Protein aggregation is typical of various neurodegenerative diseases such as Alzheimer’s, Parkinson’s and prion diseases such as Creutzfeld-Jakob disease. A research team headed by Professor Jörg Tatzelt from the Department of Biochemistry of Neurodegenerative Diseases at Ruhr University Bochum, Germany, has now used new in vitro and cell culture models to show that a lipid anchor on the outer membrane of nerve cells inhibits the aggregation of the prion protein. “Understanding the mechanisms that cause the originally folded proteins to transform into pathogenic forms is of crucial importance for the development of therapeutic strategies,” says Jörg Tatzelt. The team published their findings in the journal Proceedings of the National Academy of Sciences (PNAS) on December, 31, 2024.

A recent study, affiliated with South Korea's Ulsan National Institute of Science and Technology (UNIST) appeared in the online version before inclusion in an issue of Angewandte Chemie International Edition on November 21, 2024. This study highlights a groundbreaking development in foldable molecular paths within solid-state frameworks, illuminating their potential for dynamic pore control and transformative applications in molecular metamaterials.

Organoids, or living biobanks, are living tissue models widely used in biomedical research and drug screening. A recent review article published in the Chinese Medical Journal, systematically examines standardization efforts in organoid research, including operational procedures, laboratory establishment, and existing published guidelines related to organoid culture. The authors also discuss current challenges in the standardization of organoid construction, highlighting key areas for improvement.

Aerobic glycolysis is critical for tumor growth and metastasis. Previously, we have found that the overexpression of the inhibitor of growth 5 (ING5) inhibits lung cancer aggressiveness and epithelial–mesenchymal transition (EMT). However, whether ING5 regulates lung cancer metabolism reprogramming remains unknown. Here, by quantitative proteomics, we showed that ING5 differentially regulates protein phosphorylation and identified a new site (Y163) of the key glycolytic enzyme PDK1 whose phosphorylation was upregulated 13.847-fold. By clinical study, decreased p-PDK1Y163 was observed in lung cancer tissues and correlated with poor survival. p-PDK1Y163 represents the negative regulatory mechanism of PDK1 by causing PDHA1 dephosphorylation and activation, leading to switching from glycolysis to oxidative phosphorylation, with increasing oxygen consumption and decreasing lactate production. These effects could be impaired by PDK1Y163F mutation, which also impaired the inhibitory effects of ING5 on cancer cell EMT and invasiveness. Mouse xenograft models confirmed the indispensable role of p-PDK1Y163 in ING5-inhibited tumor growth and metastasis. By siRNA screening, ING5-upregulated TIE1 was identified as the upstream tyrosine protein kinase targeting PDK1Y163. TIE1 knockdown induced the dephosphorylation of PDK1Y163 and increased the migration and invasion of lung cancer cells. Collectively, ING5 overexpression—upregulated TIE1 phosphorylates PDK1Y163, which is critical for the inhibition of aerobic glycolysis and invasiveness of lung cancer cells.

An Osaka Metropolitan University team has devised a more accurate way of measuring an indicator of kidney function known as glomerular filtration rate (GFR) by taking aging into account.

A study published in National Science Review reveals that carbon-14 (C-14) from algae can integrate into zebrafish biomolecules through a food chain transfer pathway, causing metabolic changes and neurological alterations.