Deubiquitinases (DUBs) are enzymes used by cells to trim protein modifications made from the protein ubiquitin, and thereby regulate proteins. Malfunctioning of DUBs could lead to diseases, including cancer and neurodegenerative disorders. A protein called USP53 has been recently linked with progressive familial intrahepatic cholestasis, a hereditary liver disease in children, yet its mechanism of action has remained elusive. While its sequence made it part of a deubiquitinase family, previous attempt to detect catalytic activity had remained inconclusive. Now, a team led by Malte Gersch, group leader at the Max Planck Institute of Molecular Physiology, together with researchers from the TU Dortmund University and the Erasmus University Medical Center in Rotterdam have decoded the mode of action of USP53 and its related enzyme called USP54. Scientists revealed that both enzymes remove specifically long polyubiquitin chains from proteins. They also identified the proteins that USP53 acts on that could be associated with the liver disease, thereby suggesting how targeted treatment for such diseases could be identified.

Antibodies can improve the rehabilitation of people with acute spinal cord injury. Researchers at 13 clinics in Germany, Switzerland, the Czech Republic and Spain have investigated this with promising results. For the first time, it was possible to identify patient groups that displayed a clinically relevant treatment effect. A follow-up study will start in December 2024.

An Osaka Metropolitan University-led research team found out how AHCC, a standardized extract of cultured Lentinula edodes mycelia, might be able to suppress the progression of liver fibrosis.

In spite of intensive research, glioblastoma remains one of the most lethal types of brain cancer. Temozolomide (TMZ) is used as the front-line medicine in its treatment. While TMZ effectively penetrates the brain and targets tumors, its success depends on the tumor cells attempting to repair the DNA damage caused by the drug. Unfortunately, glioblastomas often evade treatment by inactivating the various DNA repair pathways, making them resistant to TMZ and limiting its effectiveness. In these drug-resistant cancer cells, DNA becomes mutated but does not lead to cell death.

Until now, scientists have been unable to determine how metformin, a Type 2 diabetes medication that lowers blood sugar, works.   

A new Northwestern Medicine study has provided direct evidence in mice that it reversibly cuts the cell’s energy supply by interfering with mitochondria to lower glucose levels.