TY - JOUR
T1 - Reduction by cycloheximide of lysosomal proteolytic enzyme activity and rate of protein degradation in organ-cultured hearts
AU - Wildenthal, Kern
AU - Griffin, Edmond E.
N1 - Funding Information:
This work was supported by the National Heart and Lung Institute (HL 14706 and HL 06296) and the Moss Heart Fund. Dr. Wildenthal held a USPHS Career Development Award during the time the study was performed (HL 70125). We thank Dr. J.T. Dingle and Dr. D.E. Rannels for discussions and S.C. Jasinski, M. Kennedy, P.C. Morton, A. Vasil, and J.R. Wakeland for technical assistance.
PY - 1976/9/24
Y1 - 1976/9/24
N2 - Cycloheximide, an agent whose primary action is inhibition of protein synthesis, also causes a decrease in the rate of protein degradation in cultured fetal mouse hearts. This is associated with marked decreases in the activities of cathespin D and other lysosomal hydrolases. It is suggested that reduced lysosomal proteolytic capacity may contribute to cycloheximide-induced inhibition of protein degradation.
AB - Cycloheximide, an agent whose primary action is inhibition of protein synthesis, also causes a decrease in the rate of protein degradation in cultured fetal mouse hearts. This is associated with marked decreases in the activities of cathespin D and other lysosomal hydrolases. It is suggested that reduced lysosomal proteolytic capacity may contribute to cycloheximide-induced inhibition of protein degradation.
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U2 - 10.1016/0304-4165(76)90395-0
DO - 10.1016/0304-4165(76)90395-0
M3 - Article
C2 - 971421
AN - SCOPUS:0017186753
SN - 0304-4165
VL - 444
SP - 519
EP - 524
JO - Biochimica et Biophysica Acta - General Subjects
JF - Biochimica et Biophysica Acta - General Subjects
IS - 2
ER -