Researchers at Washington University School of Medicine in St. Louis have shed new light on a process that fixes breaks in the genetic material of the body's cells. Their findings could lead to ways of enhancing chemotherapy drugs that destroy cancer cells by damaging their DNA.

Like a mechanic popping the hood of a car to get at a faulty engine, a tumor-suppressing protein allows cellular repair mechanisms to pounce on damaged DNA by overcoming a barrier to DNA access.

Like doctors making house calls, some DNA repair enzymes can relocate to the part of the cell that needs their help, a collaborative team of scientists at Emory University School of Medicine has found.

The enzyme machine that translates a cell's DNA code into the proteins of life is nothing if not an editorial perfectionist.

This month's issue of Cold Spring Harbor Protocols features two articles detailing experimental methods for the analysis of molecular processes involved in DNA repair and post-translational modification of proteins.

Scientists at Burnham Institute for Medical Research (Burnham) have demonstrated important new roles for the protein kinase complex Cdc7/Dbf4 or Cdc7/Drf1 (Ddk) in monitoring damage control during DNA replication and reinitiating replication following DNA repair.

Variants of numerous DNA repair genes initially appeared to be statistically significantly associated with cancer risk in epidemiological studies.

An abundant chromosomal protein that binds to damaged DNA prevents cancer development by enhancing DNA repair, researchers at The University of Texas M. D. Anderson Cancer Center report online this week in the Proceedings of the National Academies of Science.

U. of I. researchers have taken the first steps toward understanding how an enzyme repairs DNA.

Researchers at the University of Delaware have discovered a novel technique--that acts like a “spell-checker” for correcting a misspelling in the DNA code--to repair the defective gene that causes spinal muscular atrophy (SMA). This hereditary neuromuscular disease is the number-one genetic killer of children under two years old.

Although defects in the "breast cancer gene," BRCA1, have been known for years to increase the risk for breast cancer, exactly how it can lead to tumor growth has remained a mystery.

A biochemistry research team led by Dr. Andrew H.-J. Wang and Dr. Ting-Fang Wang at the Institute of Biological Chemistry, Academia Sinica(IBCAS), has discovered that the RecA family recombinases function as a new type of rotary motor proteins to repair DNA damages.