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- Table of Contents
Facts about Mitotic checkpoint protein BUB3.
Necessary for kinetochore localization of BUB1. Regulates chromosome segregation during oocyte meiosis.
Human | |
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Gene Name: | BUB3 |
Uniprot: | O43684 |
Entrez: | 9184 |
Belongs to: |
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WD repeat BUB3 family |
BUB3 (budding uninhibited by benzimidazoles 3, yeast) homolog; BUB3 budding uninhibited by benzimidazoles 3 homolog; Bub3; BUB3L; budding uninhibited by benomyl; budding uninhibited by benzimidazoles 3 homolog (yeast); hBUB3; mitotic checkpoint component; mitotic checkpoint protein BUB3
Mass (kDA):
37.155 kDA
Human | |
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Location: | 10q26.13 |
Sequence: | 10; NC_000010.11 (123154244..123170467) |
Nucleus. Chromosome, centromere, kinetochore. Starts to localize at kinetochores in prometaphase I (Pro-MI) stage and maintains the localization until the metaphase I-anaphase I (MI-AI) transition.
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The BUB3 marker is located on chromosome 10,q24-q26. This gene regulates DMAP1 mediated DNA methylation. The resistance to mitotic stresses in pancreatic cancer is also linked with the BUB3 genes. Several hypotheses have been proposed to explain the presence of BUB3 in this gene. These hypotheses are further discussed in this article.
This gene encodes a proteinkinase which phosphorylates BUB3 in kinetochores. BUB1 in yeast is found at kinetochores prior to chromosome alignment. Taylor et al. (1993). Taylor et.al.
BubR1 interacts with Bub3 through cooperative recognition. The C-terminal portion of the peptide may require Bub3 loop regions to undergo conformational changes. The interaction involves important contacts between Bub3R1 and Bub3. This makes the enthalpy contributions relatively high. Additional contacts are required near the peptide to prevent a low-affinity interaction. The short-lived interaction between BubR1 and Bub3 suggests that a complex-forming interaction requires important contacts between the proteins.
A disruption of the BubR1–Bub3 interaction is another possible mechanism to block SAC signaling. Inhibition of SAC signaling in human cells may involve disrupting this interaction. This interaction is vital for normal SAC Signaling. BubR1 & Bub3 are essential for the SAC pathway. A potential treatment strategy is to disable Bub3-BubR1 interactions.
It is still not clear what role the BUB3 marker plays in cancer. It has been shown that expression of the BUB3 marker in human sarcoma cells and tissues is associated to a lower overall survival rate and disease-free survival. This research may provide answers to the question "What are your best treatments for sarcomas?"
Recent research has revealed that BUBs play an important role in immune cell biology, including regulation of the cell cycle. Several of these studies are currently being conducted to determine how these proteins contribute to a healthy immune system. BUBs also play a role in the infection of human T-lymphotropic viruses. Researchers are currently studying the role of BUBs within the cell cycle. This research was funded by the National Institutes of Health, Tianjin Municipal Health Commission, and other funding agencies.
The BUB3 protein family is made up of a number proteins that participate in many body processes. The BUB3 protein is a member of this family. It binds its partner protein BUB1. Both proteins recognize eachother and work together during Mitosis. Many of these proteins play a role in controlling the cell cycle, including BUB1/BUB3 and BUB1/BUB3. BUB3 has also been found in many types of cancer, including oral. BUB3 inhibition could increase the chemosensitivity in tumors.
Bub3 plays a crucial role in regulating microtubule interaction during chromosome differentiation. Monitoring chromosome segregation is possible when microtubules are depolymerized and MBC is washed away. The presence of Bub3 is required for proper kinetochore-microtubule attachment. Bub3-deficient cells are less likely to achieve bi-orientation.
BUB3 is an extremely low-level protein. However, it is essential to the mitotic process. BUB3 could not be visually scored in the previous study because of technical difficulties. The accuracy of BUB3 counts depends on how many tumor cells are clustered. This study may help us to better understand tumor morphology. To prove its utility, however we need to validate BUB3 in modern patient cohorts.
The BUB3 genes is an essential regulator of cell-cycle progression. Low-grade luminal breast carcinoma is associated with BUB3 gene expression, and colorectal cancer is associated with mutations in the gene. Overexpression of the BUB3 marker has been shown to be associated with poor prognosis in breast carcinoma. Future research will be conducted on the marker's role in cancer progression. Researchers have already started to use it for cancer diagnostics.
The N-terminal portion of the Bub3 protein interacts tightly with the peptide. This interaction is thought to contribute to the overall binding affinity of the protein. Mutating the GLEBS domain can also be used to determine the binding kinetic parameters for the BUB3 protein. A Glu-394 salt bridge is found in the N-terminal and amino acids 400-419 are also present. The second-smallest koff is found in the mutant BUBR1392-425, E394K.
The mitotic control point complex includes the BUB3 genes. It is a member of the mitotic checkpoint complex and works with other proteins to prevent premature onset. Mutation of BUB3 in knockout mice causes tumorigenesis. Knockout mice exhibit high proliferative capacity and aneuploidy. Numerous studies in humans have linked BUB3 gene mutations to various types of cancer, including colorectal. BUB3 genes are expressed in different places in colorectal tumors. The highest levels of expression are found in CLP.
PMID: 10198256 by Seeley T.W., et al. Phosphorylation of human MAD1 by the BUB1 kinase in vitro.
PMID: 9660858 by Taylor S.S., et al. The human homologue of Bub3 is required for kinetochore localization of Bub1 and a Mad3/Bub1-related protein kinase.