The team of Prof. Babis Spilianakis provides insights on how long non-coding RNAs may regulate biallelic gene expression. Stratigi et al. suggest a role for lncRNAs in the regulation of somatic homologous spatial proximity and allelic expression control necessary for fine-tuning mammalian immune responses.
The team of Prof. Theo Fotsis reveals that VEGF integrates components of the UPR machninery to generate angiogenesis. In this repsect, Karali et al. show that the ER plays an important role in normal cellular functions, such as signaling by growth factors, and is not limited to the adaptation of the cell to stress.
Konstantinides & Averof find that crustaceans and vertebrates use a similar type of stem cell to regenerate their muscles. Their research points to a common basis for regeneration that may date back to the common ancestors of all bilaterian animals.
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 team of Prof. Mavrothalassitis 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 team of Prof. Economou in collaboration with the Kalodimos lab (Rutgers U.) reveals 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.