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Maria Eugenia Guicciardi

Researcher at Mayo Clinic

Publications -  52
Citations -  5444

Maria Eugenia Guicciardi is an academic researcher from Mayo Clinic. The author has contributed to research in topics: Apoptosis & Liver injury. The author has an hindex of 27, co-authored 52 publications receiving 4927 citations. Previous affiliations of Maria Eugenia Guicciardi include University of Modena and Reggio Emilia.

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NOTCH3 expression is linked to breast cancer seeding and distant metastasis

TL;DR: The key role of NOTCH3 oncogenic signaling in the genesis of breast cancer metastasis is demonstrated and provided a compelling preclinical rationale for the design of novel therapeutic strategies that will selectively target NotCH3 to halt metastatic seeding and to improve the clinical outcomes of patients with breast cancer.
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Tumor Necrosis Factor-related Apoptosis-inducing Ligand (TRAIL) Protein-induced Lysosomal Translocation of Proapoptotic Effectors Is Mediated by Phosphofurin Acidic Cluster Sorting Protein-2 (PACS-2)

TL;DR: It is reported that TRAIL induces recruitment of the multifunctional sorting protein phosphofurin acidic cluster sorting protein-2 (PACS-2) to DR5-positive endosomes in Huh-7 cells where it forms an immunoprecipitatable complex with Bim and Bax on lysosomal membranes.
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cFLIPL prevents TRAIL-induced apoptosis of hepatocellular carcinoma cells by inhibiting the lysosomal pathway of apoptosis.

TL;DR: It is demonstrated that lysosomal permeabilization contributes to TRAIL-induced apoptosis of hepatocellular carcinoma cells and suggested that cFLIP(L) cytoprotection is, in part, due to p42/44 MAPK-dependent inhibition of lysOSomal breakdown.
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Cellular inhibitor of apoptosis 1 (cIAP-1) degradation by caspase 8 during TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis.

TL;DR: It is demonstrated that TRAIL-induced apoptosis of liver cancer cells is associated with degradation of cI AP-1 and X-linked IAP (XIAP), whereas cIAP-2 remains unchanged, and results suggest that TRAil-mediated apoptosis proceeds through caspase 8-dependent degradation ofCiAP-1.