Dactinomycin

Publication Title: 
The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences

Previous studies indicated that renal tubular epithelial cells from some long-lived avian species exhibit robust and/or unique protective mechanisms against oxidative stress relative to murine cells.

Author(s): 
Ogburn, C. E.
Carlberg, K.
Ottinger, M. A.
Holmes, D. J.
Martin, G. M.
Austad, S. N.
Publication Title: 
The Journal of Pharmacology and Experimental Therapeutics
Author(s): 
Indacochea-Redmond, N.
Witschi, H.
Plaa, G. L.
Publication Title: 
Apoptosis: An International Journal on Programmed Cell Death

Isoflavone genistein may have beneficial effects on vascular function, but the mechanism is unclear. Here, we investigated whether genistein protects vascular endothelial cells against apoptosis induced by tumor necrosis factor-alpha. We show that genistein significantly inhibited TNF-alpha-induced apoptosis in human aortic endothelial cells as determined by caspase-3 activation, 7-amino actinomycin D staining, in situ apoptotic cell detection and DNA laddering. The anti-apoptotic effect of genistein was associated with an enhanced expression of Bcl-2 protein and its promoter activity.

Author(s): 
Si, Hongwei
Liu, Dongmin
Publication Title: 
The Journal of Biological Chemistry

hnRNP K, a member of the family of heterogeneous ribonucleoproteins, is known to exert various functional roles in the nucleus, cytoplasm, and mitochondria to affect different cellular processes including chromatin remodeling, transcription, splicing, and translation. Here we report, for the first time, that hnRNP K is specifically involved in human LDL receptor (LDLR) gene transcription in HepG2 cells. We show that depletion of hnRNP K by siRNA transfection reduces the expression of LDLR mRNA and protein by more than 50% as measured by quantitative real-time PCR and Western blot analysis.

Author(s): 
Li, Hai
Liu, Jingwen
Publication Title: 
The Journal of Clinical Investigation

The present studies were performed to elucidate the mechanisms responsible for the impairment of glucose-stimulated insulin secretion observed in fasting. Rats fasted for 48 hr displayed marked impairment in their insulin secretory response to both oral and intravenous glucose. Glucose-stimulated insulin secretion was restored within 24 hr by refeeding; actinomycin D given before refeeding blocked the expected return of normal glucose-stimulated insulin secretion despite adequate food intake.

Author(s): 
Grey, N. J.
Goldring, S.
Kipnis, D. M.
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