The hot-spot p53R172H mutant promotes formation of giant spermatogonia triggered by DNA damage

• Main Authors: Xue, Y, Raharja, A, Sim, W, Wong, E.S.M, Rahmat, S.A.B, Lane, D.P
• Other Authors: MEDICINE
• Format: Article
• Published: Nature Publishing Group 2020
• Subjects: aurora B kinase; beta galactosidase; caspase 3; cyclin A2; cyclin D1; cycline; histone gamma h2ax; histone H2AX; histone H3; protein MDM2; protein p21; protein p53; tumor suppressor p53 binding protein 1; unclassified drug; arginine; histidine; mutant protein; adult; animal cell; animal experiment; animal model; animal tissue; apoptosis; Article; cell cycle progression; cell proliferation; controlled study; DNA damage; DNA damage response; double stranded DNA break; embryo; gene expression; gene sequence; genetic transcription; giant spermatogonia; hereditary tumor; immunohistochemistry; in situ hybridization; intron; irradiation; Leydig cell; male; mouse; newborn; nonhuman; primordial germ cell; priority journal; promoter region; protein depletion; protein function; seminiferous tubule epithelium; Sertoli cell; spermatid; spermatocyte; spermatogenesis; spermatogonium; staining; amino acid substitution; animal; genetics; mammalian embryo; metabolism; mutation rate; pathology; physiology; testis; testis tumor; transgenic mouse; tumor suppressor gene; Amino Acid Substitution; Animals; Animals, Newborn; Apoptosis; Arginine; DNA Damage; Embryo, Mammalian; Genes, p53; Histidine; Male; Mice; Mice, Transgenic; Mutant Proteins; Mutation Rate; Spermatogonia; Testicular Neoplasms; Testis
• Online Access: https://scholarbank.nus.edu.sg/handle/10635/179209
• Institution: National University of Singapore

10.1038/onc.2016.374