Massimo Bonora

ORCID: 0000-0002-5752-3318
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About
Contact & Profiles
Research Areas
  • Mitochondrial Function and Pathology
  • ATP Synthase and ATPases Research
  • Adenosine and Purinergic Signaling
  • Autophagy in Disease and Therapy
  • Cell death mechanisms and regulation
  • Metabolism and Genetic Disorders
  • Acute Myeloid Leukemia Research
  • Hematopoietic Stem Cell Transplantation
  • Extracellular vesicles in disease
  • Endoplasmic Reticulum Stress and Disease
  • Immune Cell Function and Interaction
  • Calcium signaling and nucleotide metabolism
  • Multiple Sclerosis Research Studies
  • RNA modifications and cancer
  • Cardiac Ischemia and Reperfusion
  • Adipose Tissue and Metabolism
  • Cancer, Hypoxia, and Metabolism
  • Cellular transport and secretion
  • Epigenetics and DNA Methylation
  • Protein Kinase Regulation and GTPase Signaling
  • Retinoids in leukemia and cellular processes
  • Neuroscience and Neuropharmacology Research
  • Nanoplatforms for cancer theranostics
  • RNA regulation and disease
  • Cancer Immunotherapy and Biomarkers

University of Ferrara
2016-2025

Albert Einstein College of Medicine
2015-2024

Montefiore Health System
2024

Stem Cell Institute
2019

California Institute for Regenerative Medicine
2019

Montefiore Medical Center
2019

Morpho (United States)
2017

General Department of Preventive Medicine
2013

Reactive oxygen species (ROS) are highly reactive molecules, mainly generated inside mitochondria that can oxidize DNA, proteins, and lipids. At physiological levels, ROS function as “redox messengers” in intracellular signalling regulation, whereas excess induce cell death by promoting the intrinsic apoptotic pathway. Recent work has pointed to a further role of activation autophagy their importance regulation aging. This review will focus on producers targets summarize different proteins...

10.1155/2012/329635 article EN cc-by Journal of Signal Transduction 2011-11-14

The term "mitochondrial permeability transition" (MPT) refers to an abrupt increase in the of inner mitochondrial membrane low molecular weight solutes. Due osmotic forces, MPT is paralleled by a massive influx water into matrix, eventually leading structural collapse organelle. Thus, can initiate outer permeabilization (MOMP), promoting activation apoptotic caspase cascade as well caspase-independent cell death mechanisms. appears be mediated opening so-called "permeability transition pore...

10.4161/cc.23599 article EN Cell Cycle 2013-02-13

The promyelocytic leukemia (PML) tumor suppressor is a pleiotropic modulator of apoptosis. However, the molecular basis for such diverse proapoptotic role currently unknown. We show that extranuclear Pml was specifically enriched at endoplasmic reticulum (ER) and mitochondria-associated membranes, signaling domains involved in ER-to-mitochondria calcium ion (Ca(2+)) transport induction found complexes large size with inositol 1,4,5-trisphosphate receptor (IP(3)R), protein kinase Akt,...

10.1126/science.1189157 article EN Science 2010-10-29

Calcium (Ca2+) homeostasis is fundamental for cell metabolism, proliferation, differentiation, and death. Elevation in intracellular Ca2+ concentration dependent either on influx from the extracellular space through plasma membrane, or release stores, such as endoplasmic/sarcoplasmic reticulum (ER/SR). Mitochondria are also major components of calcium signalling, capable modulating both amplitude spatio-temporal patterns signals. Recent studies revealed zones close contact between ER...

10.1186/1478-811x-9-19 article EN cc-by Cell Communication and Signaling 2011-09-22

Significance Accumulating evidence has underscored the role of cytosolic p53 in promoting cell death. Different reports have revealed that participates apoptosis induction by acting directly at mitochondria. However, because can mediate without its DNA-binding domain (the proposed to be fundamental for targeting mitochondria), mitochondrial localization is likely not only transcription-independent mechanism which promotes apoptosis. Here we demonstrate endoplasmic reticulum (ER) and...

10.1073/pnas.1410723112 article EN Proceedings of the National Academy of Sciences 2015-01-26

Protein phosphorylation controls many aspects of cell fate and is often deregulated in pathological conditions. Several recent findings have provided an intriguing insight into the spatial regulation protein across different subcellular compartments how this can be finely orchestrated by specific kinases phosphatases. In review, focus will placed on (i) phosphoinositide 3-kinase (PI3K) pathway, specifically Akt mTOR phosphatases PP2a PTEN, (ii) PKC family serine/threonine kinases. We look at...

10.4061/2011/329098 article EN Enzyme Research 2011-09-04

The P2X7 receptor (P2X7R) is a known and powerful activator of the NOD-like (NLR)P3 inflammasome; however, underlying pathways are poorly understood. Thus, we investigated molecular mechanisms involved. effect P2X7R expression activation on NLRP3 recruitment was by Western blot, RT-PCR, coimmunoprecipitation, confocal microscopy in microglial mouse cell lines selected for reduced primary cells from P2X7R-/- C57BL/6 mice. We show here that ATP (EC50 = 1 mM) or benzoyl-ATP 300 μM)...

10.1096/fj.14-268714 article EN The FASEB Journal 2015-02-17

Mitochondrial fatty acid oxidation (FAO) is essential for hematopoietic stem cell (HSC) self-renewal; however, the mechanism by which mitochondrial metabolism controls HSC fate remains unknown. Here, we show that within lineage, HSCs have largest NADPH pools, are required proper and homeostasis. Bioinformatic analysis of transcriptome, biochemical assays, genetic inactivation FAO all indicate FAO-generated fuels cholesterol synthesis in HSCs. Interference with disturbs segregation toward...

10.1016/j.stem.2024.02.004 article EN cc-by-nc-nd Cell stem cell 2024-03-01
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