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Publication Metadata only Advances in template-based protein docking by utilizing interfaces towards completing structural interactome(Current Biology Ltd, 2015) N/A; N/A; N/A; Department of Chemical and Biological Engineering; Department of Computer Engineering; Muratçıoğlu, Serena; Maiorov, Emine Güven; Keskin, Özlem; Gürsoy, Attila; PhD Student; PhD Student; Faculty Member; Faculty Member; Department of Chemical and Biological Engineering; Department of Computer Engineering; The Center for Computational Biology and Bioinformatics (CCBB); Graduate School of Sciences and Engineering; Graduate School of Sciences and Engineering; College of Engineering; College of Engineering; N/A; N/A; 26605; 8745The increase in the number of structurally determined protein complexes strengthens template-based docking (TBD) methods for modelling protein-protein interactions (PPIs). These methods utilize the known structures of protein complexes as templates to predict the quaternary structure of the target proteins. The templates may be partial or complete structures. Interface based (partial) methods have recently gained interest due in part to the observation that the interface regions are reusable. We describe how available template interfaces can be used to obtain the structural models of protein interactions. Despite the agreement that a majority of the protein complexes can be modelled using the available Protein Data Bank (PDB) structures, a handful of studies argue that we need more template proteins to increase the structural coverage of PPIs. We also discuss the performance of the interface TBD methods at large scale, and the significance of capturing multiple conformations for improving accuracy.Publication Metadata only Covid-19 under spotlight: a close look at the origin, transmission, diagnosis, and treatment of the 2019-nCoV disease(Wiley, 2020) Sheervalilou, Roghayeh; Shirvaliloo, Milad; Dadashzadeh, Nahid; Shirvalilou, Sakine; Shahraki, Omolbanin; Pilehvar-Soltanahmadi, Younes; Ghaznavi, Habib; Khoei, Samideh; N/A; Nazarlou, Ziba; PhD Student; Graduate School of Sciences and Engineering; N/AMonths after the outbreak of a new flu-like disease in China, the entire world is now in a state of caution. The subsequent less-anticipated propagation of the novel coronavirus disease, formally known as COVID-19, not only made it to headlines by an overwhelmingly high transmission rate and fatality reports, but also raised an alarm for the medical community all around the globe. Since the causative agent, SARS-CoV-2, is a recently discovered species, there is no specific medicine for downright treatment of the infection. This has led to an unprecedented societal fear of the newly born disease, adding a psychological aspect to the physical manifestation of the virus. Herein, the COVID-19 structure, epidemiology, pathogenesis, etiology, diagnosis, and therapy have been reviewed.Publication Metadata only Genome-wide chromatin state transitions associated with developmental and environmental cues(CELL PRESS, 2013) Zhu, Jiang; Adli, Mazhar; Zou, James Y.; Verstappen, Griet; Coyne, Michael; Zhang, Xiaolan; Durham, Timothy; Miri, Mohammad; Deshpande, Vikram; De Jager, Philip L.; Bennett, David A.; Houmard, Joseph A.; Muoio, Deborah M.; Camahort, Ray; Cowan, Chad A.; Meissner, Alexander; Epstein, Charles B.; Shoresh, Noam; Bernstein, Bradley E.; N/A; Önder, Tamer Tevfik; Faculty Member; School of Medicine; 42946Differences in chromatin organization are key to the multiplicity of cell states that arise from a single genetic background, yet the landscapes of in vivo tissues remain largely uncharted. Here, we mapped chromatin genome-wide in a large and diverse collection of human tissues and stem cells. The maps yield unprecedented annotations of functional genomic elements and their regulation across developmental stages, lineages, and cellular environments. They also reveal global features of the epigenome, related to nuclear architecture, that also vary across cellular phenotypes. Specifically, developmental specification is accompanied by progressive chromatin restriction as the default state transitions from dynamic remodeling to generalized compaction. Exposure to serum in vitro triggers a distinct transition that involves de novo establishment of domains with features of constitutive heterochromatin. We describe how these global chromatin state transitions relate to chromosome and nuclear architecture, and discuss their implications for lineage fidelity, cellular senescence, and reprogramming.Publication Metadata only In-depth review: is hepcidin a marker for the heart and the kidney?(Springer, 2021) Afsar, Rengin Elsurer; Ibis, Avsin; Afsar, Baris; N/A; Kanbay, Mehmet; Faculty Member; School of Medicine; 110580Iron is an essential trace element involved in oxidation-reduction reactions, oxygen transport and storage, and energy metabolism. Iron in excess can be toxic for cells, since iron produces reactive oxygen species and is important for survival of pathogenic microbes. There is a fine-tuning in the regulation of serum iron levels, determined by intestinal absorption, macrophage iron recycling, and mobilization of hepatocyte stores versus iron utilization, primarily by erythroid cells in the bone marrow. Hepcidin is the major regulatory hormone of systemic iron homeostasis and is upregulated during inflammation. Hepcidin metabolism is altered in chronic kidney disease. Ferroportin is an iron export protein and mediates iron release into the circulation from duodenal enterocytes, splenic reticuloendothelial macrophages, and hepatocytes. Systemic iron homeostasis is controlled by the hepcidin-ferroportin axis at the sites of iron entry into the circulation. Hepcidin binds to ferroportin, induces its internalization and intracellular degradation, and thus inhibits iron absorption from enterocytes, and iron release from macrophages and hepatocytes. Recent data suggest that hepcidin, by slowing or preventing the mobilization of iron from macrophages, may promote atherosclerosis and may be associated with increased cardiovascular disease risk. This article reviews the current data regarding the molecular and cellular pathways of systemic and autocrine hepcidin production and seeks the answer to the question whether changes in hepcidin translate into clinical outcomes of all-cause and cardiovascular mortality, and cardiovascular and renal end-points.Publication Metadata only Mechanisms of somatic cell reprogramming(Humana Press Inc, 2013) N/A; N/A; Önder, Tamer Tevfik; Faculty Member; School of Medicine; 42946Generation of induced pluripotent stem cells (iPSCs) from somatic cell types has revolutionized the field of stem cell biology and opened the way for production of disease- and patient-specific stem cells which have tremendous potential for regenerative medicine. Despite the rapid progress and improvement in iPSC-derivation techniques, transcription factor-based reprogramming remains an inefficient and poorly understood process. Successful reprogramming requires the completion of a number of rate-limiting steps that include avoiding senescence, mesenchymal-epithelial transition, and activation of endogenous pluripotency genes. It has also become clear that the global epigenetic landscape of the somatic cell types is completely overhauled during acquisition of pluripotency. The epigenetic state is largely determined by the deposition of chromatin marks which include histone tail modifications and DNA methylation. These marks are not only indicative of a given cell state; they are also functionally important during reprogramming. In this chapter I will review our current understanding of the mechanism of reprogramming and the role chromatin marks and the associated chromatin-modifier proteins play in this process.Publication Metadata only Multiple interaction partners for cockayne syndrome proteins: implications for genome and transcriptome maintenance(Elsevier Ireland Ltd, 2013) Aamann, Maria D.; Bohr, Vilhelm A.; Stevnsner, Tinna; N/A; Müftüoğlu, Meltem; Faculty Member; School of Medicine; 105916Cockayne syndrome (CS) is characterized by progressive multisystem degeneration and is classified as a segmental premature aging syndrome. The majority of CS cases are caused by defects in the CS complementation group B (CSB) protein and the rest are mainly caused by defects in the CS complementation group A (CSA) protein. Cells from CS patients are sensitive to UV light and a number of other DNA damaging agents including various types of oxidative stress. The cells also display transcription deficiencies, abnormal apoptotic response to DNA damage, and DNA repair deficiencies. Herein we have critically reviewed the current knowledge about known protein interactions of the CS proteins. The review focuses on the participation of the CSB and CSA proteins in many different protein interactions and complexes, and how these interactions inform us about pathways that are defective in the disease.