DNA repair tagged posts

This image shows reduced levels of BRCA1 (red) in neurons (blue). Amyloid-beta plaques in the brain can deplete neurons of BRCA1, potentially contributing to cognitive deficits in Alzheimer’s disease. Credit: Elsa Suberbielle

Researchers from the Gladstone Institutes have shown for the first time that the protein BRCA1 is required for normal learning and memory and is depleted by Alzheimer’s disease. BRCA1 is a key protein involved in DNA repair, and mutations that impair its function increase the risk for breast and ovarian cancer. The new study shows Alzheimer’s disease is associated with a depletion of BRCA1 in neurons and that BRCA1 depletion can cause cognitive deficits.

“BRCA1 has so far been studied primarily in dividing (multiplying) cells and in cancer, which is characterized by a...

Highlights •Timeless interacts with PARP-1 independent of poly(ADP-ribosyl)ation •Crystal structures of Timeless PAB in free form and in complex with PARP-1 •Specific recognition of PARP-1 by Timeless does not affect its enzymatic activity •PARP-1 is required for Timeless recruitment to DSB sites to promote HR repair

A new molecular mechanism for DNA repair involving an unexpected interaction between PARP-1 protein and sleep proteins in humans has been found. While it is a well-known fact that sleep is important to the body’s recovery and healing, knowledge of the molecular mechanisms that make this possible is incomplete...

Kinesin-14 promotes DSB mobility.

It’s a discovery that could unlock secrets into how cancer operates. “Scientists knew that severely injured DNA was taken to specialized ‘hospitals’ in the cell to be repaired, but the big mystery was how it got there,” said Professor Karim Mekhail, He discovered this DNA ambulance, which is a kinesin-14 motor protein complex, by using yeast cells.

Mekhail’s team also found that the DNA hospital, ie nuclear pore complex, repairs damaged DNA inaccurately. This inaccurate fix is important because DNA contains the instructions for all our genetic information. While the repaired DNA can still replicate, it has irregular cell instructions – a scenario that could cause cancer.

Daniel Durocher, Senior Investigator at Mount Sinai’s Lunenfeld-Tanenbaum Research I...

Images showing the difference in the prevalence of p53 in the oral tissue of a 28-year-old (left) and a 74-year-old (right). Credit: Dr. Reuben Kim

UCLA researchers have found that a protein that serves as a suppressor of cancer diminishes in skin and mouth epithelial cells as the human body ages. Dr. No-Hee Park, UCLA School of Dentistry dean and his team have been studying p53, tumor suppressor protein, “guardian of the genome” involved in DNA repair, cell cycle regulation and cellular deterioration.

“Looking at ways to maintain levels of p53 as one ages may provide a therapeutic clue to preventing cancer development,” said Park. Previous studies have shown p53 accumulates in large quantities as connective tissue cells, called fibroblasts, age and stop dividing...