ArticleBiochemical and biophysical research communications2009
Cloning and characterization of the 5'UTR of the rat anti-apoptotic Bcl-w gene.
Article in Biochemical and biophysical research communications, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Suppression of miR-195 attenuates oxygen-glucose deprivation/reperfusion-induced BBB destruction, possibly via targeting BCL2L2.Frontiers in neuroscience · 2026Article
- BCL-2 protein family: attractive targets for cancer therapy.Apoptosis : an international journal on programmed cell death · 2023Review
- BCL-w: apoptotic and non-apoptotic role in health and disease.Cell death & disease · 2020Review
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Authors and funding
3 authors at 2 institutions in 1 country.
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Abstract
The anti-apoptotic Bcl-w regulator, which is expressed in the developing and mature brain, not only promotes neuronal survival, but also neuronal differentiation. However, its transcriptional regulation remains to be elucidated due to a lack of knowledge of the Bcl-w promoter. Here, we report the mapping and characterization of the rat Bcl-w promoter, which is highly conserved between the human, mouse, and rat species. Using a series of 5' and 3' deletions, we mapped the TATA-less minimal Bcl-w promoter and showed that it is under a combinatorial regulation with the neurogenic bHLH transcription factor NeuroD6 mediating its activation, validating our previous finding of increased expression of the Bcl-w protein in stably transfected PC12-NeuroD6 cells. Upon stress, NeuroD6 promotes colocalization of Bcl-w with mitochondria and endoplasmic reticulum. Finally, we provide the first evidence of Bcl-w localization in the growth cones of differentiating neuronal cells, suggestive of a potential synaptic neuroprotective role.
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