Abstract
Apoptosis is an evolutionarily conserved and tightly regulated cell death pathway. Physiological cell death is important for maintaining homeostasis and optimal biological conditions by continuous elimination of undesired or superfluous cells. The BH3-only pro-apoptotic members are strong inducers of apoptosis. The pro-apoptotic BH3-only protein Noxa activates multiple death pathways by inhibiting the anti-apoptotic Bcl-2 family protein, Mcl-1, and other protein members leading to Bax and Bak activation and MOMP. On the other hand, Puma is induced by p53-dependent and p53-independent apoptotic stimuli in several cancer cell lines. Moreover, this protein is involved in several physiological and pathological processes, such as immunity, cancer, and neurodegenerative diseases. Future heat shock research could disclose the effect of hyperthermia on both Noxa and BH3-only proteins. This suggests post-transcriptional mechanisms controlling the translation of both Puma and Noxa mRNA in heat-shocked cells. This study was also the chance to recapitulate the different reactional mechanisms investigated for caspases.
Highlights
Apoptosis is a regulated form of genetically programmed cell death that has significant roles in development, tissue homeostasis, and in response to environmental stresses.Regulated cell death was first described as shrinkage necrosis, due to morphological observations, and later renamed apoptosis
Another study has demonstrated that Noxa can bind to B-cell lymphoma-2 (Bcl-2), though this interaction can only be observed in Jurkat cells when they are treated with either bortezomib or
With the expression of this vital regulator of apoptosis characterized, we can go on to investigate what mechanisms are responsible for the altered expression of both p53 upregulated modulator of apoptosis (Puma) and Noxa seen in many disorders and diseases
Summary
Apoptosis is a regulated form of genetically programmed cell death that has significant roles in development, tissue homeostasis, and in response to environmental stresses. Life 2022, 12, 256 death promoter (Bad), Bcl-2-modifying factor (Bmf), activator of apoptosis 3ara-kiri (Hrk), Noxa, and Puma These proteins are responsible for activating Bax, Bak, and Bok upon receiving stress signals, though the exact mechanism is currently being investigated. By freeing up Bax/Bak, the sensitizers allow their activator relatives to bind and activate Bax/Bak [47,61] In this model, Bid, Bim, and Puma are strong inducers of apoptosis both because of high affinities to all of the anti-apoptotic Bcl-2 members and due to their ability to bypass the anti-apoptotic inhibition step and directly activate Bax/Bak. two alternate models exist to describe the activation of Bax/Bak in the OMM, genetic and biochemical evidences support the idea that both the direct and indirect models apply in many circumstances. This activates the mitochondrial outer membrane and initiates apoptosis [25,63]
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