Biochemical and Biophysical Research Communications
Regular Articlebcl-2 Gene Is Highly Expressed during Neurogenesis in the Central Nervous System
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The role of Bcl-2 proteins in modulating neuronal Ca<sup>2+</sup> signaling in health and in Alzheimer's disease
2021, Biochimica et Biophysica Acta - Molecular Cell ResearchCitation Excerpt :It should be noted that changes in Ca2+ homeostasis of the ER have been shown to induce apoptosis in neurons [134]. As Bcl-2 expression decreases after neurulation, Bcl-XL expression increases and remains elevated throughout neuronal ontogeny with the highest levels in differentiating cells [102,121]. It was demonstrated that Bcl-XL may regulate programmed cell death via supporting the viability of immature cells during the development of the nervous and hematopoietic systems.
Differentiated NSC-34 motoneuron-like cells as experimental model for cholinergic neurodegeneration
2013, Neurochemistry InternationalCitation Excerpt :This effect is associated with an over-expression of Bcl-2 during differentiation and diminished apoptotic response to pro-apoptotic chemicals in vitro (Itano et al., 1996; Lasorella et al., 1995; Lombet et al., 2001; Tieu et al., 1999). Immunohistochemistry data from human and mouse embryonic brain tissues furthermore revealed increased expression of Bcl-2 in developing neural cells (Abe-Dohmae et al., 1993; Merry et al., 1994) supporting the view that Bcl-2, besides being protective and anti-apoptotic might be implicated in neuronal differentiation and survival. In conclusion, differentiation of NSC-34 cells using atRA may serve as a suitable model for analyzing motoneuron development, including cholinergic and morphological maturation.
Insulin promotes neuronal survival via the alternatively spliced protein kinase CδII isoform
2012, Journal of Biological ChemistryCitation Excerpt :We are cloning a PKCδII splicing minigene to further study the molecular mechanisms of alternative splicing of PKCδII mRNA regulated by insulin, thereby evaluating the interplay of PKCδII cis-elements with their trans-factors. Here we demonstrated that insulin acts through PKCδII to increase expression of the pro-survival proteins Bcl2 and bcl-xL, which increase neurogenesis and neuronal survival (34, 46–51). Our results with insulin treatment and in cells overexpressing PKCδII show an increase in phosphorylation of BAD at Ser-136, which indicates that this increase occurs via the AKT pathway and not the ERK or PKA pathways, because we did not see increases at Ser-122 or Ser-115.
What can we learn from mice lacking pro-survival BCL-2 proteins to advance BH3 mimetic drugs for cancer therapy?
2022, Cell Death and Differentiation