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Validated All-in-One™ qPCR Primer for CDC20(NM_001255.2) Search again
Product ID:
HQP023365
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CDC20A, OOMD14, OZEMA14, bA276H19.3, p55CDC
Gene Description:
cell division cycle 20
Target Gene Accession:
NM_001255.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
CDC20 appears to act as a regulatory protein interacting with several other proteins at multiple points in the cell cycle.
Gene References into function
- localization in tail-to-tail array and expression in proliferating cells
- Destruction-box specificities of APC/C(fzy) and APC/C(fzr)& successive activation of APC/C by fzy & fzr establish the temporal substrate degradation pattern, explaining why some endogenous RXXL substrates are degraded by fzy & others by fzr complexes.
- These findings implicate RASSF1A in the regulation of both APC-Cdc20 activity and mitotic progression.
- These results indicate that Bub3 and Cdc20 play additional roles in the integration of cell cycle arrest as transcriptional repressors.
- activation of APC(Cdc20) by Tax provides an explanation for the mitotic abnormalities in HTLV-I-infected cells and is likely to play an important role in the development of adult T cell leukemia
- Up-regulation of cdc20 is associated with gastric cancer
- Functional analysis suggests that an optimum Mad2 binding efficiency of Cdc20 is required during checkpoint arrest and release.
- High level of Cdc20 appears to be more tightly associated with a poor prognosis.
- Overexpression of Cdc20 leads to impairment of the spindle assembly checkpoint and aneuploidization in oral cancer
- These results suggest that targeting molecules involved in spindle mitotic checkpoint, such as p55CDC/Cdc20, might account for the high cytotoxicity of HDAC inhibitors versus malignant cells.
- There is no interaction between RASSF1A and Cdc20.
- Overexpression of CDC20 is associated with cancer
- SCF(Skp2) and APC(Cdc20) mark MLL for degradation at S phase and late M phase, respectively.
- Data show that Cdc20 and Cks1 direct the spindle checkpoint-independent destruction of cyclin A2.
- Both MCF2 and MCC inhibit APC/C by antagonizing Cdc20, possibly by interaction with the Cdc20-binding site of APC/C.
- Over-expression of mRNA levels of IGFBP-2 and CDC20 is highly related to glioblastomas.
- Ubiquitylation of human Cdc20 is not required to release it from the checkpoint complex, but to degrade it to maintain mitotic arrest.
- The degradation of Cdc20 represents a critical control mechanism to ensure inactivation of APC/C(Cdc20) in response to the spindle assembly checkpoint.
- BubR1 competes with Cdc20 for binding to securin. Interaction of BubR1 and securin is increased by the depletion of Cdc20. Regulation of BubR1 may generate an anaphase-inhibitory signal through the Cdc20-independent interaction of BubR1 with securin.
- Results support a model in which immobilized Mad1/Mad2 at kinetochores provides a template for initial assembly of Mad2 bound to Cdc20 that is then converted to a final mitotic checkpoint inhibitor with Cdc20 bound to BubR1.