Researchers at New York University have demonstrated that protease-activated receptor 2 (PAR2) on epithelial cells of the colon continued after they were trafficked from the cell membrane.

“The premise of our whole company is that we target molecular machines, but we don’t target the engine,” Adrian Schomburg told BioWorld. Instead, “we interfere with the throttle and other highly specific controls of these machines.” “We,” in this case, is Eisbach Bio GmbH, a German startup that is developing anticancer programs aimed at exploiting synthetic lethality by targeting helicases. Founded in 2019, the company has three programs, a recently announced collaboration with MD Anderson Cancer Center in oncology, and another program in COVID-19.

The growth of some pancreatic cancers is fueled by fungus-induced production of the cytokine IL-33, and the progression of such tumors could be slowed down by treatment with antifungals or genetic deletion of IL-33, researchers reported in the February 3, 2022, online issue of Cancer Cell.

A remarkably brief exposure to a multidrug cocktail enabled frogs to re-grow largely functional limbs after amputation, investigators from Tufts University reported in the January 26, 2022, issue of Science Advances. Twenty-four hours of exposure to five factors – brain-derived neurotrophic factor (BDNF), growth hormone (GH), 1,4-dihydrophenonthrolin-4-one-3carboxylic acid (1,4-DPCA), resolvin D5 (RD5) and retinoic acid (RA) – set off regeneration processes that continued for 18 months.

Two studies published this January by separate research teams have conclusively identified Epstein-Barr virus infection as the cause of multiple sclerosis, and the mechanism by which the immune response to EBV infection triggers an attack on the myelin sheath, the insulation that enables high-speed neuronal transmission.

By using a new method to model ovarian cancer, researchers at Memorial Sloan-Kettering Cancer Center have gained new insights into the role of senescence in therapy response of high-grade serous ovarian cancers.

Tau protein aggregates are present in a group of disorders, collectively termed the tauopathies. Alzheimer's disease is the most common of those disorders, while frontotemporal dementia is most strongly linked to tau. Now, a map of the proteins that interact with tau and how those interactions differ between normal and disease-associated tau protein could give new clues on how the protein causes damage in neurodegenerative disorders, and on how to treat or prevent that damage.

Antibodies to the EBNA1 protein of Epstein-Barr virus can cross-react with glial cell adhesion molecule (GlialCAM), a component of the myelin sheath. The findings are the first to report a mechanism for how viral infections can cause autoimmune disorders.

The enzyme poly [ADP-ribose] polymerase 1 (PARP1) is well known for its role in DNA damage repair, and multiple FDA-approved PARP inhibitors are used to treat BRCA-mutated tumors. Now, researchers at the Wistar Institute have described a role for PARP in regulating the genome of Epstein-Barr virus.

Investigators have identified structural differences between amyloid-beta (Abeta) aggregates in the postmortem brains of patients with inherited and sporadic Alzheimer's disease (AD), respectively. Moreover, both were different from the aggregates that form when Abeta assembles in vitro.