2 [68], TRES ‚Äì Transcription Regulatory Element Search, which performs searches within the TRANSFAC database [69] and the PromScan program, that generates an alignment of known sequences and matrix frequency [70], were used to scan DNA sequences for potential binding sites.
Sample text:```We screened for potential TF binding sites using STAMP [59], with the motifs’ position weight matrices (PWMs) retrieved from the TRANSFAC database [60].```
Sample intent: background
Sample text:```Because previous studies indicated that hexapeptides bind the junction core (29, 32), we tested two junctions, one with an AT-rich core and the other with a GC-rich core (Fig.```
Sample intent: result



Sample text:```Illustra PuReTaq ReadyTo-Go PCR beads (0.5 ml tubes, GE healthcare) were used to amplify DTL, SLFN5, TRIM47, WRAP53 and CHN1 transcripts (denaturing at 94uC for 30 s, annealing at 58uC for 1 min and elongation at 72uC for 2 min, 25‚Äì35 cycles).```
Sample intent: background



Sample text:```Therefore, one manifestation of the BRCA1–TONSL genetic interaction may well operate at sites of UV-induced damage, where both proteins are normally engaged in complex DNA damage responses (Duro et al. 2010; O’Connell et al. 2010; O’Donnell et al. 2010; Piwko et al. 2010; Pathania et al. 2011).```
Sample intent: method



Sample text:```Our results further confirm previous findings on the differential regulatory mechanisms for Hoxa3 and Hoxb3 expression in r5 and r6 by kreisler (Manzanares et al., 1997, 1999a,b, 2001).```
Sample intent: result



Sample text:```A number of studies have been published recently, which analyze the location, orientation, and identity ofmacromolecular complexes, based on the outcome of template-matching (Brandt et al., 2009; Ortiz et al., 2010).```
Sample intent: method
Sample text:```Therefore, one manifestation of the BRCA1–TONSL genetic interaction may well operate at sites of UV-induced damage, where both proteins are normally engaged in complex DNA damage responses (Duro et al. 2010; O’Connell et al. 2010; O’Donnell et al. 2010; Piwko et al. 2010; Pathania et al. 2011).```
Sample intent: method



Sample text:```Illustra PuReTaq ReadyTo-Go PCR beads (0.5 ml tubes, GE healthcare) were used to amplify DTL, SLFN5, TRIM47, WRAP53 and CHN1 transcripts (denaturing at 94uC for 30 s, annealing at 58uC for 1 min and elongation at 72uC for 2 min, 25‚Äì35 cycles).```
Sample intent: background



Sample text:```3, top) was constructed from the previously described 0.85-kb promoter construct (construct 6, Drews et al. 2005) by digestion with AscI and MluI followed by religation.```
Sample intent: method



Sample text:```A number of studies have been published recently, which analyze the location, orientation, and identity ofmacromolecular complexes, based on the outcome of template-matching (Brandt et al., 2009; Ortiz et al., 2010).```
Sample intent: method



Sample text:```Our genealogy, based on many alleles but only the first exon of bindin, is not entirely consistent with that of McCartney and Lessios (2004), based on fewer alleles but incorporating the entire molecule.```
Sample intent: result



Sample text:```Unlabeled DNA substrates containing consensus 12-RSS, 23-RSS, Hox11 or non-specific DNA sequences (DAR81/82) were prepared from oligonucleotides described previously [11,24].```
Sample intent: background



Sample text:```This process is controlled not only by the protein-coding segments of the genome but also by non-coding regions, including loci that produce small RNAs (Grivna et al., 2006; He et al., 2009; Thomson and Lin, 2009).```
Sample intent: method



Sample text:```Our results further confirm previous findings on the differential regulatory mechanisms for Hoxa3 and Hoxb3 expression in r5 and r6 by kreisler (Manzanares et al., 1997, 1999a,b, 2001).```
Sample intent: result



Sample text:```We screened for potential TF binding sites using STAMP [59], with the motifs’ position weight matrices (PWMs) retrieved from the TRANSFAC database [60].```
Sample intent: background



Sample text:```The vast majority of mutations in FUS/TLS-related familial ALS cases were identified in C-terminal NLS, which result in the retention and the inclusion of FUS/TLS in the cytoplasm [2,3,5,8,14], and FUS/TLS as well as TDP-43 is recruited to SGs under stress conditions such as arsenite, heat shock and hypoxia [28,29,30].```
Sample intent: method