Advance could suggest new ways to synthesize proteins with bespoke functions in medicine and biotechnology
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Human DNA-PKcs promotes broken DNA-end structure independence during NHEJ
Whether DNA-PKcs is necessary for non-homologous end joining has been biochemically obscure. Through optimization of reaction conditions, Fujii and Modesti show that DNA-PKcs plays a constructive role, which leads to indistinguishable repair efficiencies between cohesive-end and blunt-end DNA substrates.
Abstract: Metabolic syndrome and excessive alcohol consumption lead to liver injury and fibrosis, characterized by increased collagen deposition from hepatic stellate cells
https://doi.org/10.1172/JCI197923 Here, David A. Brenner & team discover the RNA-binding protein LARP6 as a master coordinator of hepatic stellate cell activation and fibrosis, using human tissue and liver spheroid models of MASH and MetALD.
The image shows collagen labeling (red) in human liver spheroids MASH model with LARP6-targeting ASO (DAPI, blue). Collagen labeling is decreased compared with MASH control.
11 Center for Epigenomics, UCSD, La Jolla, California, USA.
12 Sanford Burnham Prebys Medical Discovery Institute, La Jolla, California, USA.
13 Department of Biomedical Sciences, College of Medicine, Florida State University, Tallahassee, Florida, USA.
Experiments advance efforts to restore vision with transplanted neurons
Researchers at Johns Hopkins Medicine say they have successfully demonstrated that disrupting an eye structure long suspected of blocking the growth and survival of transplanted nerve cells may help restore vision in people with optic nerve damage.
A report on the experiments with animals, stem cells and donated eye tissue was published in Science Translational Medicine. It suggests that altering or removing a thin layer of tissue called the internal limiting membrane, which separates the light-sensing retinal tissue at the back of the eye from the gel-like vitreous fluid that fills the eye, could help transplanted retinal ganglion cells (RGCs) survive and grow in people with blinding optic nerve damage.
Such damage, also known as optic neuropathy, occurs when retinal ganglion cells die of disease, inflammation or injury and stop carrying electrical signals to the brain. Common causes of damage include glaucoma, optic nerve inflammation (optic neuritis) and ischemic optic neuropathy (sudden loss of blood flow to the optic nerve).
Neuromodulation for gait disorders
Gait impairments such as freezing, weakness and imbalance remain resistant to standard therapies across neurological disorders. This Review examines advances in neuromodulation, from refining deep brain stimulation to integrating spinal and distributed strategies. It discusses adaptive neurotechnologies, mechanistic insights and a framework for tailoring spatiotemporally precise interventions to restore gait control.
