scholarly journals Biochemical and cross-resistance studies with HeLa cell mutants resistant to cardiac glycoside SC4453. Regulation of the resistant form of Na+/K+-ATPase in the mutant cells.

1986 ◽  
Vol 261 (5) ◽  
pp. 2034-2040
Author(s):  
A Chopra ◽  
R S Gupta
2003 ◽  
Vol 376 (1) ◽  
pp. 253-260 ◽  
Author(s):  
Pachiyappan KAMARAJAN ◽  
Nian-Kang SUN ◽  
Chuck C.-K. CHAO

Cisplatin-selected cervix carcinoma HeLa cell lines induced less apoptosis, and weaker activation by cisplatin or Fas-activating antibody, of mitochondrial-associated caspase-9 and death receptor-mediated caspase-8 than did parental cells. Furthermore, less DISC (death-inducing signalling complex) was formed in cisplatin-selected cell lines than in parental cells. Ac-IETD-CHO (acetyl-Ile-Glu-Thr-Asp-aldehyde), which has a certain preference for inhibiting caspase-8, or Fas-antagonistic antibody, significantly inhibited cisplatin-induced apoptosis in both parental and cisplatin-selected HeLa cell lines. These results imply that cell-surface death signalling is inducible by cisplatin; that reduction of this pathway is associated with drug resistance, and that cisplatin-selected cells acquire cross-resistance to cell-surface death signalling. Sequential up-regulation of FLIP (FLICE-like inhibitory protein), but not Bcl-2, Bcl-xL or inhibitors of apoptosis protein (IAPs), was observed in resistant cells but not in parental cells. The inhibition of FLIP by FLIP antisense oligonucleotides promotes cisplatin and Fas-antibody-induced apoptosis. However, the modulation of apoptosis by FLIP antisense oligonucleotides in resistant cells is greater than that in parental cells. The presented data reveal that the up-regulation of FLIP may contribute to the suppression of apoptosis and thereby change cells that are resistant to cisplatin and Fas-mediated death signals. The results also show that cancer cells that have undergone long-term chemotherapy and become chemoresistant may change the FLIP level, becoming cross-resistant to death factors such as Fas.


1993 ◽  
Vol 71 (1) ◽  
pp. 174-182 ◽  
Author(s):  
Douglas F. Bray ◽  
John R. Bagu ◽  
Kazuo Nakamura

A mutant (NL-51) of the unicellular green alga Chlamydomonas reinhardtii Dangeard isolated from a wild-type strain (137c+) was shown to be resistant to the bipyridilium herbicide paraquat at the concentration at which growth of the wild type was inhibited. Tetrad analysis from a cross between the mutant and the wild type showed 2:2 segregation, indicating that the resistance is under control of a single gene. Cross-resistance of the mutant to methionine and to methionine combined with riboflavin suggested that the resistance is due to increased levels of one of the enzymes capable of detoxifying active oxygens. Ultrastructural examination of mutant and wild-type cells exposed to paraquat revealed that the mutant cells were 3 to 4 times more resistant, but both strains showed the same sequence of deterioration. Damage was first manifested as swelling of the mitochondria and dilation of the perinuclear space. This was followed by disintegration of the nuclear matrix and the chloroplast thylakoids. Key words: Chlamydomonas reinhardtii, methionine resistance, paraquat, paraquat-resistant mutant, ultrastructure.


Blood ◽  
2005 ◽  
Vol 105 (10) ◽  
pp. 4021-4027 ◽  
Author(s):  
Ping-Hui Tseng ◽  
Ho-Pi Lin ◽  
Jiuxiang Zhu ◽  
Kuen-Feng Chen ◽  
Erinn M. Hade ◽  
...  

AbstractResistance to the Ableson protein tyrosine (Abl) kinase inhibitor imatinib mesylate has become a critical issue for patients in advanced phases of chronic myelogenous leukemia. Imatinib-resistant tumor cells develop, in part, as a result of point mutations within the Abl kinase domain. As protein kinase B (Akt) plays a pivotal role in Abl oncogene-mediated cell survival, we hypothesize that concurrent inhibition of Akt will sensitize resistant cells to the residual apoptotic activity of imatinib mesylate, thereby overcoming the resistance. Here, we examined the effect of OSU-03012, a celecoxib-derived phosphoinositide-dependent kinase-1 (PDK-1) inhibitor, on imatinib mesylate-induced apoptosis in 2 clinically relevant breakpoint cluster region (Bcr)-Abl mutant cell lines, Ba/F3p210E255K and Ba/F3p210T315I. The 50% inhibitory concentration (IC50) values of imatinib mesylate to inhibit the proliferation of Ba/F3p210E255K and Ba/F3p210T315I were 14 ± 4 and 30 ± 2 μM, respectively. There was no cross-resistance to OSU-03012 in these mutant cells with an IC50 of 5 μM irrespective of mutations. Nevertheless, in the presence of OSU-03012 the susceptibility of these mutant cells to imatinib-induced apoptosis was significantly enhanced. This synergistic action was, at least in part, mediated through the concerted effect on phospho-Akt. Together these data provide a novel therapeutic strategy to overcome imatinib mesylate resistance, especially with the Abl mutant T315I.


Author(s):  
Karen S. Howard ◽  
H. D. Braymer ◽  
M. D. Socolofsky ◽  
S. A. Milligan

The recently isolated cell wall mutant slime X of Neurospora crassa was prepared for ultrastructural and morphological comparison with the cell wall mutant slime. The purpose of this article is to discuss the methods of preparation for TEM and SEM observations, as well as to make a preliminary comparison of the two mutants.TEM: Cells of the slime mutant were prepared for thin sectioning by the method of Bigger, et al. Slime X cells were prepared in the same manner with the following two exceptions: the cells were embedded in 3% agar prior to fixation and the buffered solutions contained 5% sucrose throughout the procedure.SEM: Two methods were used to prepare mutant and wild type Neurospora for the SEM. First, single colonies of mutant cells and small areas of wild type hyphae were cut from solid media and fixed with OSO4 vapors similar to the procedure used by Harris, et al. with one alteration. The cell-containing agar blocks were dehydrated by immersion in 2,2-dimethoxypropane (DMP).


Planta Medica ◽  
2015 ◽  
Vol 81 (11) ◽  
Author(s):  
M Choules ◽  
Y Yu ◽  
SH Cho ◽  
J Anderson ◽  
W Gao ◽  
...  
Keyword(s):  

ENTOMON ◽  
2019 ◽  
Vol 44 (2) ◽  
pp. 127-132
Author(s):  
M. Visnupriya ◽  
N. Muthukrishnan

Field population of Spodoptera litura from tomato ( resistant to the majority of the conventional insecticide molecules) were subjected to the in vivo toxicity of spinetoram 12 SC to assess whether cross resistance exists or not. Untreated larvae of both field and laboratory strains showed no mortality during 48 hours of feeding. After 48 hours of feeding on spinetoram 12 SC treated leaves, LC50s of field larvae were 0.28, 0.93, 3.71 and 7.11 ppm for the 2nd, 3rd, 4th and 5th instars of S. litura respectively. However, in the laboratory strain these values were 1.12, 5.86, 36.72 and 91.55 ppm for 2nd, 3rd, 4th and 5th instars of S. litura respectively. Resistance ratio was 0.25, 0.16, 0.10 and 0.08 for the 2nd instar up to the 5th instar of S. litura.


2016 ◽  
Vol 2 (2) ◽  
pp. 1-30 ◽  
Author(s):  
Sandra Harvey

This essay reads the narratives of HeLa cell contamination as accusations of racial and gender passing. It argues that the passing narrative is much more complex, rarely confined to an individual’s autonomous will, and far more entrenched in state building and concepts of social progress than previously considered. I urge us to move away from the desire of the passing subject, and back to our own to ask after the sort of anxiety, excitement, and panic that animate our attempts to see, classify, and regulate bodies. Thus, what becomes significant is an examination of an “ethics of knowing” within science. The paper draws on a collection of correspondence, lab notes, published articles, and newspaper clippings related to Henrietta Lacks and HeLa from the George O. Gey Collection at the Medical Archives of the Johns Hopkins Medical Institutions (1918-1974) and articles on HeLa published in scientific journals, science journalism, and cultural studies articles (1950-present). In doing so, it traces the narratives of science (and its complex of industries—journalism and cultural studies) and HeLa’s passing. Tracing the reactions to HeLa contamination, the paper asks after the ways national, racial, and sexual desire, fantasy, anxiety, and paranoia have animated the cells through time. Particularly it examines the agency of HeLa, a cell line that is passed through race and genders and ideas of mortality, as it makes clear its own vital, creative, and destructive forces.


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