scholarly journals Detrimental effects of UV-B radiation in a xeroderma pigmentosum-variant cell line

2014 ◽  
Vol 55 (5) ◽  
pp. 375-384 ◽  
Author(s):  
Kimberly N. Herman ◽  
Shannon Toffton ◽  
Scott D. McCulloch
1983 ◽  
Vol 39 (4) ◽  
pp. 415-416 ◽  
Author(s):  
R. Gambari ◽  
G. Raschellà ◽  
R. Biagini ◽  
M. Tripodi ◽  
M. G. Farace ◽  
...  

1990 ◽  
Vol 10 (8) ◽  
pp. 4155-4162
Author(s):  
M Nori ◽  
L K Shawver ◽  
M J Weber

To study the relationship between oncogenesis by v-src and normal cellular signalling pathways, we determined the effects of v-src on 3T3-TNR9 cells, a Swiss 3T3 variant which does not respond mitogenically to tumor promoters such as 12-O-tetradecanoyl-phorbol-13-acetate (TPA). We found that src was unable to transform these variant cells, whether the oncogene was introduced by infection with a murine retrovirus vector or by transfection with plasmid DNA. 3T3-TNR9 cells were not inherently resistant to transformation, since infection with similar recombinant retroviruses containing either v-ras or v-abl did induce transformation. Further analysis of Swiss 3T3 and 3T3-TNR9 cell populations infected with the v-src-containing retrovirus revealed that although the amount of v-src DNA in each was approximately the same, the level of the v-src message and protein and the overall level of phosphotyrosine expressed in the infected variants was much less than in infected parental cells. Cotransfection experiments using separate v-src and neo plasmids revealed a decrease in the number of G418-resistant colonies when transfections of TNR9 cells occurred in the presence of the src-containing plasmid, suggesting a growth inhibitory effect of v-src on 3T3-TNR9 cells, as has also been found for TPA itself. Since v-src cannot transform this variant cell line, which does not respond mitogenically to the protein kinase C agonist TPA, we suggest that src makes use of the protein kinase C pathway as part of its signalling activities.


1995 ◽  
Vol 14 (2) ◽  
pp. 175-188 ◽  
Author(s):  
ROBERT DAY ◽  
SUZANNE BENJANNET ◽  
LINDA MATSUUCHI ◽  
REGIS B. KELLY ◽  
MIECZYSLAW MARCINKIEWICZ ◽  
...  

1988 ◽  
Vol 8 (2) ◽  
pp. 833-842 ◽  
Author(s):  
M Nori ◽  
M R Stallcup

The expression of mouse mammary tumor virus (MMTV) glycoproteins on the surface of stably infected mouse lymphoma cell line W7MG1 is dramatically increased by glucocorticoid hormones. A variant cell line, W7M.TS1, was selected from W7MG1 for its lack of expression of MMTV glycoproteins on the cell surface in response to treatment with glucocorticoid. Hormonal stimulation of MMTV RNA levels and hormone-induced cytolysis occurred normally in the variant cells. Furthermore, the rates of production of the precursor and mature forms of MMTV glycoproteins in the presence of glucocorticoid were similar in variant and wild-type cells. However, the accumulation of MMTV glycoproteins on the cell surface after hormone treatment was delayed by about 8 h in the variant relative to wild-type cells. The steady-state level of a constitutively expressed cellular protein, T200, on the variant cell surface was comparable to that on wild-type cells. However, in pulse-chase experiments, the appearance of newly synthesized T200 on the cell surface was delayed in the variant compared with wild-type cells. Another glucocorticoid hormone response, removal of H-2 class I antigens from the cell surface, was also delayed in the variant relative to wild-type cells, suggesting that turnover or internalization of cell surface glycoproteins may also be affected in the variant. The defects in the variant cell line were observed at 37 degrees C, but not at 31 degrees C; the variant cells grew normally at both temperatures. This variant phenotype defines a new genetic entity that is important for transport of glycoproteins between internal microsomal compartments and the cell surface.


1990 ◽  
Vol 14 ◽  
pp. 256
Author(s):  
M GARCIASANZ ◽  
M BOBADILLA ◽  
A VALLS ◽  
E HILARIO

1984 ◽  
Vol 159 (5) ◽  
pp. 1464-1472 ◽  
Author(s):  
R B Levy ◽  
S K Dower ◽  
G M Shearer ◽  
D M Segal

Several anti-H-2Kk but not anti-H-2Dd monoclonal antibodies (mAb) exhibited enhanced binding to B10.A murine spleen cells after modification of the cells with trinitrobenzene sulfonate (TNBS). The number of antibody molecules bound to TNP-modified B10.A spleen cells increased by a factor of two or more. The same anti-2Kk mAb that exhibited enhanced binding to modified B10.A cells did not bind to unmodified C57BL/10 spleen cells, as expected, but did bind to TNP-modified C57BL/10 spleen cells. This TNP-dependent binding was not a result of cross-reactions with cell surface TNP groups nor with Fc receptors. TNP modification of a variant cell line that does not express class I H-2 products did not result in enhanced binding by these mAb. These findings can account for preferential recognition of TNP-Kk by B10.A and B10.BR CTL, and also for cross-reactive lysis by C57BL/10 CTL stimulated by C57BL/10-TNP against unmodified H-2Kk targets.


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