H ομάδα του Καθ. Θεόδωρου Φώτση δείχνει ότι το ενδοπλασματικό δίκτυο και ο μηχανισμός UPR παίζουν σημαντικό ρόλο σε φυσιολογικές λειτουργίες του κυττάρου, όπως είναι η σηματοδότηση της αγγειογένεσης από τον VEGF, και δεν περιορίζονται μόνο στην προσαρμογή του κυττάρου στο στρες.
The Economou lab reveal that the protein export nanomotor SecA is highly dynamic. Gouridis etal, show that the nanomotor undergoes a finely orchastrtaed series of quaternary changes that are coupled to defined protein translocation steps.
Using mice defective in DNA repair, Karakasilioti et al., show that DNA damage triggers a chronic auto-inflammatory response leading to fat depletion. The findings highlight the role of irreparable DNA lesions in adipose tissue degeneration with important ramifications for progressive lipodystrophies and natural aging.
The Eliopoulos lab in collaboration with the Liloglou team at the University of Liverpool uncovered a novel function of the TPL2 kinase as suppressor of lung carcinogenesis. By combining genomic analyses of human tumors with cell and animal model systems,Gkirtzimanaki, Gkouskou et al report the operation of multiple genetic and epigenetic mechanisms which lead to loss of TPL2 expression in lung tumors and link TPL2 to key pathways regulating the apoptosis barrier to cancer.
The Mavrothalassitis lab in collaboration with the Wilkie lab combining human genetics and animal model systems, identified the genetic basis of a newly recognized clinical disorder, ERF-related craniosynostosis. Twigg et al reveal that ERF haploinsufficiency causes multiple-suture synostosis, craniofacial dysmorphism, Chiari malformation and language delay.
Research at IMBB, published today in the premier international scientific journal Nature, uncovers a universal and potent protective mechanism against neuronal necrosis. By developing and characterizing models of heat stroke, Kourtis and Nikoletopoulou in theTavernarakis lab reveal a novel molecular mechanism that defends against neurodegeneration triggered by extreme temperature and multiple, diverse insults.
Work from IMBB has uncovered a role for bHLH-O (a.k.a. Hes) proteins Dpn and E(spl) in neural stem cell maintenance in Drosophila. By exerting an anti-differentiation activity they ensure long-term proliferation, which is needed to produce the myriad of neural cells. However, aberrant cell signalling that leads to bHLH-O overexpression can cause pathological over-proliferation of neural stem cells. Zacharioudaki et al, Development 2012.
IMBB researchers reveal similarities in the development of insect and vertebrate body segments. Sarrazin et al. show that a segmentation clock, analogous to the one found in vertebrates, underpins segmentation in insects.
IMBB researchers uncover a novel molecular mechanism for Nucleotide Excision Repair during mammalian development. Kamileri et al reveal that key proteins in this pathway activate the transcription of genes involved in mammalian growth.
IMBB researchers uncover a novel, unexpected molecular mechanism required for the degeneration of nerve cells. Troullinaki and Tavernarakis reveal that two processes normally essential for cell survival, endocytosis and intracellular trafficking, also contribute to necrotic cell death.
The Economou lab in collaboration with the Kalodimos lab (Rutgers U.) reveal a novel regulatory mechanism in protein-protein interactions. Chen et al show that the interaction of a chaperone with its substrate is mediated by finely tuned structural instability and is coupled to molecular mimicry.
IMBB researchers contribute to the unraveling of the molecular mechanism of Notch signalling. Daskalaki et al show that ubiquitylation of the Notch ligand Delta simultaneously triggers its endocytosis and its signalling activity.