5 Papers
16 Citations
C Maas is an academic researcher from Netherlands Cancer Institute. The author has contributed to research in topics: Receptor & Apoptosis. The author has an hindex of 5, co-authored 5 publications.
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Papers
Apoptosis induction by Bid requires unconventional ubiquitination and degradation of its N-terminal fragment
TL;DR: It is concluded that unconventional ubiquitination and proteasome-dependent degradation of tBid-N is required to unleash the proapoptotic activity of t Bcl-2 homology 3 (BH3) domain in the cleaved complex.
Bid can mediate a pro-apoptotic response to etoposide and ionizing radiation without cleavage in its unstructured loop and in the absence of p53.
TL;DR: It is demonstrated that the Bid-dependent apoptotic pathway induced by IR and etoposide operates in MEFs that are transformed by SV40, but is not evident in E1A/Ras-transformed MEFs, implying relevance for treatment outcome.
Radiation and anticancer drugs can facilitate mitochondrial bypass by CD95/Fas via c-FLIP downregulation
TL;DR: In this article, the potential of combined modality treatment with APO010 was analyzed, and the authors concluded that c-FLIP downregulation represents a mechanism by which diverse anticancer regimens can facilitate tumor cell execution by CD95/Fas through the direct pathway of caspase activation.
Ubiquitination by the Membrane-associated RING-CH-8 (MARCH-8) Ligase Controls Steady-state Cell Surface Expression of Tumor Necrosis Factor-related Apoptosis Inducing Ligand (TRAIL) Receptor 1
Bert van de Kooij,Inge Verbrugge,Evert de Vries,Merel Gijsen,Veronica Montserrat,C Maas,Jacques Neefjes,Jannie Borst +7 more
TL;DR: It is demonstrated that TRAIL-R1 is down-regulated from the cell surface, with great preference over TRAil-R2, by exogenous expression of MARCH ligases that are implicated in endosomal trafficking, such as MARCH-1 and -8.
Smac/DIABLO release from mitochondria and XIAP inhibition are essential to limit clonogenicity of Type I tumor cells after TRAIL receptor stimulation
C Maas,Inge Verbrugge,Inge Verbrugge,E de Vries,G Savich,G Savich,L W van de Kooij,Stephen W.G. Tait,Stephen W.G. Tait,Jannie Borst +9 more
TL;DR: The mitochondrial pathway is essential for apoptotic execution of Type I tumor cells by death receptors, when long-term clonogenicity is taken into account, and this finding is relevant for cancer therapy using death receptor agonists.