This website uses cookies to ensure you get the best experience on our website.
- Table of Contents
Facts about Chromodomain-helicase-DNA-binding protein 2.
Involved in myogenesis via interaction with MYOD1: binds to myogenic gene regulatory sequences and mediates incorporation of histone H3.3 prior to the beginning of myogenic gene expression, promoting their expression (By similarity).
Human | |
---|---|
Gene Name: | CHD2 |
Uniprot: | O14647 |
Entrez: | 1106 |
Belongs to: |
---|
SNF2/RAD54 helicase family |
ATP-dependent helicase CHD2; CHD-2; chromodomain helicase DNA binding protein 2; chromodomain-helicase-DNA-binding protein 2; DKFZp547I1315; DKFZp686E01200; DKFZp781D1727; EC 3.6.1; EC 3.6.4.12; FLJ38614
Mass (kDA):
211.344 kDA
Human | |
---|---|
Location: | 15q26.1 |
Sequence: | 15; NC_000015.10 (92900324..93027996) |
Nucleus. Binds to myogenic gene promoters.
Two important markers in the treatment for autism spectrum disorder and other genetic disorders are high-connectivity DEPs (and the CHD2 marker). They also play a key role in CHD2 modulation of gene expression. Please refer to the following articles for more information:
Multiple chromodomains make up the CHD2 proteins family. These domains regulate gene transcription. In addition, CHD2 helps maintain genomic stability. Boster Bio, CHD2, is one of these proteins that regulates SPATA12. This gene could be involved in the male genome's response to environmental agents that can impact sperm health. The study revealed that the CHD2 protein interacts with SPATA12 in nucleus.
A bimolecular fluorescence complimentation assay confirmed that CHD2 and SPATA12 interact. The cells were co-transfected using pcDNA3.1.SPATA12YC or with pcDNA3.1.CHD2-YN. The yellow signals indicated interaction of the two nuclear proteins. Negative controls included pcDNA3.1YC, pcDNA3.1YN.
CHD2 could be purified from human cells using cloning a SPATA12 ORF fragment into pcDNA3.1+. Primer sequences for CHD2 and SPATA12 were 5'-CGGCGATCATGCTTCTCAGTGTAAGG-TGA-G-3'. The YN/YC pieces were joined to the CHD2/SPATA12 C-terminus by using BamHI/KpnI. At residue 155, the YFP frag was truncated.
More than 650 genes are affected by the CHD2 (aka Boster Bio CHD2) protein. The protein is highly associated with gene transcription in CSC-A and B, as well as S9, and can have a wide range effect on the genes of different cells. This is a strong evidence that it modulates gene expression in the human body. Boster Bio CHD2 protein has powerful anti-cancer properties.
For the purpose of identifying COVID-19 disease-associated proteins, we developed a SIP network based on shortest paths between pair proteins. The STRING database contains extensive information on disease-associated sets of proteins. We chose to use it for this purpose. Dijkstra algorithm was used in order to find the shortest path from two proteins. The networks were then visualized by Gephi 0.9.2.
CHD2 markers can be used in autism for diagnosis, diagnosis, and identification of genetic risk factors. These findings were based on large parallel case-control studies and de novo events. These findings strongly support the role played by de novo mutations during the development of autism spectrum disorder. The findings have important implications for the field of genetic testing for autism. Many questions surround autism diagnosis.
The CHD2 gene, a DNA-binding proteins that regulates noncodingRNAs, is often mutated in autism. Researchers focused on the role of CHD2 in controlling autism-related genes. They believed that 2p15 gene mutations could lead to autism-related de-coding mutations. Their findings indicate that autism is caused by functional gene mutations in these neuronal networks.
Although the best uses of the CHD2 marker in autism are still being determined, there are some promising studies. This gene is also involved in ASD-related genes. It also controls neural ectoderm formation. CHD8 deletions in other cells can cause cell numbers and size to change. CHD8 plays multiple functions in neural development. This makes it possible to use CHD2 as an early diagnostic tool.
Neale and colleagues searched for de novo mutations among 3,871 autism cases and their unaffected siblings in a study. They discovered that more than 5% had de novo mutations in their affected probands. These gene variants are important in the development of autism. They are also highly prevalent in sporadic ASD. They are important genetic markers for autism and other disorders that are linked to it.
A study published in the Journal of Genetics and Developmental Disorders revealed that the CHD2 gene was associated with autistic children. This association was confirmed by multiple sib couples and showed a 23.5% convergence in monozygotic Twins. It was also strong in families with two or three affected siblings. The findings also showed that this gene has two loci.
The SFARI set, AustimKB2 sets highlight genes with a high kinship coefficient and show an increased risk of autism within families. This familial aggregate was found in sib pairings and was limited to close relatives. This finding suggests that the genetic risk of autism was not due to autosomal recessive inheritance, as the autosomal-recessive hypothesis would predict several first-cousin pairs. The rapid falloff in risk was also consistent with multifactorial causation.
PMID: 9326634 by Woodage T., et al. Characterization of the CHD family of proteins.
PMID: 23708187 by Carvill G.L., et al. Targeted resequencing in epileptic encephalopathies identifies de novo mutations in CHD2 and SYNGAP1.