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Researchers at the University of Illinois Urbana-Champaign’s Beckman Institute for Advanced Science and Technology led by Professor Nien-Pei Tsai (right) and Kwan Young Lee have established the protein p53 as critical for regulating sociability, repetitive behavior, and hippocampus-related learning and memory in mice, illuminating the relationship between the protein-coding gene TP53 and neurodevelopmental and psychiatric disorders like autism spectrum disorder. Credit: University of Illinois/L. Brian Stauffer
Researchers have established the protein p53 as critical for regulating sociability, repetitive behavior, and hippocampus-related learning and memory in mice, illuminating the relationship between the protein-coding gene TP53 and neurodevelopmental and psychiatric disorders like ...
The analysis of human samples and animal experiments demonstrate that the presence of p53 gene mutations in the blood increases the risk of developing atherosclerosis, the principle cause of cardiovascular disease. Credit: CNIC
A team at the Centro Nacional de Investigaciones Cardiovasculares (CNIC), working in collaboration with institutes in the U.S., has demonstrated that acquired mutations in the gene encoding the protein p53 contribute to the development of atherosclerotic cardiovascular disease.
Known as the “guardian of the genome,” p53 helps to maintain the integrity of the hereditary material inside cells by regulating multiple cell functions in response to cellular stresses.
Every day, an adult person generates hundreds of thousands of blood cells...
•p53 is poorly expressed and conformationally unstable •A spider silk domain boosts p53 translation in vitro •The spider silk-p53 fusion protein adopts a compact state and is biologically active •Reducing N-terminal disorder in fusion proteins increases expression and stability
The p53 protein protects our cells from cancer and is an interesting target for cancer treatments. The problem is, however, that it breaks down rapidly in the cell. Researchers at Karolinska Institutet in Sweden have now found an unusual way of stabilising the protein and making it more potent. By adding a spider silk protein to p53, they show that it is possible to create a protein that is more stable and capable of killing cancer cells. The study is published in the journal Structure.
This illustration depicts how retrotransposons are “handcuffed” by the tumor suppressor gene p53. But when p53 is lost, these mobile elements can erupt. Credit: Study authors Amanda Jones and Bhavana Tiwari. Artwork by Angela Diehl.
Finding sheds light on why mutations of the gene p53 are associated with cancer and could lead to new diagnostics or treatments About half of all tumors have mutations of the gene p53, normally responsible for warding off cancer. Now, UT Southwestern scientists have discovered a new role for p53 in its fight against tumors: preventing retrotransposons, or “jumping genes,” from hopping around the human genome. In cells with missing or mutated p53, the team found, retrotransposons move and multiply more than usual...
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