Publications by authors named "J Paul Werthenbach"

Article Synopsis
  • cIAPs are proteins that play a crucial role in regulating TNF signaling by modifying RIPK1, and mutations in cIAP1/2 lead to severe embryonic development issues in mice due to apoptosis.
  • While a modified version of RIPK1 can rescue embryonic development, its absence in cIAP1/2 mice results in inflammation and early death after weaning.
  • The study reveals that cIAPs also control TNFR1-mediated toxicity independently of RIPK1 and RIPK3, providing new insights into TNF signaling and creating a mouse model to help evaluate treatments involving TNF inhibitors.
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Elevated expression of the X-linked inhibitor of apoptosis protein (XIAP) has been frequently reported in malignant melanoma suggesting that XIAP renders apoptosis resistance and thereby supports melanoma progression. Independent of its anti-apoptotic function, XIAP mediates cellular inflammatory signalling and promotes immunity against bacterial infection. The pro-inflammatory function of XIAP has not yet been considered in cancer.

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The vasculature represents a highly plastic compartment, capable of switching from a quiescent to an active proliferative state during angiogenesis. Metabolic reprogramming in endothelial cells (ECs) thereby is crucial to cover the increasing cellular energy demand under growth conditions. Here we assess the impact of mitochondrial bioenergetics on neovascularisation, by deleting cox10 gene encoding an assembly factor of cytochrome c oxidase (COX) specifically in mouse ECs, providing a model for vasculature-restricted respiratory deficiency.

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Caspase-8 is the initiator caspase of extrinsic apoptosis and inhibits necroptosis mediated by RIPK3 and MLKL. Accordingly, caspase-8 deficiency in mice causes embryonic lethality, which can be rescued by deletion of either Ripk3 or Mlkl. Here we show that the expression of enzymatically inactive CASP8(C362S) causes embryonic lethality in mice by inducing necroptosis and pyroptosis.

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