ORCID Profile
0000-0002-5070-1329
Current Organisation
Karl-Franzens-Universität Graz
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Publisher: Springer Science and Business Media LLC
Date: 23-01-2018
Publisher: Informa UK Limited
Date: 02-09-2014
Publisher: Elsevier BV
Date: 03-2020
Publisher: EMBO
Date: 30-08-2021
Publisher: Springer Science and Business Media LLC
Date: 21-08-2011
DOI: 10.1038/NM.2439
Publisher: Cold Spring Harbor Laboratory
Date: 15-01-2004
DOI: 10.1101/GAD.287604
Abstract: During Drosophila embryogenesis, developing muscles extend growth-cone–like structures to navigate toward specific epidermal attachment sites. Here, we show that the homolog of Glutamate Receptor–Interacting Proteins (DGrip) acts as a key component of proper muscle guidance. Mutations in dgrip impair patterning of ventral longitudinal muscles (VLMs), whereas lateral transverse muscles (LTMs) that attach to intrasegmental attachment sites develop normally. Myoblast fusion, stabilization of muscle contacts, and general muscle function are not impaired in the absence of DGrip. Instead, the proper formation of cellular extensions during guidance fails in dgrip mutant VLMs. DGrip protein concentrates at the ends of VLMs while these muscles guide toward segment border attachment sites. Conversely, LTMs overexpressing DGrip form ectopic cellular extensions that can cause attachment of these muscles to other muscles at segment borders. Our data suggest that DGrip participates in the reception of an attractive signal that emanates from the epidermal attachment sites to direct the motility of developing muscles. This dgrip phenotype should be valuable to study mechanistic principles of Grip function.
Publisher: American Association for the Advancement of Science (AAAS)
Date: 28-09-2012
Abstract: Cancer cells are often aneuploid that is, they have an abnormal number of chromosomes. But to what extent this contributes to the tumorigenic phenotype is not clear. Senovilla et al. (p. 1678 see the Perspective by Zanetti and Mahadevan ) found that tetraploidization of cancer cells can cause them to become immunogenic and thus aid in their clearance from the body by the immune system. Cells with excess chromosomes put stress on the endoplasmic reticulum, which leads to movement of the protein calreticulin to the cell surface. Calreticulin exposure in turn caused recognition of cancer cells in mice by the host immune system. Thus, the immune system appears to serve a protective role in eliminating hyperploid cells that must be overcome to allow unrestricted growth of cancer cells.
Publisher: Informa UK Limited
Date: 04-2012
DOI: 10.4161/AUTO.19496
Publisher: EMBO
Date: 08-06-2017
Abstract: Over the past two decades, the molecular machinery that underlies autophagic responses has been characterized with ever increasing precision in multiple model organisms. Moreover, it has become clear that autophagy and autophagy‐related processes have profound implications for human pathophysiology. However, considerable confusion persists about the use of appropriate terms to indicate specific types of autophagy and some components of the autophagy machinery, which may have detrimental effects on the expansion of the field. Driven by the overt recognition of such a potential obstacle, a panel of leading experts in the field attempts here to define several autophagy‐related terms based on specific biochemical features. The ultimate objective of this collaborative exchange is to formulate recommendations that facilitate the dissemination of knowledge within and outside the field of autophagy research.
Publisher: Wiley
Date: 22-04-2015
DOI: 10.1111/ACEL.12338
Publisher: Springer Netherlands
Date: 2011
Publisher: Elsevier BV
Date: 06-2016
Publisher: The Company of Biologists
Date: 15-08-2008
DOI: 10.1242/JCS.028977
Abstract: Understanding the mechanisms underlying lipid-induced cell death has significant implications in both cell biology and human diseases. Previously, we showed that fission-yeast Schizosaccharomyces pombe cells deficient in triacylglycerol synthesis display apoptotic markers upon entry into stationary phase. Here, we characterize the sequential molecular events that take place at the onset of cell death in S. pombe, including a surge of diacylglycerol, post-mitotic arrest, alterations in mitochondrial activities and in intracellular redox balance, chromatin condensation, nuclear-envelope fragmentation, and eventually plasma-membrane permeabilization. Our results demonstrated active roles of mitochondria and reactive oxygen species in cell death, and identified novel cell-death regulators – including metacaspase Pca1, BH3-domain protein Rad9, and diacylglycerol-binding proteins Pck1 and Bzz1. Most importantly, we show that, under different conditions and stimuli, failure to maintain intracellular-lipid homeostasis can lead to cell death with different phenotypic manifestations, genetic criteria and cellular mechanisms, pointing to the existence of multiple lipotoxic pathways in this organism. Our study represents the first in-depth analysis of cell-death pathways in S. pombe.
Publisher: Informa UK Limited
Date: 02-01-2016
Publisher: Frontiers Media SA
Date: 20-11-2015
No related grants have been discovered for Frank Madeo.