Product Pathways - Cell Cycle / Checkpoint
CDC20 (D6C2Q) Rabbit mAb #14866
|14866S||100 µl ( 10 western blots )||￥3,100.00 现货查询||购买询价|
|14866||carrier free & custom formulation / quantity||email request|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting, IP=Immunoprecipitation,
Specificity / Sensitivity
CDC20 (D6C2Q) Rabbit mAb recognizes endogenous levels of total CDC20 protein. This antibody does not cross-react with FZR1 protein.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of human CDC20 protein.
Western blot analysis of extracts from various cell lines using CDC20 (D6C2Q) Rabbit mAb.
Immunoprecipitation of CDC20 from 293T cell extracts using Rabbit (DA1E) mAb IgG XP® Isotype Control #3900 (lane 2) or CDC20 (D6C2Q) Rabbit mAb (lane 3). Lane 1 is 10% input. Western blot analysis was performed using CDC20 (D6C2Q) Rabbit mAb.
Western blot analysis of extracts from 293T cells, mock transfected (-) or transfected with constructs expressing Myc/DDK-tagged full-length human CDC20 protein (hCDC20-Myc/DDK; +) and Myc/DDK-tagged full-length human FZR1 protein (hFZR1-Myc/DDK; +), using CDC20 (D6C2Q) Rabbit mAb (upper) and DYKDDDDK Tag Antibody #2368 (lower).
The cell division cycle demands accuracy to avoid the accumulation of genetic damage. This process is controlled by molecular circuits called "checkpoints" that are common to all eukaryotic cells (1). Checkpoints monitor DNA integrity and cell growth prior to replication and division at the G1/S and G2/M transitions, respectively. The cdc2-cyclin B kinase is pivotal in regulating the G2/M transition (2,3). Cdc2 is phosphorylated at Thr14 and Tyr15 during G2-phase by the kinases Wee1 and Myt1, rendering it inactive. The tumor suppressor protein retinoblastoma (Rb) controls progression through the late G1 restriction point (R) and is a major regulator of the G1/S transition (4). During early and mid G1-phase, Rb binds to and represses the transcription factor E2F (5). The phosphorylation of Rb late in G1-phase by CDKs induces Rb to dissociate from E2F, permitting the transcription of S-phase-promoting genes. In vitro, Rb can be phosphorylated at multiple sites by cdc2, cdk2, and cdk4/6 (6-8). DNA damage triggers both the G2/M and the G1/S checkpoints. DNA damage activates the DNA-PK/ATM/ATR kinases, which phosphorylate Chk at Ser345 (9), Chk2 at Thr68 (10) and p53 (11). The Chk kinases inactivate cdc25 via phosphorylation at Ser216, blocking the activation of cdc2.
CDC20 binds to and activates the APC/C during mitosis and G1 phase of the cell cycle (12). Moreover, CDC20 is necessary for ubiquitin ligase activity of the APC/C. In metaphase MAD2L1 inactivates the CDC20-APC/C complex, while in anaphase this inhibition is lost and CDC20-APC/C degrades its substrates (13). p53 and p21 suppress expression of CDC20 upon genotoxic stresses and ectopic introduction of p53. siRNA mediated knock-down of CDC20 in cancer cells leads to attenuated cell growth and induces G2/M arrest, suggesting that CDC20 is a possible therapeutic target of cancer (14). Organization of neuronal circuits requires presynaptic axonal differentiation and synapse formation. CDC20-APC regulates presynaptic differentiation in post-mitotic neurons by triggering the required degradation of the transcription factor NeuroD2 (15).
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