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Now showing 1 - 6 of 6
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    Conservation of migratory species
    (Cell Press, 2018) Horns, Joshua J.; Department of Molecular Biology and Genetics; Şekercioğlu, Çağan Hakkı; Faculty Member; Department of Molecular Biology and Genetics; College of Sciences; 327589
    N/A
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    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/A
    Months 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.
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    Extracellular glucose level regulates dependence on 78 for cell surface localization of multipass transmembrane proteins in HeLa cells
    (Wiley, 2018) Toyoda, Yusuke; Sarov, Mihail; Saitoh, Shigeaki; Department of Molecular Biology and Genetics; Akarlar, Büşra; Other; Faculty Member; Department of Molecular Biology and Genetics; College of Sciences; N/A; 105301
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    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; 42946
    Differences 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.
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    Intraductal tubulopapillary neoplasm (ITPN) of the pancreas: a distinct entity among pancreatic tumors
    (Wiley, 2022) Paolino, G.; Esposito, I.; Hong, S.-M.; Baştürk, O.; Mattiolo, P.; Kaneko, T.; Veronese, N.; Scarpa, A.; Luchini, C.; Adsay, Nazmi Volkan; Faculty Member; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); School of Medicine; Koç University Hospital; 286248
    Aims: intraductal tubulopapillary neoplasm (ITPN)of the pancreas is a recently recognized pancreatictumor entity. Here we aimed to determine the mostimportant features with a systematic review coupledwith an integrated statistical approach.Methods and results: PubMed, SCOPUS, and Embasewere searched for studies reporting data on pancreaticITPN. The clinicopathological, immunohistochemical,and molecular data were summarized. Then a compre-hensive survival analysis and a comparative analysis ofthe molecular alterations of ITPN with those of pancre-atic ductal adenocarcinoma (PDAC) and intraductalpapillary mucinous neoplasm (IPMN) from referencecohorts (including the International Cancer GenomeConsortium- ICGC dataset and The Cancer GenomeAtlas, TCGA program) were conducted. The core find-ings of 128 patients were as follows: (i) Clinicopathologi-cal parameters: pancreatic head is the most commonsite; presence of an associated adenocarcinoma wasreported in 60% of cases, but with rare nodal metastasis.(ii) Immunohistochemistry: MUC1 (>90%) and MUC6(70%) were the most frequently expressed mucins. ITPNlacked the intestinal marker MUC2; unlike IPMN, it didnot express MUC5AC. (iii) Molecular landscape: Com-pared with PDAC/IPMN, the classic pancreatic driversKRAS,TP53,CDKN2A,SMAD4,GNAS,andRNF43were less altered in ITPN (P<0.001), whereasMCLamplifications,FGFR2fusions, andPI3KCAmutationswere commonly altered (P<0.001). (iv) Survival anal-ysis: ITPN with a “pure” branch duct involvementshowed the lowest risk of recurrence.Conclusion: ITPN is a distinct pancreatic neoplasmwith specific clinicopathological and molecular char-acteristics. Its recognition is fundamental for its clini-cal/prognostic implications and for the enrichment ofpotential targets for precision oncology.
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    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; 105916
    Cockayne 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.