scholarly journals Effects of Trypanocidal drugs on DNA synthesis: new insights into melarsoprol growth inhibition

Parasitology ◽  
2021 ◽  
pp. 1-30
Author(s):  
Stephen Larson ◽  
McKenzie Carter ◽  
Galadriel Hovel-Miner
Keyword(s):  
Growth Inhibition ◽  
Dna Synthesis ◽  
Trypanocidal Drugs

Stimulation of cell division and DNA replication inPrototheca richardsiby passage through larval amphibian guts

Parasitology ◽  
1993 ◽  
Vol 107 (2) ◽  
pp. 119-124 ◽  
Author(s):  
T. J. C. Beebee ◽  
A. L.-C. Wong
Keyword(s):  
Cell Division ◽  
Dna Replication ◽  
Growth Inhibition ◽  
Dna Synthesis ◽  
Free Living ◽  
Leucine Uptake ◽  
Amphibian Larvae ◽  
Larval Amphibian ◽  
Stimulation Of

SUMMARYPrototheca richardsi, an unpigmented heterotrophic alga, causes growth inhibition in amphibian larvae and has proved refractory to culturein Vitro.P. richardsireplication is dependent on regular passaging through tadpole digestive systems; uptake of thymidine by free-livingProtothecacells and incorporation into DNA are very low by comparison with leucine uptake and incorporation into protein, but DNA synthesis is detectable in cells isolated from tadpole intestines. DNA replication was elicited 6–8 h after ingestion in protothecans fed to tadpoles and subsequently re-isolated from them, providing that the tadpoles were fed subsequent to the ingestion. It appears that passaging through tadpole intestines provides an essential stimulus to maintaining an active cell division cycle inP. richardsi.

scholarly journals Growth inhibition by the muscarinic M3 acetylcholine receptor: evidence for p21Cip1/Waf1 involvement in G1 arrest

2002 ◽  
Vol 367 (2) ◽  
pp. 549-559 ◽  
Author(s):  
Drew BURDON ◽  
Rajnikant PATEL ◽  
R.A. John CHALLISS ◽  
Jonathan L. BLANK
Keyword(s):  
Growth Inhibition ◽  
Dna Synthesis ◽  
Acetylcholine Receptors ◽  
Chinese Hamster ◽  
Phase Cell ◽  
G1 Arrest ◽  
Growth Responses ◽  
Interacting Protein ◽  
Extracellular Signal ◽  
Mitogen Activated Protein

We have assessed the growth response of Chinese-hamster ovary (CHO) cells to activation of recombinantly expressed G-protein-coupled muscarinic M2 or M3 acetylcholine receptors (AChRs). We show that activation of these receptors leads to divergent growth responses: M2 AChR activation causes an increase in DNA synthesis, whereas M3 AChR activation causes a dramatic decrease in DNA synthesis. We have characterized the M3 AChR-mediated growth inhibition and show that it involves a G1 phase cell-cycle arrest. Further analysis of this arrest indicates that it involves an increase in expression of the cyclin-dependent kinase (CDK) inhibitor, p21Cip1/Waf1 (where Cip1 is CDK-interacting protein 1 and Waf1 is wild-type p53-associated fragment 1), in response to M3 AChR activation. This increase in protein expression leads to an increase in p21Cip1/Waf1 association with CDK2, a decrease in CDK2 activity and an accumulation of hypophosphorylated retinoblastoma protein. The increased p21Cip1/Waf1 expression is due, at least in part, to an increase in p21Cip1/Waf1 mRNA, and receptor-mediated changes in phosphorylation of c-Jun provide a mechanism to account for this p21Cip1/Waf1 transcriptional regulation. Evaluation of the extracellular signal-regulated protein kinase and c-Jun N-terminal kinase activities has shown striking differences in the profiles of activation of these mitogen-activated protein kinases by the M2 and M3 AChRs, and their potential involvement in mediating growth arrest by the M3 AChR is discussed.

The role of HMG CoA reductase and dolichol synthesis in the control of 3T6 cell proliferation: effects of cell crowding, serum depletion and addition of epidermal growth factor

1988 ◽  
Vol 90 (4) ◽  
pp. 613-620
Author(s):  
O. Larsson
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Growth Inhibition ◽  
Dna Synthesis ◽  
Experimental Conditions ◽  
Hmg Coa Reductase ◽  
Dependent Inhibition ◽  
Epidermal Growth ◽  
Coa Reductase

The proliferation of 3T6 cells was substantially decreased when the monolayer cultures were allowed to reach confluency. This growth inhibition (so-called density-dependent inhibition) was of the same magnitude as that following serum depletion in non-confluent cultures. Each type of growth inhibition was correlated to a depression of the activity of 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG CoA) reductase, an enzyme that regulates the biosynthesis of cholesterol and isoprenoid derivatives (e.g. dolichol) by catalysing the reduction of HMG CoA (which is derived from acetyl-CoA) into mevalonate. However, the depression of enzyme activity was more substantial in cells exposed to cell crowding than that in serum-depleted cells (87 and 48%, respectively). On the other hand, there was a 60–65% inhibition of the incorporation of mevalonate into dolichol due to serum deprivation, while it remained at normal level in confluent cultures, which implies that the inhibitory effects on dolichol synthesis due to these two experimental conditions were approximately equipotent. Addition of epidermal growth factor (EGF) to the cell cultures, whose proliferation was inhibited due to serum depletion, restored DNA synthesis completely, and these effects were related to a normalization of the activity of HMG CoA reductase and of the incorporation of mevalonate into dolichol. In contrast, in confluent cells addition of EGF only caused a slight increase in DNA synthesis and activity of HMG CoA reductase, and there was no significant increase in the incorporation of mevalonate into dolichol either.(ABSTRACT TRUNCATED AT 250 WORDS)

QUANTITATIVE ASPECTS OF OXYGEN TOXICITY IN THE NEWBORN: INHIBITION OF LUNG DNA SYNTHESIS IN THE MOUSE

PEDIATRICS ◽  
1972 ◽  
Vol 50 (1) ◽  
pp. 67-72
Author(s):  
William H. Northway ◽  
Rita Petriceks ◽  
Lee Shahinian
Keyword(s):  
Growth Inhibition ◽  
Dna Synthesis ◽  
Cultured Cells ◽  
Oxygen Toxicity ◽  
Newborn Mouse ◽  
Cell Replication ◽  
Lung Growth ◽  
Lung Weight ◽  
Newborn Mice ◽  
Total Dna

The incorporation of 3H-thymidine into lung DNA in newborn mice was inhibited by increasing exposure to 96-100% oxygen. Twenty-four hours following the onset of this inhibition both total DNA per lung and lung weight decreased in the oxygen-exposed animals relative to the air-exposed control animals. These data indicate that 96-100% oxygen retards lung growth in the newborn mouse by inhibiting DNA synthesis and cell replication. These results are consistent with observations on cultured cells of nonpulmonary origin. Such growth inhibition may occur at oxygen concentrations below 96 -100%.

scholarly journals p53 Differentially Inhibits Cell Growth Depending on the Mechanism of Telomere Maintenance

2004 ◽  
Vol 24 (13) ◽  
pp. 5967-5977 ◽  
Author(s):  
Zaineb R. Abdul Razak ◽  
Robert J. Varkonyi ◽  
Michelle Kulp-McEliece ◽  
Corrado Caslini ◽  
Joseph R. Testa ◽  
...  
Keyword(s):  
Growth Inhibition ◽  
Dna Synthesis ◽  
Cell Lines ◽  
Current Data ◽  
Telomere Maintenance ◽  
Temperature Sensitive ◽  
Telomere Repeat ◽  
Alternative Lengthening ◽  
Clonal Cell Lines ◽  
Inhibition Of Dna Synthesis

ABSTRACT Telomere stabilization is critical for tumorigenesis. A number of tumors and cell lines use a recombination-based mechanism, alternative lengthening of telomeres (ALT), to maintain telomere repeat arrays. Current data suggest that the mutation of p53 facilitates the activation of this pathway. In addition to its functions in response to DNA damage, p53 also acts to suppress recombination, independent of transactivation activity, raising the possibility that p53 might regulate the ALT mechanism via its role as a regulator of recombination. To test the role of p53 in ALT we utilized inducible alleles of human p53. We show that expression of transactivation-incompetent p53 inhibits DNA synthesis in ALT cell lines but does not affect telomerase-positive cell lines. The expression of temperature-sensitive p53 in clonal cell lines results in ALT-specific, transactivation-independent growth inhibition, due in part to the perturbation of S phase. Utilizing chromatin immunoprecipitation assays, we demonstrate that p53 is associated with the telomeric complex in ALT cells. Furthermore, the inhibition of DNA synthesis in ALT cells by p53 requires intact specific DNA binding and suppression of recombination functions. We propose that p53 causes transactivation-independent growth inhibition of ALT cells by perturbing telomeric recombination.

Use of Antibody to aid Visualization of Protein at the Termini of Bacteriophage Ø29 DNA

1980 ◽  
Vol 38 ◽  
pp. 540-541
Author(s):  
Dwight Anderson ◽  
Charlene Peterson ◽  
Gursaran Notani ◽  
Bernard Reilly
Keyword(s):  
Electron Microscopy ◽  
Bacillus Subtilis ◽  
Dna Synthesis ◽  
Restriction Endonuclease ◽  
Protein Complex ◽  
Protein Product ◽  
Viral Dna ◽  
Small Proteins ◽  
Antibody Labeling ◽  
Subtilis Bacteriophage

The protein product of cistron 3 of Bacillus subtilis bacteriophage Ø29 is essential for viral DNA synthesis and is covalently bound to the 5’-termini of the Ø29 DNA. When the DNA-protein complex is cleaved with a restriction endonuclease, the protein is bound to the two terminal fragments. The 28,000 dalton protein can be visualized by electron microscopy as a small dot and often is seen only when two ends are in apposition as in multimers or in glutaraldehyde-fixed aggregates. We sought to improve the visibility of these small proteins by use of antibody labeling.

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