Publications by authors named "Emika Nishida"
Article Synopsis
- Research indicates that etoposide causes Apaf-1 to interact with Cullin-4B, leading to increased ubiquitination and potential degradation of Apaf-1 in healthy cells.
- In situations where the proteasome is impaired, such as with MG132 treatment, ubiquitinated Apaf-1 can activate caspase-9 by forming aggregates with p62 in the cytosol, suggesting a new role for Apaf-1 in cell death pathways.
Article Synopsis
- Olfaxin is a protein mainly found in mitral and tufted cells of the olfactory bulb, with similar properties to another protein called Caytaxin, which is linked to motor dysfunction in humans and mice.
- Researchers created Prune2 gene mutant mice (Olfaxin knockouts) using CRISPR/Cas9 to study Olfaxin, resulting in reduced levels of both Olfaxin mRNA and protein in the olfactory bulb and piriform cortex.
- The knockout mice showed impaired odor preference and disrupted odor-associative learning, suggesting that Olfaxin is crucial for olfactory memory and preference though sensory and motor functions remained intact.
Patients with Alzheimer's disease (AD) experience a wide array of cognitive deficits, which typically include the impairment of explicit memory. In previous studies, the authors reported that a flavonoid, quercetin, reduces the expression of ATF4 and delays memory deterioration in an early-stage AD mouse model. In the present study, the effects of long-term quercetin intake on memory recall were assessed using contextual fear conditioning in aged wild-type mice.
View Article and Find Full Text PDFCED-4 is an mRNA-binding protein that delivers ced-3 mRNA to ribosomes.
Biochem Biophys Res Commun
January 2016
Cell death abnormal (ced)-3 and ced-4 genes regulate apoptosis to maintain tissue homeostasis in Caenorhabditis elegans. Apoptosome formation and CED-4 translocation drive CED-3 activation. However, the precise role of CED-4 translocation is not yet fully understood.
View Article and Find Full Text PDFThe production of amyloid β (Aβ) in the brain from Aβ precursor protein (APP) through γ-secretase is important for the pathogenesis of Alzheimer's disease (AD). Our previous studies have demonstrated that autophagy impairment and endoplasmic reticulum stress increase presenilin 1 expression and enhance γ-secretase activity through the phosphorylation of eukaryotic translation initiation factor 2α (eIF2α) and the translation of activating transcription factor 4 (ATF4). However, the inhibitory molecules for γ-secretase are largely unknown.
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