anti-Cell Division Cycle 20 Homolog (S. Cerevisiae) (CDC20) Antibodies

Human Cell Division Cycle 20 Homolog (S. Cerevisiae) (CDC20) interaction partners

1. Cdc20 exerts its oncogenic role partly due to regulation of Bim and p21 in osteosarcoma cells.

2. Study indicates that CDC20 knockdown inhibited migration, a key component of the tumor metastatic process, in chemoresistant pancreatic cancer cells and metastatic breast cancer cells. By contrast, the overexpression of CDC20 by plasmid transfection promoted the metastasizing capacities of these cells. Results suggest that CDC20 is a critical regulator of cancer metastasis.

3. knockdown of CDC20 can be used for therapeutic benefit and represents an effective adjuvant anti-cancer treatment to eliminate CSCs during prostate cancer progression.

4. Study demonstrated that CDC20 is overexpressed in cutaneous squamous cell carcinoma (cSCC) tissues and cell lines, and its expression is associated with tumor progression. Knockdown of CDC20 suppressed cell growth and migration, and promoted apoptosis and cell cycle arrest in cSCC.

5. The expression levels of CDC20 and PTGDS were able to predict overall survival in diffuse large B-cell lymphoma patients.

6. Knockdown of CDC20 enhanced the drug sensitivity of TR cells to Temozolomide.

7. Results showed that CENPA, CDK1 and CDC20 were highly expressed in lung adenocarcinoma (LAC) tissue with co-expression patterns. Also, the integrated microarray analysis demonstrated that CENPA, CDK1 and CDC20 might serve as novel cluster of prognostic biomarkers for LAC.

8. our data collectively demonstrated that Cdc20 overexpression facilitates the docetaxel resistant of the castration-resistant prostate cancer cell lines in a Bim-dependent manner

9. findings suggest that application of the CDC20-M signature may permit more selective use of adjuvant therapies for glioma patients and that dysregulated CDC20-M members may provide a therapeutic vulnerability in glioma.

10. Study indicated that AURKA, CDC20 and TPX2 are over-expressed in smoking related lung adenocarcinoma tissues and their higher mRNA expression levels have a worse prognosis.

11. we demonstrate that the CDC20-MAD2 complex could also be formed independently of the SAC. Moreover, in prolonged arrest caused by nocodazole treatment, the overall levels of the CDC20-MAD2 complex are gradually, but significantly, reduced and this is associated with lower levels of cyclin B1, which brings a new insight into the mechanism of mitotic "slippage" of the arrested cells.

12. Cdc20 may be a promising molecular target for chemotherapy.

13. Long non-coding RNA SPRY4-IT1 promotes cell proliferation and invasion by regulation of Cdc20 in pancreatic cancer cells

14. Cdc20 functions as an important negative regulator of SMAR1 in higher grades of cancer

15. Data provide support for the recent structure-based models and functionally dissect three elements of Cdc20 inhibition: sequestration of Cdc20 in the core mitotic checkpoint complex, sufficient at low Cdc20 concentrations; inhibition of a second Cdc20 through the Mad3 C terminus, independent of Mad2 binding to this Cdc20 molecule; and occupancy of the APC/C with full MCC, where Mad3 and Apc15 are involved.

16. CDC20 gene, related to cell proliferation in protein complex A, might play momentous roles in the initiation and development of consecutive Trauma-Induced Sepsis.

17. A mitotic phosphorylation site on Cdc20, known to be a substrate of PP2A(B56), modulates APC/C(Cdc20) assembly.

18. c-Myc is a driver when combined with kRas/Akt3 oncogenic signals in gliomagenesis, whereas Cdc20 overexpression is a passenger

19. The ABBA-KEN-ABBA amino acid motif cassette holds the Mitotic Checkpoint Complex (MCC) onto the Anaphase-Promoting Complex-Cyclosome (APC/C) by binding the two Cdc20 molecules in the MCC-APC/C complex.

20. It discuses the roles of Cdc20 in SAC signalling and mitotic exit, describe how the integration of traditional approaches with emerging technologies has revealed new details of Cdc20 functions, comment about the potential of Cdc20 as a therapeutic target for the treatment of human malignancies.

Xenopus laevis Cell Division Cycle 20 Homolog (S. Cerevisiae) (CDC20) interaction partners

1. Cdc20 auto-ubiquitylation does not play a major role in terminating Cdc20 activation.

2. Dephosphorylation of Cdc20 is required for its loading and activation of the APC/C ubiquitin ligase.

3. A role for the fizzy/cdc20 family of proteins in activation of the APC/C distinct from substrate recruitment is reported.

Mouse (Murine) Cell Division Cycle 20 Homolog (S. Cerevisiae) (CDC20) interaction partners

1. PPM1K Regulates Hematopoiesis and Leukemogenesis through CDC20-Mediated Ubiquitination of MEIS1 and p21.

2. Enforced expression of CDC20 in cardiomyocytes and in the heart aggravated the hypertrophic response. Furthermore, the authors found that CDC20 directly targeted LC3, a key regulator of autophagy, and promoted LC3 ubiquitination and degradation by the proteasome, which inhibited autophagy leading to cardiac hypertrophy.

3. Cdc20 hypomorphism causes chromatin bridging and chromosome misalignment, revealing a requirement for Cdc20 in efficient sister chromosome separation and chromosome-microtubule attachment.

4. The physiologically effective threshold level of Cdc20 is high for female meiosis I.

5. Results indicate that Cdc20 also contributes to post-anaphase activation of the APC/C.

6. This cell division cycle protein is a key regulator of the cell cycle.

7. The seven tandem WD motifs of Cdc20 they are required for speriolin binding and for localization of Cdc20 to the centrosomes and nucleus, suggesting that speriolin might regulate or stabilize the folding of Cdc20 during meiosis in spermatogenic cells

8. Data suggest that Mad2 and BubR1 must cooperate to inhibit Cdc20 activity.

9. Cdc20 is degraded through two independent degradation signals (degrons), the KEN box and a newly described CRY box.

10. Cdc20 and securin double mutant embryos could not maintain the metaphase arrest, suggesting a role of securin in preventing mitotic exit

11. Expression of the cdc20 gene is down-regulated by zif268 in neuronal cells; altered expression of proteasome-regulatory genes following zif268 induction may be a key component of long-lasting CNS plasticity.

12. Cdc20 is required for the anaphase onset of the first meiosis but not the second meiosis in mouse oocytes

13. findings suggest a novel function of HSF1 frequently overexpressed in cancer cells, to inhibit APC/C activity by interacting with Cdc20, and to result in aneuploidy development and genomic instability

14. Data show that the BubR1 N terminus binds to Cdc20 to inhibit APC/C activity in interphase, thereby allowing accumulation of cyclin B in G(2) phase prior to mitosis onset.

15. Results indicate that the spindle assembly checkpoint-mediated inhibition of Cdc20 is an important tumor-suppressing mechanism.

Pig (Porcine) Cell Division Cycle 20 Homolog (S. Cerevisiae) (CDC20) interaction partners

1. porcine FZR1 and CDC20 work on the maintenance of meiotic arrest at the first meiotic prophase and on the exit from M1