'Our group has been studying the proteins that are targeted by the phytoplasma effector proteins for almost 30 years,' said Günter Theißen, one of the scientists involved in the study. 'In our latest research, based on just few data and some simple assumptions, we predicted the structure of the respective effector protein (termed SAP54) about 5 years ago. With the new work, we tested our hypothesis experimentally, and found that our prediction was quite accurate.'
Scientists at Fujita Health University, Japan, have discovered how deficiencies of the IL-36Ra protein -- caused by mutations in the IL36RN gene -- delay wound healing via the flooding of the wound with several types of immune cells. However, by inhibiting the functioning of proteins and the signaling pathways involved in activating the immune system at a wound, this delay can be offset. These findings could aid efforts to develop ways of regulating wound healing in IL36RN mutation-related skin disorders.
With insights into a molecular pathway that regulates the activity of Tregs, a type of T cell involved in immunosuppression, research by the University of Pennsylvania's George Hajishengallis and colleagues opens up possibly new avenues for treating inflammatory and autoimmune diseases.
In a painstaking experiment, scientists suspended a single protein filament between two microscopic beads. Their results have shed light on an elusive process in which cells receive and respond to mechanical cues.
The dynamic change in root growth of plants plays an important role in their adjustment to soil conditions. Depending on the location, nutrients or moisture can be found in higher or lower soil layers. This is why, depending on the situation, a short or a long root is advantageous. Caroline Gutjahr, Professor of Plant Genetics at the Technical University of Munich (TUM), and her team investigate how plant hormones influence the growth of roots.
Researchers from Tokyo Metropolitan University have discovered a new mechanism by which clumps of tau protein are created in the brain, killing brain cells and causing Alzheimer's disease. A specific mutation to an enzyme called MARK4 changed the properties of tau, usually an important part of the skeletal structure of cells, making it more likely to aggregate, and more insoluble. Getting to grips with mechanisms like this may lead to breakthrough treatments.
Oncotarget recently published "Evaluation of cellular alterations and inflammatory profile of mesothelial cells and/or neoplastic cells exposed to talc used for pleurodesis"
What about the kidneys make them a hotspot for COVID-19's cytokine storm? A research team says it's the presence of a protein found on specialized renal transport cells.
People with diabetes -- especially those with diabetic kidney disease -- are among the most at risk for COVID-19. A new study peered inside the kidney cells of COVID-19 patients and diabetic kidney disease patients and made a surprising discovery: Similar molecular processes were activated in both sets of patients. The results suggest that diabetes may predispose patients to SARS-CoV-2 infection or more severe COVID-19 by spurring biological processes used by the virus to infect and replicate.
A new study led by Marc Veldhoen, principal investigator at Instituto de Medicina Molecular with an interdisciplinary team of clinicians and researchers from FMUL and CHLN and collaborators at IPST, shows that 90% of subjects have detectable antibodies 40 days up to 7 months post contracting COVID-19. These results, now published in the scientific journal European Journal of Immunology, also show that age is not a confounding factor in levels of antibodies produced, but disease severity is.