Measuring Composition of CD95 Death-Inducing Signaling Complex and Processing of Procaspase-8 in this Complex

Hillert-Richter, Laura K.; Lavrik, Inna N.

doi:10.3791/62842

Cited by 4 publications

(1 citation statement)

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“…Subsequently, the death-inducing signalling complex (DISC), a ligand-receptor-adaptor protein complex, is formed by a sequential process. The death ligand of DISC binds to DR to recruit an adaptor protein in order (98,99). The DISC activates caspase-8, which initiates apoptosis through cleavage of the downstream caspases (97).…”

Section: The Mechanism Of Apoptosis In Glaucomamentioning

confidence: 99%

Apoptosis in glaucoma: A new direction for the treatment of glaucoma (Review)

Xia,

Zhang

2024

Mol Med Rep

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Glaucoma is a group of progressive optic nerve disorders characterized by the loss of retinal ganglion cells, a thinner retinal nerve fibre layer and cupping of the optic disk. Apoptosis is a physiological cell death process regulated by genes and plays a crucial role in maintaining tissue homeostasis, ensuring the natural development and immune defence of organisms. Apoptosis has been associated with glaucoma and inhibiting apoptosis by activating phosphatidylinositol 3-kinase-protein kinase B or other medicines can rescue pathological changes in glaucoma. Due to the complex crosstalk of apoptosis pathways, the pathophysiological mechanism of apoptosis in glaucoma needs to be fully elucidated. The present review aimed to discuss the mechanism of cell apoptosis in glaucoma, improve the understanding of the pathophysiology of glaucoma, summarize new directions for the treatment of glaucoma and lay the foundation for new treatment strategies for glaucoma.

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Section: The Mechanism Of Apoptosis In Glaucomamentioning

confidence: 99%

Apoptosis in glaucoma: A new direction for the treatment of glaucoma (Review)

Xia,

Zhang

2024

Mol Med Rep

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IRE1 RNase controls CD95-mediated cell death

Pelizzari-Raymundo,

Maltret,

Nivet

et al. 2024

EMBO Rep

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Signalling by the Unfolded Protein Response (UPR) or by the Death Receptors (DR) are frequently activated towards pro-tumoral outputs in cancer. Herein, we demonstrate that the UPR sensor IRE1 controls the expression of the DR CD95/Fas, and its cell death-inducing ability. Both genetic and pharmacologic blunting of IRE1 activity increased CD95 expression and exacerbated CD95L-induced cell death in glioblastoma (GB) and Triple-Negative Breast Cancer (TNBC) cell lines. In accordance, CD95 mRNA was identified as a target of Regulated IRE1-Dependent Decay of RNA (RIDD). Whilst CD95 expression is elevated in TNBC and GB human tumours exhibiting low RIDD activity, it is surprisingly lower in XBP1s-low human tumour samples. We show that IRE1 RNase inhibition limited CD95 expression and reduced CD95-mediated hepatic toxicity in mice. In addition, overexpression of XBP1s increased CD95 expression and sensitized GB and TNBC cells to CD95L-induced cell death. Overall, these results demonstrate the tight IRE1-mediated control of CD95-dependent cell death in a dual manner through both RIDD and XBP1s, and they identify a novel link between IRE1 and CD95 signalling.

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