Research in our laboratory is focused on the understanding of molecular mechanisms that regulate the mitochondrial contribution to programmed cell death and inflammation signaling. Both processes are fundamental to a variety of diseases, including cancer, neurodegeneration and infectious diseases. In this context we are specifically interested in mitochondrial autophagy and interorganellar interactions, including with the endolysosomal compartment. We are applying a combination of fluorescence microscopy, molecular and cell biological, and biochemical approaches. Our studies aim at uncovering novel cell biological insights that can be exploited to combat diseases.
Ugolino J, Ji YJ, Conchina K, Chu J, Nirujogi RS, Pandey A, Brady NR, Hamacher-Brady A, Wang J. Loss of C9orf72 Enhances Autophagic Activity via Deregulated mTOR and TFEB Signaling. PLoS Genet. 2016 PubMed PMID: 27875531.
Marin Zapata PA, Beese CJ, Jünger A, Dalmasso G, Brady NR, Hamacher-Brady A. Time course decomposition of cell heterogeneity in TFEB signaling states reveals homeostatic mechanisms restricting the magnitude and duration of TFEB responses to mTOR activity modulation. BMC Cancer. 2016 PubMed PMID: 27268034.
Hamacher-Brady A, Brady NR. Mitophagy programs: mechanisms and physiological implications of mitochondrial targeting by autophagy. Cell Mol Life Sci. 2016 PubMed PMID: 26611876.
Hamacher-Brady A, Choe SC, Krijnse-Locker J, Brady NR. Intramitochondrial recruitment of endolysosomes mediates Smac degradation and constitutes a novel intrinsic apoptosis antagonizing function of XIAP E3 ligase. Cell Death Differ. 2014 PubMed PMID: 25080938.
Zhu Y, Massen S, Terenzio M, Lang V, Chen-Lindner S, Eils R, Novak I, Dikic I, Hamacher-Brady A, Brady NR. Modulation of serines 17 and 24 in the LC3-interacting region of Bnip3 determines pro-survival mitophagy versus apoptosis. J Biol Chem. 2013 PubMed PMID: 23209295.