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Example sentences for: sv-
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SV-40 large T antigen transfected ovarian surface epithelial cell lines from women with and without an amino-terminal BRCA1 mutation were employed to ascertain the function of the amino-terminal RING domain in apoptosis [ 31 ] . To confirm BRCA1 status in these cell lines, whole cell lysates were western blotted using a monoclonal anti-BRCA1 antibody against the amino-terminal (Figure 1).
Murine podocytes immortalized with interferon-inducible temperature-sensitive SV-40 T antigen ( ts -SV-40 T) were isolated and infected with replication incompetent GFP-expressing HIV-1 virus, replication incompetent GFP-expressing single-gene mutants of HIV-1, or replication incompetent GFP-expressing control lentivirus containing GFP but no HIV-1 genes as previously described [ 7 8 ] . In all cases, 70% to 80% of podocytes showed GFP expression 4 days post infection (data not shown).
Unless otherwise indicated, all studies were conducted at cell confluency and 14 days after inactivation of ts -SV-40 T at the non-permissive temperature (37°C) when wild-type podocytes are fully differentiated [ 27 28 ] .
SV-40 large T-antigen transfected human ovarian surface epithelial cell lines, MCC5 and HIO3261-77, were derived from women with and without a family history of breast/ovarian cancer, respectively [ 31 ] . While MCC5 cells were derived from a patient denoted as wild type BRCA1 status, HIO3261-77 cells were derived from a patient characterized as 185delAG mutated [ 39 ] . Dr. W. Bai (USF) kindly provided the MCF7 breast cancer carcinoma line.
In comparison to the two general alternative mechanisms utilized by known transforming viruses to promote cell-cycle progression, namely, by activating or bypassing endogenous D-type cyclins (herein, referred to as "cyclin D"), it has not been established whether HIV-1 gene products trigger either cyclin D-dependent or cyclin D-independent proliferation in non-lymphoid tissues [ 15 ] . In infected renal epithelium, HIV-1 could disrupt the inhibitory binding of pRb to E2F independent of endogenous cyclin D, analogous to transforming viral mechanisms that bypass and down-regulate endogenous cyclin D, such as SV-40 T antigen binding to pRb [ 16 ] , HHV-8 v -cyclin binding to and activating cyclin-dependent kinase-6 (CDK) [ 17 ] , and activation of cyclin E by EBV-induced c -myc [ 18 ] . Alternatively, HIV-1 could activate cyclin D-dependent proliferation, as exemplified by RSV v -src-mediated signaling [ 19 ] . In most tissues, the selective activation of these cell-cycle pathways is readily discernable.
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