The phrase "alt cell" is not standard in written English and may cause confusion without context.
It could be used in specific technical or gaming contexts, such as referring to an alternative cell in a spreadsheet or a game.
Example: "In the spreadsheet, you can use the alt cell to input different data without affecting the main cells."
Alternatives: "alternative cell" or "alternate cell".
We have recently shown that chromatin remodelling at the telomerase gene promoters is associated with a lack of expression of hTR and hTERT in some ALT cell lines, highlighting one potential mechanism for regulating the activation of ALT or telomerase (Atkinson et al, 2005).
A comprehensive analysis of several ALT cell lines has indicated that loss or mutations of ATRX are hallmarks of ALT cell lines.
Inhibition of Topo III expression by siRNA reduced ALT cell survival, but did not affect telomerase positive cell lines.
We have not found any fundamental differences between APBs in asynchronously growing ALT cell populations and those where senescence is experimentally induced.
As noted above, large APBs (henceforth referred to as APBs) are usually found in ∼5% of cells within asynchronously growing ALT cell populations [11].
Little was known about the effect of telomestatin or other G-quadruplex ligands in telomerase-negative ALT cell lines, except that cell proliferation is inhibited [8], [16], [17], [52].
The cellular response to down regulation of Ku70/80 closely resembles that of ALT cells depleted of the MRE11/RAD50/NBS1 complex, as shown by analysis of ALT cells transduced with lentiviral vectors for the expression of shRNAs targeting MRE11/NBS1 (Supplementary Figure S2).
This marker spread to other chromosome ends much more frequently in ALT cells than in telomerase-plus cells, suggesting that the telomeres in ALT cells (or a subset, such as the shortest telomeres?) were more recombinogenic than telomeres maintained by telomerase.
A number of recent papers have been directed at the above question, by examining the consequences of reconstitution of telomerase activity in ALT cells as a result of ectopic expression of telomerase subunits (Perrem et al., 2001; Cerone et al., 2001; Ford et al., 2001; Grobelny et al., 2001) or by fusion of ALT cells with telomerase-positive tumor cell lines (Perrem, et al. 2001).
Reddel and co-workers did not observe inhibition of ALT when telomerase was ectopically expressed, but when ALT cells were fused with telomerase-positive tumor cells, telomeres showed rapid initial decreases in length, followed by more gradual shortening (Perrem et al., 2001).
These data indicate the importance of G-quadruplex stabilization during telomere maintenance in ALT cells.
