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

Saved in:

書目詳細資料
Main Authors:	Xue, Y, Raharja, A, Sim, W, Wong, E.S.M, Rahmat, S.A.B, Lane, D.P
其他作者:	MEDICINE
格式:	Article
出版:	Nature Publishing Group 2020
主題:	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
在線閱讀:	https://scholarbank.nus.edu.sg/handle/10635/179209
標簽:	添加標簽沒有標簽, 成為第一個標記此記錄!
機構:	National University of Singapore

實物特徵
總結:	10.1038/onc.2016.374