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John M. Parant

Researcher at University of Alabama at Birmingham

Publications -  34
Citations -  5301

John M. Parant is an academic researcher from University of Alabama at Birmingham. The author has contributed to research in topics: Mutant & Zebrafish. The author has an hindex of 17, co-authored 30 publications receiving 4824 citations. Previous affiliations of John M. Parant include University of Utah & University of Texas MD Anderson Cancer Center.

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The Tol2kit: a multisite gateway-based construction kit for Tol2 transposon transgenesis constructs.

TL;DR: The Tol2kit greatly facilitates zebrafish transgenesis, simplifies the sharing of clones, and enables large‐scale projects testing the functions of libraries of regulatory or coding sequences.
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Gain of Function of a p53 Hot Spot Mutation in a Mouse Model of Li-Fraumeni Syndrome

TL;DR: In vivo validation for the gain-of-function properties of certain p53 missense mutations are provided and a mechanistic basis for these phenotypes is suggested.
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Pirh2, a p53-Induced Ubiquitin-Protein Ligase, Promotes p53 Degradation

TL;DR: Pirh2, a gene regulated by p53 that encodes a RING-H2 domain-containing protein with intrinsic ubiquitin-protein ligase activity, is described and it is proposed that Pirh2 is involved in the negative regulation of p53 function through physical interaction and ubiquit in-mediated proteolysis.
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Rescue of embryonic lethality in Mdm4 -null mice by loss of Trp53 suggests a nonoverlapping pathway with MDM2 to regulate p53

TL;DR: MDM2 and MDM4 are nonoverlapping critical regulators of p53 in vivo, which define a new pathway of p 53 regulation and raise the possibility that increasedMDM4 levels and the resulting inactivation of p52 contribute to the development of human tumors.
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Chromosome stability, in the absence of apoptosis, is critical for suppression of tumorigenesis in Trp53 mutant mice.

TL;DR: The ability of mutant p53-R172P to induce a partial cell cycle arrest and retain chromosome stability are crucial for suppression of early onset tumorigenesis.