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Julian Gannon

Researcher at University of Cambridge

Publications -  31
Citations -  5288

Julian Gannon is an academic researcher from University of Cambridge. The author has contributed to research in topics: Cyclin-dependent kinase & Cyclin B. The author has an hindex of 23, co-authored 31 publications receiving 5139 citations. Previous affiliations of Julian Gannon include The Hertz Corporation & Lincoln's Inn.

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p53 mutations in colorectal cancer.

TL;DR: It is concluded that overexpression of p53 is synonymous with mutation, but some mutations would not be detected by a simple immunohistochemical analysis.
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Activating mutations in p53 produce a common conformational effect. A monoclonal antibody specific for the mutant form.

TL;DR: It is proposed that immunoprecipitation of p53 by PAb240 is diagnostic of mutation in both murine and human systems and suggested that the different point mutations which convert p53 from a recessive to a dominant oncogene exert a common conformational effect on the protein.
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CDK-dependent phosphorylation of BRCA2 as a regulatory mechanism for recombinational repair

TL;DR: It is shown that the carboxy-terminal region of BRCA2, which interacts directly with the essential recombination protein RAD51, contains a site that is phosphorylated by cyclin-dependent kinases, indicating that S3291 phosphorylation might provide a molecular switch to regulate RAD51 recombination activity.
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Anaphase-promoting complex/cyclosome-dependent proteolysis of human cyclin A starts at the beginning of mitosis and is not subject to the spindle assembly checkpoint.

TL;DR: Microinjection of antibodies against subunits of the anaphase-promoting complex/cyclosome (APC/C) or against human Cdc20 (fizzy) arrested cells at metaphase and stabilized both cyclins A and B1 suggest that the APC/ C is activated as cells enter mitosis and immediately targets cyclin A for degradation, whereas the spindle assembly checkpoint delays the degradation of cyclin B1 until the metaphase to anaphases transition.
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Cyclin B2-null mice develop normally and are fertile whereas cyclin B1-null mice die in utero

TL;DR: Observations suggest that cyclin B1 may compensate for the loss ofcyclin B2 in the mutant mice, and implies that cycl in B1 is capable of targeting the p34(cdc2) kinase to the essential substrates of cyclinB2.