Key Spec Table
|Species Reactivity||Key Applications||Host||Format||Antibody Type|
|H, M, R||WB, IP||Rb||Serum||Polyclonal Antibody|
|Presentation||Unpurified rabbit serum containing 0.05% NaN3.|
|Safety Information according to GHS|
|Storage and Shipping Information|
|Storage Conditions||Stable for 2 years at -20°C from date of receipt.
Handling Recommendations: Upon receipt, and prior to removing the cap, centrifuge the vial and gently mix the solution.
|Material Size||100 µL|
|Anti-CDT1 - 2051947||2051947|
|Anti-CDT1 - NG1618263||NG1618263|
|Anti-CDT1 - NG1806854||NG1806854|
|Anti-CDT1 Polyclonal Antibody||2964471|
|Anti-CDT1 Polyclonal Antibody||2970628|
|Reference overview||Pub Med ID|
|Human papillomavirus E7 induces rereplication in response to DNA damage.|
Fan, X; Liu, Y; Heilman, SA; Chen, JJ
Journal of virology 87 1200-10 2013
Human papillomavirus (HPV) infection is necessary but not sufficient for cervical carcinogenesis. Genomic instability caused by HPV allows cells to acquire additional mutations required for malignant transformation. Genomic instability in the form of polyploidy has been demonstrated to play an important role in cervical carcinogenesis. We have recently found that HPV-16 E7 oncogene induces polyploidy in response to DNA damage; however, the mechanism is not known. Here we present evidence demonstrating that HPV-16 E7-expressing cells have an intact G(2) checkpoint. Upon DNA damage, HPV-16 E7-expressing cells arrest at the G(2) checkpoint and then undergo rereplication, a process of successive rounds of host DNA replication without entering mitosis. Interestingly, the DNA replication initiation factor Cdt1, whose uncontrolled expression induces rereplication in human cancer cells, is upregulated in E7-expressing cells. Moreover, downregulation of Cdt1 impairs the ability of E7 to induce rereplication. These results demonstrate an important role for Cdt1 in HPV E7-induced rereplication and shed light on mechanisms by which HPV induces genomic instability.