A transcription inhibitor, actinomycin D, partially inhibits the rhabdomeral renewal induced by a diacylglycerol lipase inhibitor, U-57908 in crab retinas

1994 ◽  
Vol 174 (6) ◽  
Author(s):  
A.D. Blest ◽  
S. Stowe ◽  
A. Delaney
Keyword(s):  
Actinomycin D ◽  
Lipase Inhibitor ◽  
Diacylglycerol Lipase ◽  
Transcription Inhibitor

A Transcription Inhibitor, Actinomycin D, Enhances HIV-1 Replication Through an Interleukin-6-Dependent Pathway

2005 ◽  
Vol 40 (4) ◽  
pp. 388-397 ◽  
Author(s):  
Tomozumi Imamichi ◽  
Thomas P Conrads ◽  
Ming Zhou ◽  
Yuxin Liu ◽  
Joseph W Adelsberger ◽  
...  
Keyword(s):  
Interleukin 6 ◽  
Actinomycin D ◽  
Transcription Inhibitor ◽  
Dependent Pathway ◽  
Hiv 1

scholarly journals Actinomycin D enhances killing of cancer cells by immunotoxin RG7787 through activation of the extrinsic pathway of apoptosis

2016 ◽  
Vol 113 (38) ◽  
pp. 10666-10671 ◽  
Author(s):  
Xiu Fen Liu ◽  
Laiman Xiang ◽  
Qi Zhou ◽  
Jean-Philippe Carralot ◽  
Marco Prunotto ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Phase I Trial ◽  
Actinomycin D ◽  
Rna Expression ◽  
Extrinsic Pathway ◽  
Western Blots ◽  
Protein Levels ◽  
Apoptotic Protein ◽  
Transcription Inhibitor ◽  
High Cytotoxic Activity

RG7787 is a mesothelin-targeted immunotoxin designed to have low-immunogenicity, high-cytotoxic activity and fewer side effects. RG7787 kills many types of mesothelin-expressing cancer cells lines and causes tumor regressions in mice. Safety and immunogenicity of RG7787 is now being assessed in a phase I trial. To enhance the antitumor activity of RG7787, we screened for clinically used drugs that can synergize with RG7787. Actinomycin D is a potent transcription inhibitor that is used for treating several cancers. We report here that actinomycin D and RG7787 act synergistically to kill many mesothelin-positive cancer cell lines and produce major regressions of pancreatic and stomach cancer xenografts. Analyses of RNA expression show that RG7787 or actinomycin D alone and together increase levels of TNF/TNFR family members and NF-κB–regulated genes. Western blots revealed the combination changed apoptotic protein levels and enhanced cleavage of Caspases and PARP.

The diacylglycerol lipase inhibitor RHC-80267 potentiates the relaxation to acetylcholine in rat mesenteric artery by anti-cholinesterase action

2005 ◽  
Vol 517 (1-2) ◽  
pp. 97-102 ◽  
Author(s):  
Philippe Ghisdal ◽  
Greet Vandenberg ◽  
Marie-Christine Hamaide ◽  
Maurice Wibo ◽  
Nicole Morel
Keyword(s):  
Mesenteric Artery ◽  
Lipase Inhibitor ◽  
Diacylglycerol Lipase ◽  
Rat Mesenteric Artery

scholarly journals Aldosterone sensitizes connecting tubule glomerular feedback via the aldosterone receptor GPR30

2014 ◽  
Vol 307 (4) ◽  
pp. F427-F434 ◽  
Author(s):  
YiLin Ren ◽  
Martin A. D'Ambrosio ◽  
Jeffrey L. Garvin ◽  
Pablo Leung ◽  
Kristopher Kutskill ◽  
...  
Keyword(s):  
Renal Damage ◽  
Actinomycin D ◽  
Control Period ◽  
Maximal Response ◽  
Connecting Tubule ◽  
Aldosterone Receptor ◽  
Epithelial Na Channels ◽  
Transcription Inhibitor ◽  
Sodium Hydrogen Exchanger ◽  
And Control

Increasing Na delivery to epithelial Na channels (ENaC) in the connecting tubule (CNT) dilates the afferent arteriole (Af-Art), a process we call connecting tubule glomerular feedback (CTGF). We hypothesize that aldosterone sensitizes CTGF via a nongenomic mechanism that stimulates CNT ENaC via the aldosterone receptor GPR30. Rabbit Af-Arts and their adherent CNTs were microdissected and simultaneously perfused. Two consecutive CTGF curves were elicited by increasing luminal NaCl in the CNT. During the control period, the concentration of NaCl that elicited a half-maximal response (EC50) was 37.0 ± 2.0 mmol/l; addition of aldosterone 10−8 mol/l to the CNT lumen caused a left-shift (decrease) in EC50 to 19.3 ± 1.3 mmol/l ( P = 0.001 vs. control; n = 6). Neither the transcription inhibitor actinomycin D nor the translation inhibitor cycloheximide prevented the effect of aldosterone (control EC50 = 34.7 ± 1.9 mmol/l; aldosterone+actinomycin D EC50 = 22.6 ± 1.6 mmol/l; P < 0.001 and control EC50 = 32.4 ± 4.3 mmol/l; aldosterone+cycloheximide EC50 = 17.4 ± 3.3 mmol/l; P < 0.001). The aldosterone antagonist eplerenone prevented the sensitization of CTGF by aldosterone (control EC50 = 33.2 ± 1.7 mmol/l; aldosterone+eplerenone EC50 = 33.5 ± 1.3 mmol/l; n = 7). The GPR30 receptor blocker G-36 blocked the sensitization of CTGF by aldosterone (aldosterone EC50 = 16.5 ± 1.9 mmol/l; aldosterone+G-36 EC50 = 29.0 ± 2.1 mmol/l; n = 7; P < 0.001). Finally, we found that the sensitization of CTGF by aldosterone was mediated, at least in part, by the sodium/hydrogen exchanger (NHE). We conclude that aldosterone in the CNT lumen sensitizes CTGF via a nongenomic effect involving GPR30 receptors and NHE. Sensitized CTGF induced by aldosterone may contribute to renal damage by increasing Af-Art dilation and glomerular capillary pressure (glomerular barotrauma).

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