Hypoxia-induced deacetylation is required for tetraploid differentiation in response to testicular ischemia-reperfusion (IR) injury

Journal of Andrology

Volumn 33, Issue 6, 2012, Pages 1379-1386

  Hou, Wugang ^a   Dong, Yushu ^b   Zhang, Jinshan ^c   Yin, Zhongmin ^b   Wen, Hua ^b   Xiong, Lize ^a   Li, Wei ^b  

^a FOURTH MILITARY MEDICAL UNIVERSITY   (China)

^b Shenyang 463 Hospital   (China)

^c FOURTH MILITARY MEDICAL UNIVERSITY   (China)

Author keywords

Apoptosis; Histone deacetylase (HDAC); Tetraploid Pachytene Spermatocytes

Indexed keywords

ACYLTRANSFERASE; HISTONE DEACETYLASE 2; HISTONE DEACETYLASE INHIBITOR; PROTEIN P53;

ANIMAL EXPERIMENT; ANIMAL MODEL; APOPTOSIS; ARTICLE; CELL DIFFERENTIATION; DEACETYLATION; ENZYME ACTIVITY; GENOME; HYPOXIA; IN VITRO STUDY; IN VIVO STUDY; INFORMATION PROCESSING; MALE; MEIOSIS; MOUSE; NONHUMAN; PACHYTENE; PRIORITY JOURNAL; PROTEIN EXPRESSION; REPERFUSION INJURY; SPERMATOCYTE; SPERMATOGENESIS; TESTIS INJURY; TETRAPLOIDY;

ANIMALS; ANOXIA; APOPTOSIS; CELL DIFFERENTIATION; HISTONE DEACETYLASE INHIBITORS; HISTONE DEACETYLASES; HYDROXAMIC ACIDS; MALE; MICE; MICE, INBRED C57BL; OKADAIC ACID; REPERFUSION INJURY; TESTIS; TETRAPLOIDY; TUMOR SUPPRESSOR PROTEIN P53;

EID: 84870028855     PISSN: 01963635     EISSN: 19394640     Source Type: Journal    
DOI: 10.2164/jandrol.112.016584     Document Type: Article

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