The Role of the Loop in Binding of an Actinomycin D Analog to Hairpins Formed by Single-Stranded DNA

2000 ◽  
Vol 384 (1) ◽  
pp. 199-203 ◽  
Author(s):  
Randy M. Wadkins ◽  
Chang-Shung Tung ◽  
Peter M. Vallone ◽  
Albert S. Benight
Keyword(s):  
Actinomycin D ◽  
Single Stranded Dna

Single stranded-DNA detection: the role of Wip1 in ATR-dependent pathway

2018 ◽  
Vol 46 (1) ◽  
Author(s):  
Monika Kurpas ◽  
Katarzyna Jonak ◽  
Krzysztof Puszynski
Keyword(s):  
Dna Detection ◽  
Single Stranded Dna ◽  
Dependent Pathway

scholarly journals Role of EGR-1 in thapsigargin-inducible apoptosis in the melanoma cell line A375-C6.

1995 ◽  
Vol 15 (11) ◽  
pp. 6262-6272 ◽  
Author(s):  
S Muthukkumar ◽  
P Nair ◽  
S F Sells ◽  
N G Maddiwar ◽  
R J Jacob ◽  
...  
Keyword(s):  
Actinomycin D ◽  
Interleukin 1 ◽  
Growth Control ◽  
Melanoma Cells ◽  
Dominant Negative ◽  
Dominant Negative Mutant ◽  
Functional Relevance ◽  
Antisense Oligomer ◽  
Negative Mutant

Induction of apoptosis by diverse exogenous signals is dependent on elevation of intracellular Ca2+. This process of cell death can be blocked by actinomycin D, indicating that it requires gene transcription events. To identify genes that are required for apoptosis, we used thapsigargin (TG), which inhibits endoplasmic reticulum-dependent Ca(2+)-ATPase and thereby increases cytosolic Ca2+. Exposure to TG led to induction of the zinc finger transcription factor, EGR-1, and apoptosis in human melanoma cells, A375-C6. To determine the functional relevance of EGR-1 expression in TG-inducible apoptosis, we employed a dominant negative mutant which functionally competes with EGR-1 in these cells. Interestingly, the dominant negative mutant inhibited TG-inducible apoptosis. Consistent with this observation, an antisense oligomer directed against Egr-1 also led to a diminution of the number of cells that undergo TG-inducible apoptosis. These results suggest a novel regulatory role for EGR-1 in mediating apoptosis that is induced by intracellular Ca2+ elevation. We have previously shown that in these melanoma cells, EGR-1 acts to inhibit the growth arresting action of interleukin-1. Together, these results imply that EGR-1 plays inducer-specific roles in growth control.

Genomic and nongenomic dose-dependent biphasic effect of aldosterone on Na+/H+ exchanger in proximal S3 segment: role of cytosolic calcium

2008 ◽  
Vol 295 (5) ◽  
pp. F1342-F1352 ◽  
Author(s):  
D. C. A. Leite-Dellova ◽  
M. Oliveira-Souza ◽  
G. Malnic ◽  
M. Mello-Aires
Keyword(s):  
Actinomycin D ◽  
Cytosolic Calcium ◽  
Inhibitory Effect ◽  
Ru 486 ◽  
Nongenomic Action ◽  
Biphasic Effect ◽  
S3 Segment ◽  
Dose Dependent Increase ◽  
Dose Dependent

The effects of aldosterone on the intracellular pH recovery rate (pHirr) via Na+/H+ exchanger and on the [Ca2+]i were investigated in isolated rat S3 segment. Aldosterone [10−12, 10−10, or 10−8 M with 1-h, 15- or 2-min preincubation (pi)] caused a dose-dependent increase in the pHirr, but aldosterone (10−6 M with 1-h, 15- or 2-min pi) decreased it (these effects were prevented by HOE694 but not by S3226). After 1 min of aldosterone pi, there was a transient and dose-dependent increase of the [Ca2+]i and after 6-min pi there was a new increase of [Ca2+]i that persisted after 1 h. Spironolactone, actinomycin D, or cycloheximide did not affect the effects of aldosterone (15- or 2-min pi) but inhibited the effects of aldosterone (1-h pi) on pHirr and on [Ca2+]i. RU 486 prevented the stimulatory effect of aldosterone (10−12 M, 15- or 2-min pi) on both parameters and maintained the inhibitory effect of aldosterone (10−6 M, 15- or 2-min pi) on the pHirr but reversed its stimulatory effect on the [Ca2+]i to an inhibitory effect. The data indicate a genomic (1 h, via MR) and a nongenomic action (15 or 2 min, probably via GR) on [Ca2+]i and on the basolateral NHE1 and are compatible with stimulation of the NHE1 by increases in [Ca2+]i in the lower range (at 10−12 M aldosterone) and inhibition by increases at high levels (at 10−6 M aldosterone) or decreases in [Ca2+]i (at 10−6 M aldosterone plus RU 486).

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