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Facts about G2/mitotic-specific cyclin-B1.
Human | |
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Gene Name: | CCNB1 |
Uniprot: | P14635 |
Entrez: | 891 |
Belongs to: |
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cyclin family |
CCNB; CCNB1; Cyclin B1; G2/mitotic-specific cyclin B1; G2/mitotic-specific cyclin-B1
Mass (kDA):
48.337 kDA
Human | |
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Location: | 5q13.2 |
Sequence: | 5; NC_000005.10 (69167010..69178245) |
Cytoplasm. Nucleus. Cytoplasm, cytoskeleton, microtubule organizing center, centrosome.
CCNB1 is a biomarker that ER+ breast cancer cells. It is part of the family of caspase proteases that respond to various Apoptotic stimuli. These triggers include DNA damage, cell death and growth factor receptor-bound proteins. Boster offers reagents and convenient solutions for all PCR needs.
CCNB1 is a biomarkers for ER+ breast cancer and its expression may provide useful information regarding the prognosis for patients who are receiving hormonal therapy. CCNB1 may also be a promising target for developing strategies that overcome resistance to hormone therapy. It may help physicians monitor the patients receiving hormone therapy and adapt their treatment to the patients' responses. But more multicenter , randomized controlled trials are needed to establish the value of CCNB1 as a biomarker to detect ER+ breast cancer.
The results revealed that CCNB1 is prominently expressed in patients suffering from G3-4 and G1-2 grade HCC. It also was associated with HCC patients with vascular invasive. In patients with ovarian cancers the poor prognosis was related to the expression of CDC7 or BUB1B. Potential candidates for the development of new anti-cancer drugs could include inhibitors of CDC7 and BUB1B.
CCNB1 is a member of the Cyclin family and is the main in the process of initiating mitosis. It forms a complex with CDK1 that it phosphorylates its substrate in order to facilitate the transition of cells. Recent evidence suggests that CCNB1 is involved in tumorigenesis. However, an imbalance in the regulation of CCNB1 has been detected in a variety of human cancers.
CDK1 and CCNB1 have also been discovered as potential biomarkers for ER+ breast cancer. However, further studies are needed to determine their biological basis. These genes could be biomarkers for ER+ as well as therapeutic targets for RMS. These findings are a significant improvement in treatment options for patients suffering from ER+ breast cancer.
Researchers looked at two datasets to determine whether CCNB1 is a biomarker for ER+ melanoma. One dataset included 38 samples that were not cancerous and the second included 235 primary tumors. The second data set showed that CCNB1 was differentially expressed within tumor samples that have ER+ expression. Additionally, the data provided insight into the prognosis of patients with ER+ breast cancer.
This marker is used to examine the expression of several genes that are involved in cell proliferation, differentiation, and death. It attaches to the CCNB1 gene to stimulate the expression of a variety of epithelial cell markers, including E'-cadherin, and p120-catenin. It is also found in certain mesothelial cell kinds, like MMQ. In this study, cells were placed in six-well plates, and then treated for 48 hours with inhibitors or shRNA.
CCNB1 is highly expressed in different types of cells, including tumor cells. This marker is essential for identifying the cell-specific mechanisms that are involved in these processes. Lentiviral vectors have been utilized to create shRNAs for this gene. 293T cells were used to package the lentivirus. Cells from GH3 as well as MMQ were transfected with lentiviral vectors at 70-80% confluence.
The CCNB1 marker is versatile and can be utilized in many ways. It can also be used to track the growth of tumors. The scientists behind this kit have validated it using the most reliable methods that ensure that it is reproducible. Boster Bio offers the CCNB1 ELISA kit. The authors thank Zhao, Yuguang, and Benjamin Clay for their detailed analysis. Boster has verified each lot and ensured reproducibility.
Furthermore, miR210-3p is also known to inhibit function of SIN3A, which is which is a protein that plays a crucial role in cell growth and differentiation. In vitro experiments have shown that miR210-3p inhibits cell proliferation and apoptosis. These findings have implications for human healthcare. It could be a treatment tool in cancer research.
The CCNB1 protein can be found in most human tissues. It is a part of an intricate complex with p34, a member the cyclin superfamily. This protein is essential to ensure the proper control of the G2/M transition phase. It is the most abundant protein in the S phase, but it increases dramatically during the G2 phase. It reaches its highest level at the M stage. CCNB1 is frequently expressed in cervical and breast cancers, as well as lung and esophageal squamous cell carcinomas.
The CCNB1 marker is an essential tool in cancer research. The protein encoded by this gene is believed to control the expression of genes that are involved in cancer. This marker is used to identify cell types that contribute to different forms of tumor growth. Cancer cells can produce more FBXO45 when they are treated with DEN/CCl4 treatment.
Caspase activation in mammalian cells may be activated at three levels: the upstream regulatory level (death receptor), the terminal phase (death receptor), and the downstream regulatory level (upstream regulatory). Figure 7 shows regulation at the death receptor level. It isn't known whether caspases regulate downstream levels. It's still a subject of debate, but it is important to know how these mechanisms interact.
The caspases family is a diverse group of cysteine proteases, which play an essential role in programming cell death. They are closely associated with pro-apoptotic signaling and bind to cell proteins. DNA damage triggers the expression of PIDD, RAIDD and caspase-2. These proteins break down cell proteins, and begin the death cascade.
Proapoptotic signals are converged at the mitochondrial level, where they induce the activation of caspases, which cause the death of cells. In the process, the mitochondrial membrane becomes unstable, it collapses the electrical gradient needed for aerobic respiration, and releases the proteins from the respiratory chain, including cytochrome c. However, the exact role of tBid in intrinsic apoptosis is still unclear.
Apoptosis is a process that is highly controlled, is the removal of extra cells in the embryonic development and the culling of damaged cells throughout your body. This process is dependent on conservation of evolutionary proteins like caspases to perform their functions. Caspases are necessary for this process to take place, but failure to activate caspases is associated with a number of human diseases.
Proapoptotic Bcl-2 family members react to a variety of apoptotic stimuli and trigger cell death. Cell death occurs as the result of an increase in mitochondrial permeability. Caspase-9 activates caspase-3, which is responsible for activating caspase-9 and triggering caspase-mediated death. Caspase-3 has been proven to be essential for the death of granulosa-cells.
The Induced Proximity model summarizes key research, but it does not consider caspase activation from the initiator. The model does not take into account the conformation of the caspase which is crucial for homodimerization. Furthermore, the mechanism claims that the caspases dimerize by specific interfaces, while the other two mechanisms do not.
There are many advantages when using a CCNB1-based marker for cancer monitoring. The marker is able to increase the likelihood of success of a targeted treatment. This marker is created from gene sequences rather than an RNAi test. While the CCNB1 RNAi test has high specificity and sensitivity, it does have limitations. To identify cancerous cells CCNB1 gene mRNA levels must be high. Different methods for identifying cancerous cells are available, for example, a cell cycle assay.
Cancer cells that express CCNB1 have an inferior prognostic significance due to high levels of CCNB1 could cause chromosomal instabilities. Moreover, tumor cells expressing high levels of CCNB1 have a higher aneuploidy that is linked to aggressiveness, poor clinical outcomes, and a higher chance of developing chromosomal instability. In addition, the CCNB1/CDK1 fusion is able to interact with CDK1 to speed up early mitosis.
PMID: 2570636 by Pines J., et al. Isolation of a human cyclin cDNA: evidence for cyclin mRNA and protein regulation in the cell cycle and for interaction with p34cdc2.
PMID: 7843284 by Piaggio G., et al. Structure and growth-dependent regulation of the human cyclin B1 promoter.
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