to play important roles in proapoptotic and anti-apoptotic processes, respectively, during programmed cell death (Jia et al 2014).…”

Section: Discussionmentioning

confidence: 99%

Upregulation of Interferon Regulatory Factor 6 Promotes Neuronal Apoptosis After Traumatic Brain Injury in Adult Rats

Lin

et al. 2015

Cell Mol Neurobiol

View full text Add to dashboard Cite

The interferon regulatory factor (IRF) family was first discovered as a set of transcriptional regulators of the type I interferon system in 1988. In mammals, the IRF family includes nine members that play important roles in the immune system, oncogenesis, and apoptosis. However, the distribution and the function of IRF6 in the central nervous system are limited. In this study, we established an adult rat traumatic brain injury (TBI) model. Compared to the sham brain cortex, Western blot and immunohistochemistry showed significant upregulation of IRF6 in the ipsilateral brain cortex after TBI. Immunofluorescence double-labeling showed that IRF6 completely co-localized with neurons, not astrocytes or oligodendrocytes. Furthermore, we detected that the neuronal apoptosis marker active caspase-3 co-localized with IRF6 in neurons. Additionally, IRF6 knockdown in PC12 cells in vitro resulted in a decrease in active caspase-3 expression and an increase in Bcl-2 and p-Akt expression. We conclude that IRF6 might promote neuronal apoptosis by inhibiting Akt phosphorylation after TBI.

show abstract

Section: Discussionmentioning

confidence: 99%

Upregulation of Interferon Regulatory Factor 6 Promotes Neuronal Apoptosis After Traumatic Brain Injury in Adult Rats

Lin

et al. 2015

Cell Mol Neurobiol

View full text Add to dashboard Cite

show abstract

“…Caspases, a family of thiol proteases, are activated during the neurodegenerative process of AD and play an important regulating role in the apoptotic cascade [37, 38]. A feature of caspases in the cell is that they exist as zymogens, termed pro-caspases, which are inactive until a biochemical change causes their activation [39].…”

Section: Discussionmentioning

confidence: 99%

Cerebral mTOR signal and pro-inflammatory cytokines in Alzheimer’s disease rats

Wang

et al. 2016

Translational Neuroscience

View full text Add to dashboard Cite

As a part of Alzheimer’s disease (AD) development the mammalian target of rapamycin (mTOR) has been reported to play a crucial role in regulating cognition and can be used as a neuronal marker. Neuro-inflammation is also a cause of the pathophysiological process in AD. Thus, we examined the protein expression levels of mTOR and its downstream pathways as well as pro-inflammatory cytokines (PICs) in the brain of AD rats. We further examined the effects of blocking mTOR on PICs, namely IL-1β, IL-6 and TNF-α. Our results showed that the protein expression of p-mTOR, mTOR-mediated phosphorylation of 4E-binding protein 4 (4E-BP1) and p70 ribosomal S6 protein kinase 1 (S6K1) pathways were amplified in the hippocampus of AD rats compared with controls. Blocking mTOR by using rapamycin selectively enhanced activities of IL-6 and TNF-α signaling pathways, which was accompanied with an increase of Caspase-3, indicating cellular apoptosis and worsened learning performance. In conclusion, our data for the first time revealed specific signaling pathways engaged in the development of AD, including a regulatory role by the activation of mTOR in PIC mechanisms. Stimulation of mTOR is likely to play a beneficial role in modulating neurological deficits in AD.Targeting one or more of these signaling molecules may present with new opportunities for treatment and clinical management of AD

show abstract

“…69 Caspase-3 cleaves DCTN2. 70 PKC-zeta phosphorylates PLD2 and increases its activity. 71 PLD2 was cleaved by caspase-3, 8 and 9.…”

Section: Network Analysis Of Selected Proteinsmentioning

confidence: 99%

“…83 CXCR4 has been predicted as microRNA 9 target, using three algorithms TargetscanS, MiRanda and PicTar. 84 Caspase-3 cleaves Calponin-3. 84 UHRF1 binds histone lysine methyltransferase G9a, and both are co-localized in the nucleus in a cell-cycle-dependent manner.…”

Section: Network Analysis Of Selected Proteinsmentioning

confidence: 99%

See 1 more Smart Citation

Bioinformatics Predictions of Fas Related Protein Network

WeijunGuan

2016

j comput theor nanosci

View full text Add to dashboard Cite

Fas is a cell surface receptor that, when engaged by Fas ligand (FasL) or specific agonistic antibodies, triggers apoptosis. Binding of an adaptor protein, FADD, to the death-effector domain of Fas activates a cascade of cysteine proteases known as caspases that cleave cellular substrates, resulting in cell death. The aim of this study was to systematically construct the global proteinprotein interaction (PPI) network and predict Fas related protein connections by network analysis using MetaCore.

show abstract

Anamorsin, a Novel Caspase-3 Substrate in Neurodegeneration

Cited by 10 publications

References 54 publications

Upregulation of Interferon Regulatory Factor 6 Promotes Neuronal Apoptosis After Traumatic Brain Injury in Adult Rats

Upregulation of Interferon Regulatory Factor 6 Promotes Neuronal Apoptosis After Traumatic Brain Injury in Adult Rats

Cerebral mTOR signal and pro-inflammatory cytokines in Alzheimer’s disease rats

Bioinformatics Predictions of Fas Related Protein Network

Contact Info

Product

Resources

About