Deficiency of Bax and Bak protects photoreceptors from light damage in vivo

Cell Death and Differentiation

Volumn 11, Issue 11, 2004, Pages 1192-1197

  Hahn, P ^a,b   Lindsten, T ^b   Lyubarsky, A ^a,b   Ying, G S ^b   Pugh Jr , E N ^a,b   Thompson, C B ^b   Dunaief, J L ^a,b,c  

^a UNIVERSITY OF PENNSYLVANIA   (United States)

^b UNIVERSITY OF PENNSYLVANIA   (United States)

^c Stellar Chance Laboratories   (United States)

Author keywords

Apoptosis; Bak; Bax; Light damage; Photoreceptors; Protection

Indexed keywords

PROTEIN BAK; PROTEIN BAX;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CELL DEATH; CELL MATURATION; CELL NUCLEUS; CELL PROTECTION; CELL STIMULATION; CONTROLLED STUDY; IN VIVO STUDY; LIGHT DAMAGE; LIGHT EXPOSURE; MOUSE; NICK END LABELING; NONHUMAN; PHOTORECEPTOR CELL; PHOTOSTIMULATION; PRIORITY JOURNAL; PROTEIN DEFICIENCY; RETINA;

ANIMALS; APOPTOSIS; BCL-2 HOMOLOGOUS ANTAGONIST-KILLER PROTEIN; BCL-2-ASSOCIATED X PROTEIN; CELL NUCLEUS; DNA; DNA DAMAGE; ELECTRORETINOGRAPHY; EYE; EYE INJURIES; IN SITU NICK-END LABELING; LIGHT; MEMBRANE PROTEINS; MICE; MICE, TRANSGENIC; PROTO-ONCOGENE PROTEINS C-BCL-2; RETINA; ROD OUTER SEGMENTS; TIME FACTORS;

EID: 8844219687     PISSN: 13509047     EISSN: None     Source Type: Journal    
DOI: 10.1038/sj.cdd.4401486     Document Type: Article

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