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- Table of Contents
Facts about Chromobox protein homolog 8.
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Mouse | |
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Gene Name: | Cbx8 |
Uniprot: | Q9QXV1 |
Entrez: | 30951 |
Belongs to: |
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No superfamily |
chromobox homolog 8 (Drosophila Pc class); chromobox homolog 8 (Pc class homolog, Drosophila); chromobox homolog 8; HPC3; Pc3; PC3chromobox protein homolog 8; Polycomb 3 homolog; polycomb 3; RC1Pc class 3 homolog; Rectachrome 1
Mass (kDA):
39.86 kDA
Mouse | |
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Location: | 11|11 E2 |
Sequence: | 11; |
CBX8 has many benefits. Please refer to the Boster Bio article on the Best Uses of the Cell-CBX8 marker for more information. The CBX8 marker has a negative effect on H3K27Me3 activity and interacts with PTEN. The marker for cell cycle CBX8 can also be in phosphorylation during mitosis. This makes it an excellent marker for epigenetic machinery.
The CD of CBX8 demonstrates weak affinity for H3K27me3 over H3K9me3 in the laboratory. This affinity is correlated with binding to chromatin within live cells. The CD was shown to preferentially be associated in T98G cells with H3K27me3 over H3K9me3. Although the mechanism that underlies this association is not fully understood It is vital to know the function of CBX8 in the regulation of H3K27me3 levels.
The CD of CBX8 interacts with DNA and H3K27me3 chromatin. The CD has a high affinity to DNA and H3K27me3, which suggests that its role in chromatin interaction depends on its interaction with DNA. CBX2's DNA-binding activity has not been examined. Further studies are required to determine the importance of CBX8 as opposed to DNA binding.
Incredibly, the CD interaction with H3K27me3 is controlled by nuclear PTEN which regulates cell division and mitotic development. In Drosophila, CBX8 physically interacts with the PTEN complex and mitotic checkpoint components. The CD-CBX8 molecular complex blocks the trimethylation of H3K27me3, a critical requirement for mitotic exit and G1 entry.
In vitro studies have shown that CD binds to both the H3K27me3 as well as the H3K9me3. However, the binding was so weak that the specificity of the interaction could not be distinguished. To explore these interactions we used nuclear magnetic resonance. A spectrum of CD-NMR revealed 49 main chain resonances and 53 methyl-lysine binding.
Although the interactions between CD-CBX8 and H3K27Me3 can be complex however, it is feasible to disrupt CBX8 binding in vitro by disrupting this binding. A more potent inhibitor might be capable of blocking DNA binding as well as inhibit CBX8 activity. These findings do not necessarily indicate that CBX8 inhibitors will be 100% effective. Rather, this interaction could facilitate the development of drugs for H3K27Me3-mediated disorders.
A recent study indicates that the human chromatin-suppressive protein PTEN physically interacts with the CBX8 gene, a marker of embryonic stem cells. PTEN regulates PI3K signalling in the cytosol. However, it also has an important nuclear function, reducing the chromosomal stability of cells during division. The interaction between CBX8 & PTEN can be controlled through the ubiquitination process. This is believed to be responsible for maintaining PTEN's stability as well as its position within the nucleus.
Mitotic exit is marked by the absence of cyclins B1 phospho H3, cyclinD2 and the phospho–H3. BubR1 was dephosphorylated rapidly and destroyed rapidly, while cyclin A2 (a marker for G1 phase) was elevated in mitotic exit. CBX8 and PTEN are involved in regulating epigenetics throughout the cell cycle.
Recent studies show that CBX8 regulates the functions of several proteins in the genome. It is a key component of the EMT program. This includes stemness cell movement, BMP4-related genes that are signatures. Interestingly, CBX8 is associated with metastasis and invasion of neoplasms. These findings suggest that CBX8 is responsible for stemness, tumor invasion, and migration.
The CBX8 marker is part of the Polycomb family. It is co-localized in the nucleus with PTEN and its levels are associated with the phosphorylation. In addition, CBX8-mediated phosphorylation is seen in mitosis and is closely associated with monoubiquitinated PTEN and phosphorylated BubR1 on chromatin. The epigenetic marker H3K27Me3 has been created when the promoter activity of CBX8 is inhibited.
A variety of other diseases have been linked to mutations in the PTEN gene. One example is PTEN hamartoma tumor syndrome. These are genetic conditions where the PTEN gene is unable to make the enzyme. It is not known whether these mutations are linked to autism or other diseases. If they are, further studies will be needed to determine if CBX8 is a reliable treatment for PTEN Hamartoma.
The CBX8 gene is an important regulator of the progression of mitosis. The high expression of this gene during mitosis causes its phosphorylation which assists in PTEN binding. The gene could also be involved in the progression of mitosis. Boster Bio has identified two applications for CBX8 that are most beneficial in mitosis. Phosphorylated CBX8 can increase G1-phase markers during mitosis.
Condensed chromatin is a structure that can be found in mitotic cells. They contain nuclear PTEN and other mitotic checkpoint proteins. CBX8 physically interacts with PTEN, which regulates the H3K27Me3 levels. In addition the CBX8 molecular structure blocks the trimethylation of histone H3's lysine 27. These modifications are crucial to chromatin condensation and mitotic exit.
The expression of this gene was significantly upregulated in cells treated with nocodazole, and the expression of CBX8 during mitosis greatly reduced H3K27Me3 levels. The treatment with nocodazole also increased levels of phosphoH3 and Cyclin A, which may suggest that CBX8 plays a role in the process of mitotic exit. Although the interaction may not be caused by the C-tails of PTEN however, it aids in stabilizing the CBX8/PTEN interaction.
Although the CBX8 marker in mitoses doesn't function as a single gene it can be used to study PRC1 or PRC2 gene expression. Both of these proteins are needed to ensure the stemness of a variety of adult stem cells. If their functions are not controlled, they could affect development and malignant transformation of cancer cells. It also influences the expression of genes in the process of cell cycle progression.
There are a few factors that make CBX8 a great marker for epigenetic machinery. It has high intra- and intermolecular interactions. It is also highly expressed during mitosis and phosphorylated. Thirdly, it could play an impact on the progress of the cell cycle. CBX8 is strongly interconnected with MCC and PTEN.
Incredibly, neuroblastoma is one of the rare childhood cancer that accounts for the largest percentage of cancer-related deaths in children. Neuroblastoma patients aren't affected by somatic mutations. This suggests that epigenetic changes can play a role in the progression of the disease. Recent reports have been linked MYCN to epigenetic machinery. While the mechanisms behind MYCN and epigenetic interactions within neuroblastoma cell cells remain elusive However, chemogenomic methods have demonstrated the general MYCN–epigenetic relationship. HDACs and SMARCs were identified as possible MYCN target genes as well as MYDs (SMYDs).
Another factor that could contribute to the role of CBX8 in the epigenetic machinery is its interaction with PTEN. Additionally, PTEN interacts with CBX8 which blocks the expression of certain genes during mitosis. PRC1 and PRC2 both are essential for stemness in embryonic stem cells along with certain kinds of adult stem cell. These genes could cause cancer, or other complications, in the event that they are not managed.
MYCN ChIP–seq data shows that MYCN transcriptional regulators have been linked with cell growth and repair of DNA. This confirms the idea that CBX8 is a good marker for epigenetic machinery. The marker won't be effective if the CBX8 gene is not involved in DNA repair. The epigenetic system may not work properly if the enzyme isn't involved in DNA repair.
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PMID: 10721694 by Hemenway C.S., et al. Identification and analysis of a third mouse Polycomb gene, MPc3.
PMID: 16359901 by Cao R., et al. Role of Bmi-1 and Ring1A in H2A ubiquitylation and Hox gene silencing.