summary: The researchers have revealed a sudden link between the signal of the signal related to cancer and blood barriers in the brain and blood. The study shows that the protein that divides the p53 tumor weakens the Norrin/Frzled4 path, which is very important to maintain these protective barriers.
This indicates that cancer treatments enhance P53 may unintentionally question the integrity of the brain and the eye. The results also highlight NCAPH as a possible prisoner involved in inherited retinal disease and vascular disorders.
Main facts:
- The susceptibility of the barrier: Increased P53 levels can weaken blood and blood barriers in the blood by disrupting norrin/frizzled4 signals.
- Treatment risk: MDM2 inhibitors, designed to lift the P53 to treat cancer, nervous inflammation and vascular imbalance.
- Disease gene: NCAPH is promoted as a potential contributor to family skeletal skeleton and other vascular diseases.
source: Minnesota University
A research team led by the University of Minnesota Medical College has discovered that the course of cancer signals has unknown ropes and brain in the brain.
The results were recently published in Science signs.
CNS blood barriers act as a preventive border between the bloodstream and the central nervous system by regulating the transmission of nutrients, hormones and metabolic waste and preventing retinal and brain swelling.
One of the main brokers of this mechanism is the Norrin/Frzzled4 signal. To date, the relationship between this path and the MDM2 – P53 axis has not been identified – which suppresses the tumors -.
“The results we have found reveals an unexpected link between the P53 stress response path and the signal of Norrene in the blood vessels in the central nervous system,” said Harald Jong, an associate professor at the University of Minnesota Medical College.
“This has effects on cancer treatments targeting MDM2 and increases the abundance of P53. It is important to look that these treatments can affect the barrier function, which can lead to a transmission of blood defects between the blood and the nervous system pain, nervousness and swelling.”
The study found that the P53 – a protein known to protect against cancer – weakens the Norrin/Frzzled4 signals in the blood vessels by lowering other protein levels called NCAPH. These results indicate medications that enhance the levels of P53 – such as MDM2 inhibitors – may accidentally damage the protective barriers in the brain and eyes.
The study also sheds light on NCAPH as a new, nominated, family -linked -to -neutoprine (FEVR) – a rare genetic eye that affects the growth of blood vessels in the retina.
Looking at the decisive role of P53 in organizing the vascular barrier function, it is important to evaluate whether MDM2 inhibitors-currently in clinical tests of cancer-can negatively affect blood barriers or blood barriers in the blood.
The results also support more investigation into the role of NCAPH in the ventricular cells, whether as a response to the P53 and a potential disease of vascular disorders such as FEVR.
Finance: This study was supported by the grants of the National Institute of Eye and National Institutes of Health (R01Ey024261, R01Ey033316 and 1R21DA056728-01A1).
About this news of this brain cancer research
author: Alexandra Smith
source: Minnesota University
communication: Alexandra Smith – Minnesota University
image: The image is attributed to news of neuroscience
The original search: Open access.
“The MDM2-P53 axis is organizedWritten by Harald Jong and others. Science signs
a summary
The MDM2-P53 axis is organized
The revitalization of the NORRIN signals caused by Cat-Catenin through FRIZZLED receptors in the lining cells (ECS) is necessary to create and keep the blood barrier function.
We sought to determine how to adjust this path under stress or disease conditions. Specifically, we have investigated the role of P53 in the hypnothetic blood barriers because increasing the abundance of the P53 copy factor in ECS is associated with CNS blood vessels that are leaked in type 2 diabetes.
Using relative genetic methods, cell -based, and mouse, we identified the interaction between the P53 and its negative MDM2 and Norrin/Frzzled4 signals.
Mice with EC MDM2 The decrease in norrin/friazled4 signals, low EC proliferation and the formation of blood vessels in the retina, and disrupting the blood barrier function in the blood, all were largely restored by synchronous TP53 Delete.
The decrease in Norrin/Frzzled4 signals and the inhibition of EC proliferation are associated with the P53 with a decrease in the expression of the complex component of the SMC CONDENSIN I (NCAPH).
This study determines an organizer of Norrin/Frzzled4 signals and indicates that the clinical use of MDM2 inhibitors may weaken the blood barrier CNS.
In addition, NCAP may be influential in the direction of the river course of the P53 in ECS and Jin filter for family cultural vertebral artery (FEVR), which occurs due to flaws in NORRIN signals.
2025-07-10 20:48:00
