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

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

10.1038/onc.2016.374

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Bibliographic Details
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
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Institution:	National University of Singapore

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Summary:	10.1038/onc.2016.374