Publications by authors named "H Ozgur Ozdemirel"

Article Synopsis
  • Aggregations of misfolded proteins are linked to various diseases, including a rare condition called Autosomal dominant neurohypophyseal diabetes insipidus (ADNDI) caused by mutations in the AVP-NPII gene leading to cellular dysfunction due to accumulated proteins in the endoplasmic reticulum (ER).
  • The study aimed to investigate the formation of amyloid-like aggregates from mutant precursor proteins linked to specific mutations found in ADNDI patients, examining factors such as glycosylation patterns and degradation pathways.
  • Results indicated that mutant precursors maintained their glycan structure, were involved in degradation pathways, formed oligomers, and demonstrated fibril formation in bacterial models, providing insights into the mechanisms underlying ADNDI.
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The human intestine is a habitat for microorganisms and, recently, the composition of the intestinal microbiota has been correlated with the etiology of diseases such as inflammations, sores, and tumors. Although many studies have been conducted to understand the composition of that microbiota, expanding these studies to more samples and different backgrounds will improve our knowledge. In this work, we showed the colon microbiota composition and diversity of healthy subjects, patients with inflammatory bowel disease (IBD), and colon cancer by metagenomic sequencing.

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Archaea are a major part of Earth's microbiota and extremely diverse. Yet, we know very little about the process of mutation that drives such diversification. To expand beyond previous work with the moderate halophilic archaeal species Haloferax volcanii, we performed a mutation-accumulation experiment followed by whole-genome sequencing in the extremely halophilic archaeon Halobacterium salinarum.

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Since antibiotic resistance is a growing public health problem worldwide, it is important to understand how antibiotics and spontaneous mutations cooperate and shape the genome-wide mutation rate and spectrum. Here, we quantitatively evaluate genome-wide mutational profiles of Escherichia coli after long-term subinhibitory exposure to a broad-spectrum (streptomycin) and a narrow-spectrum antibiotic (nalidixic acid), using a mutation accumulation design combined with whole-genome resequencing of replicate lines as a mutagenicity test. We determined that, while the genome-wide mutation rate is slightly higher in the streptomycin-treated lines compared to the control lines, there is a significant increase in the nalidixic acid-treated lines.

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