Publications by authors named "T E Mertz"
CAG/CTG repeats are prone to expansion, causing several inherited human diseases. The initiating sources of DNA damage which lead to inaccurate repair of the repeat tract to cause expansions are not fully understood. Expansion-prone CAG/CTG repeats are actively transcribed and prone to forming stable R-loops with hairpin structures forming on the displaced single-stranded DNA (S-loops).
View Article and Find Full Text PDFAPOBEC-induced mutations occur in 50% of sequenced human tumors, with APOBEC3A (A3A) being a major contributor to mutagenesis in breast cancer cells. The mechanisms that cause A3A activation and mutagenesis in breast cancers are still unknown. Here, we describe factors that influence basal A3A mRNA transcript levels in breast cancer cells.
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- APOBEC cytidine deaminases, specifically APOBEC3A, contribute to genetic instability in cancer, particularly through the creation of mutations in breast cancer.
- The study reveals that using proteasome inhibitors boosts the levels of A3A mRNA significantly, by approximately 100 times, suggesting that this treatment activates the transcription of A3A rather than just preventing its breakdown.
- Increased A3A levels lead to greater cytidine deaminase activity, reduced cell growth, and more DNA damage, indicating that proteasome dysfunction may enhance genetic diversity in tumors and affect how patients respond to treatments.
Article Synopsis
- Three main surgical approaches to the forearm (Henry's, Thompson's, ulnar) carry risks of nerve injury, affecting hand function.
- A review of existing literature revealed specific "safe zones" for incisions that minimize nerve damage: radial to the flexor carpi radialis for the anterior approach, over Lister's tubercle for Thompson's, and on the ulnar side near the ulnar styloid for the ulnar approach.
- Surgeons must be aware of anatomical variations and the branching of nerves to prevent intraoperative injuries, emphasizing the importance of following established surgical techniques.
The cytidine deaminases APOBEC3A (A3A) and APOBEC3B (A3B) are prominent mutators of human cancer genomes. However, tumor-specific genetic modulators of APOBEC-induced mutagenesis are poorly defined. Here, we used a screen to identify 61 gene deletions that increase A3B-induced mutations in yeast.
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