IMBB researchers showed that NAM, a form of vitamin B3, can enhance myelin production after demyelination by signaling to microglia to stop causing myelin damage and to astrocytes to reduce inflammation. NAM is an FDA-approved caloric restriction mimetic that induces autophagy
[PubMed]
PML is a protein that regulates important cellular decisions about life or death. A new study by IMBB researchers proposes that PML is a breast - tumor suppressor and can serve as a new biomarker. They found that PML limits breast cancer metastasis by inhibiting cancer stem cell survival, tumor cell migration and blood vessel formation.
Anopheles mosquitoes transmit malaria, exerting a tremendous public health burden, with the control heavily relying on insecticides. A new study published by IMBB researchers shows that a transporter, found in mosquito legs can remove the insecticide out of the organism acting like a pump.This mechanism could be targeted to restore insecticide toxicity.
[PLOS]
IMBB researchers have used a neural cancer model in the fruitfly Drosophila to examine how deregulation of differentiation and growth pathways, as well as interactions with host macrophages, drive tumor progression to malignancy.
[Press Release] [PNAS]
A new study by IMBB researchers shows that molecular condensates that store or degrade mRNA tightly associate with mitochondria to regulate their biogenesis and function. Their balanced association is important for regulating lifespan and adaptation to stress.
In a Preview article published in Cell Metabolism, Prof. Nektarios Tavernarakis discusses a study that delineates a signaling cascade that is mobilized by neurons in the hypothalamus to modulate autophagy and metabolism in the liver.
Malaria parasites cause malaria, a devastating disease in many poor countries. A study by researchers from IMBB and University of Bergen investigated a parasite specific actin to understand its structure and function. The findings have implications for strategies to control the disease.
Recent study at IMBB, published in Cell Death and Disease revealed that CISD-1, an iron sulfur cluster binding protein implicated in the pathogenesis of the neurodegenerative disorder Wolfram Syndrome type 2, modulates longevity and proteostasis by engaging autophagy and the mitochondrial intrinsic apoptosis pathway.
Interdisciplinary scientific collaboration between the Institute of Molecular Biology and Biotechnology (IMBB, FORTH), the Institute of Electronic Structure and Laser (IESL, FORTH) and the Medical School of National and Kapodistrian University of Athens (NKUA), sheds light into the molecular mechanisms that regulate nuclear lipid droplets accumulation during ageing.
Dendrites are complex neuronal structures with a key role in information processing in the brain. Researchers at IMBB have developed new software that allows the incorporation of important dendritic properties into neural network models. Such models advance our understanding of brain function and lead to new artificial intelligence systems.
IMBB and NYU researchers joined forces to study how the brain conveys important environmental cues and contexts such as novelty and reward information. Using dendritic electrophysiology recordings, optogenetic circuit mapping, and multi-compartment computational modeling they uncovered a disinhibitory microcircuit that gates dendritic spikes in hippocampal pyramidal neurons driven by lateral entorhinal cortex inputs. These inputs are among the first to be affected in Alzheimer's disease.
Research at IMBB, published in Nature Aging, reveals a fundamental quality control mechanism that operates in cells to safeguard the integrity and function of the nucleus. By maintaining nuclear homeostasis, this molecular mechanism contributes critically to promote longevity and fertility.
In a paper published in Metabolism, Kardassis lab reveals a novel role of the nuclear receptor HNF4A in glucose homeostasis and in the liver-α-cell axis in mice. The results shed light on the relationship between diabetes and liver steatosis and could be exploited for the development of new therapies.
[PubMed]
In this work, SpilianakisLab identified SATB1 protein to regulate gene promoter-enhancer communication in developing murine T cells. SATB1 absence altered transcription programs, leading to impaired thymocyte development and deregulation of T cell populations in secondary lymphoid organs, affecting T cell homeostasis and sustaining an autoimmune-like phenotype.
[PubMed] [Nature] [Press Release]
B cells in lupus erythematosus patients exhibit an autoreactive phenotype characterized by excessive activation and antibodies production. We reveal that ATR-mediated DNA damage response (DDR) drives the pathogenicity of B cell responses in SLE. Pharmacological targeting of ATR, attenuated B-cell immunogenic profile, proposing DDR as a novel therapeutic target.
[PubMed]
Some phytopathogenic bacteria produce an effector protein that inhibits exocytosis by affecting the proper assembly of the exocyst complex.
Under normal conditions (A), the exocyst complex is properly assembled to transfer the secretory vesicles to the cell membrane for the secretion their content into the apoplast.
When the cell is infected by the bacterium Xanthomonas (B), an effector protein blocks the proper assembly of the exocyst complex, thereby inhibiting the process of extracellular secretion.
Interdisciplinary scientific collaboration between the Institute of Molecular Biology and Biotechnology (IMBB, FORTH), and the Institute of Chemical Engineering Sciences (ICE-HT, FORTH), sheds light onto the interplay between metabolism and the rate of ageing.
Work by the Laboratory of Rheumatology, Autoimmunity and Inflammation demonstrates neutrophil extracellular traps (NETs) decorated with bioactive IL-33 in the blood and inflamed tissues of patients with Systemic Lupus Erythematosus (SLE). IL-33-decorated NETs induce IFNα synthesis by plasmatocytoid dendritic cells through the ST2L receptor.
International collaboration between IMBB-FORTH and the Ludwig Maximilian University of Munich (Germany), with the contribution of researchers from the Universities of Groningen (The Netherlands) and Leuven (Belgium) shaded light on the role of Structural Dynamics in protein evolvability.
IMBB Researchers revealed that DNA damage triggers the release of cytoplasmic ssDNAs leading to chronic inflammation in mice. The team has developed a therapeutic strategy to deliver recombinant nucleases in vivo and remove cytoplasmic ssDNAs, alleviating inflammation.
[Pubmed] [Press Release]