-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
- Cosmetic Ingredient
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
This article is converted Medicine original, reproduced please indicate the source Author: chen Introduction: Recently, the University of North Carolina School of Medicine, first identified microRNA-29 CH- methylation is an important regulatory factor, and explains why the methyl CH- It is important for normal brain maturation to limit the transformation to a critical period.
They explained the important process of the normal maturation of the brain and pointed out that disrupting this process may lead to a variety of human brain diseases.
Previously, researchers at Harvard University in an article published in the journal Neuron confirmed that the brain does not mature until the age of 30.
Some netizens joked: The brain is still a child, but the hair is already bald.
.
.
So how much do you know about the maturity of the brain? Although there is a lot of knowledge surrounding brain development (for example, neurogenesis, neuron migration, and post-mitotic differentiation), there is still very little understanding of how the brain matures after this period and how to maintain brain homeostasis in adulthood.
Recently, a research team at the University of North Carolina School of Medicine (UNC School of Medicine) has identified a molecule called microRNA-29, which is a powerful control factor for mammalian brain maturation.
The research was published in "Cell Reports", entitled "MicroRNA-29 is an essential regulator of brain maturation through regulation of CH methylation".
They found that the deletion of microRNA-29 in the mouse brain or the knockout mutation that prevents microRNA-29 from targeting DNMT3A can lead to increased expression of DNMT3A, increased CH methylation, and inhibition of genes related to neuronal activity.
.
MicroRNA is a short chain of ribonucleic acid that regulates gene expression in cells.
Each microRNA can directly bind to the RNA transcript of other specific genes, thereby preventing it from being translated into protein.
Therefore, miRNA effectively acts as an inhibitor of gene activity, and a typical microRNA can regulate multiple genes in this way, so as not to overexpress genetic information.
The researchers found that a group of microRNAs stood out in the comparison of the brain activity of adult mice and young mice.
The levels of the microRNA-29 family in the brains of adult mice are 50 to 70 times higher than in the brains of young mice.
The researchers examined the mouse model and deleted genes from the microRNA-29 family in the brain.
They observed that although these mice were born normally, they quickly developed a series of problems, including repetitive behaviors, hyperactivity, and other abnormalities common in mouse models of autism and other neurodevelopmental disorders.
In severe cases, seizures may occur.
In order to understand the causes of these abnormalities, the researchers examined the gene activity in the mouse brain and compared it with the activity in the brain of mice with microRNA-29.
Unsurprisingly, when microRNA-29 no longer inhibits the activity of many genes, their gene activity is even higher.
But scientists unexpectedly discovered a large number of genes related to brain cells, these genes are less active in the absence of microRNA-29.
In the picture on the right, the important enzyme DNMT3A in microRNA-29-deficient mice is significantly increased (light blue).
So the scientists explained: One of the target genes that MicroRNA-29 usually blocks is the gene called DNMT3A enzyme.
This enzyme applies a special chemical modification called CH-methylation to DNA, thereby silencing nearby genes.
In the mouse brain, the gene activity of DNMT3A usually rises at birth, and then drops sharply after a few weeks.
Scientists have found that inhibiting the release of microRNA-29 from DNMT3A is usually the cause of this sharp decline.
Therefore, in mice lacking microRNA-29 in the brain, DNMT3A is not inhibited, the CH-methylation process continues abnormally, and instead, many brain cell genes that should be active continue to be inhibited.
Some of these genes, as well as the genes of DNMT3A itself, have been found to be missing or mutated in individuals with neurodevelopmental disorders such as autism, epilepsy, and schizophrenia.
To confirm the role of DNMT3A, the scientists created a unique mouse model that prevents microRNA-29 from inhibiting DNMT3A, but does not affect other targets of microRNA-29.
The results showed that the release of DNMT3A can cause many problems, such as seizures and early death, as seen in mice without miR-29.
These findings shed light on a crucial process in the later stages of brain development: turning off DNMT3A to release many genes that were originally more active in the adult brain.
Dr.
Mohanish Deshmukh said: "These results confirm for the first time that microRNA-29 is an important regulator of CH-methylation and reveal why limiting CH-methylation to a critical period is important for normal brain maturation.
" And more broadly, they are studying how to regulate the activity of microRNA-29 in childhood to improve their health.
Adjust brain functions to give humans a unique personality.
Dr.
Mohanish Deshmukh reference materials: 2FS2211124721002606%3Fshowall%3Dtrue Note: This article aims to introduce the progress of medical research and cannot be used as a reference for treatment options.
If you need health guidance, please go to a regular hospital for treatment.
They explained the important process of the normal maturation of the brain and pointed out that disrupting this process may lead to a variety of human brain diseases.
Previously, researchers at Harvard University in an article published in the journal Neuron confirmed that the brain does not mature until the age of 30.
Some netizens joked: The brain is still a child, but the hair is already bald.
.
.
So how much do you know about the maturity of the brain? Although there is a lot of knowledge surrounding brain development (for example, neurogenesis, neuron migration, and post-mitotic differentiation), there is still very little understanding of how the brain matures after this period and how to maintain brain homeostasis in adulthood.
Recently, a research team at the University of North Carolina School of Medicine (UNC School of Medicine) has identified a molecule called microRNA-29, which is a powerful control factor for mammalian brain maturation.
The research was published in "Cell Reports", entitled "MicroRNA-29 is an essential regulator of brain maturation through regulation of CH methylation".
They found that the deletion of microRNA-29 in the mouse brain or the knockout mutation that prevents microRNA-29 from targeting DNMT3A can lead to increased expression of DNMT3A, increased CH methylation, and inhibition of genes related to neuronal activity.
.
MicroRNA is a short chain of ribonucleic acid that regulates gene expression in cells.
Each microRNA can directly bind to the RNA transcript of other specific genes, thereby preventing it from being translated into protein.
Therefore, miRNA effectively acts as an inhibitor of gene activity, and a typical microRNA can regulate multiple genes in this way, so as not to overexpress genetic information.
The researchers found that a group of microRNAs stood out in the comparison of the brain activity of adult mice and young mice.
The levels of the microRNA-29 family in the brains of adult mice are 50 to 70 times higher than in the brains of young mice.
The researchers examined the mouse model and deleted genes from the microRNA-29 family in the brain.
They observed that although these mice were born normally, they quickly developed a series of problems, including repetitive behaviors, hyperactivity, and other abnormalities common in mouse models of autism and other neurodevelopmental disorders.
In severe cases, seizures may occur.
In order to understand the causes of these abnormalities, the researchers examined the gene activity in the mouse brain and compared it with the activity in the brain of mice with microRNA-29.
Unsurprisingly, when microRNA-29 no longer inhibits the activity of many genes, their gene activity is even higher.
But scientists unexpectedly discovered a large number of genes related to brain cells, these genes are less active in the absence of microRNA-29.
In the picture on the right, the important enzyme DNMT3A in microRNA-29-deficient mice is significantly increased (light blue).
So the scientists explained: One of the target genes that MicroRNA-29 usually blocks is the gene called DNMT3A enzyme.
This enzyme applies a special chemical modification called CH-methylation to DNA, thereby silencing nearby genes.
In the mouse brain, the gene activity of DNMT3A usually rises at birth, and then drops sharply after a few weeks.
Scientists have found that inhibiting the release of microRNA-29 from DNMT3A is usually the cause of this sharp decline.
Therefore, in mice lacking microRNA-29 in the brain, DNMT3A is not inhibited, the CH-methylation process continues abnormally, and instead, many brain cell genes that should be active continue to be inhibited.
Some of these genes, as well as the genes of DNMT3A itself, have been found to be missing or mutated in individuals with neurodevelopmental disorders such as autism, epilepsy, and schizophrenia.
To confirm the role of DNMT3A, the scientists created a unique mouse model that prevents microRNA-29 from inhibiting DNMT3A, but does not affect other targets of microRNA-29.
The results showed that the release of DNMT3A can cause many problems, such as seizures and early death, as seen in mice without miR-29.
These findings shed light on a crucial process in the later stages of brain development: turning off DNMT3A to release many genes that were originally more active in the adult brain.
Dr.
Mohanish Deshmukh said: "These results confirm for the first time that microRNA-29 is an important regulator of CH-methylation and reveal why limiting CH-methylation to a critical period is important for normal brain maturation.
" And more broadly, they are studying how to regulate the activity of microRNA-29 in childhood to improve their health.
Adjust brain functions to give humans a unique personality.
Dr.
Mohanish Deshmukh reference materials: 2FS2211124721002606%3Fshowall%3Dtrue Note: This article aims to introduce the progress of medical research and cannot be used as a reference for treatment options.
If you need health guidance, please go to a regular hospital for treatment.
