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

10.1038/onc.2016.374

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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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spelling	sg-nus-scholar.10635-1792092024-04-18T03:08:02Z The hot-spot p53R172H mutant promotes formation of giant spermatogonia triggered by DNA damage Xue, Y Raharja, A Sim, W Wong, E.S.M Rahmat, S.A.B Lane, D.P MEDICINE 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 DNA damage genetics mammalian embryo metabolism mutation rate pathology physiology spermatogonium 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 10.1038/onc.2016.374 Oncogene 36 14 2002-2013 2020-10-23T02:30:37Z 2020-10-23T02:30:37Z 2017 Article Xue, Y, Raharja, A, Sim, W, Wong, E.S.M, Rahmat, S.A.B, Lane, D.P (2017). The hot-spot p53R172H mutant promotes formation of giant spermatogonia triggered by DNA damage. Oncogene 36 (14) : 2002-2013. ScholarBank@NUS Repository. https://doi.org/10.1038/onc.2016.374 09509232 https://scholarbank.nus.edu.sg/handle/10635/179209 Attribution 4.0 International http://creativecommons.org/licenses/by/4.0/ Nature Publishing Group Unpaywall 20201031
institution	National University of Singapore
building	NUS Library
continent	Asia
country	Singapore Singapore
content_provider	NUS Library
collection	ScholarBank@NUS
topic	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 DNA damage genetics mammalian embryo metabolism mutation rate pathology physiology spermatogonium 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
spellingShingle	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 DNA damage genetics mammalian embryo metabolism mutation rate pathology physiology spermatogonium 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 Xue, Y Raharja, A Sim, W Wong, E.S.M Rahmat, S.A.B Lane, D.P The hot-spot p53R172H mutant promotes formation of giant spermatogonia triggered by DNA damage
description	10.1038/onc.2016.374
author2	MEDICINE
author_facet	MEDICINE Xue, Y Raharja, A Sim, W Wong, E.S.M Rahmat, S.A.B Lane, D.P
format	Article
author	Xue, Y Raharja, A Sim, W Wong, E.S.M Rahmat, S.A.B Lane, D.P
author_sort	Xue, Y
title	The hot-spot p53R172H mutant promotes formation of giant spermatogonia triggered by DNA damage
title_short	The hot-spot p53R172H mutant promotes formation of giant spermatogonia triggered by DNA damage
title_full	The hot-spot p53R172H mutant promotes formation of giant spermatogonia triggered by DNA damage
title_fullStr	The hot-spot p53R172H mutant promotes formation of giant spermatogonia triggered by DNA damage
title_full_unstemmed	The hot-spot p53R172H mutant promotes formation of giant spermatogonia triggered by DNA damage
title_sort	hot-spot p53r172h mutant promotes formation of giant spermatogonia triggered by dna damage
publisher	Nature Publishing Group
publishDate	2020
url	https://scholarbank.nus.edu.sg/handle/10635/179209
_version_	1800914542823211008

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

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