TRANSFAC(R): transcriptional regulation, from patterns to profiles

Abstract

The TRANSFAC database on eukaryotic transcriptional regulation, comprising data on transcription factors, their target genes and regulatory binding sites, has been extended and further developed, both in number of entries and in the scope and structure of the collected data. Structured fields for expression patterns have been introduced for transcription factors from human and mouse, using the CYTOMER database on anatomical structures and developmental stages. The functionality of Match, a tool for matrix-based search of transcription factor binding sites, has been enhanced. For instance, the program now comes along with a number of tissue-(or state-)specific profiles and new profiles can be created and modified with Match Profiler. The GENE table was extended and gained in importance, containing amongst others links to LocusLink, RefSeq and OMIM now. Further, (direct) links between factor and target gene on one hand and between gene and encoded factor on the other hand were introduced. The TRANSFAC public release is available at http://www.gene-regulation.com. For yeast an additional release including the latest data was made available separately as TRANSFAC Saccharomyces Module (TSM) at http://transfac.gbf.de. For CYTOMER free download versions are available at http://www.biobase.de:8080/index.html.

Identification of novel androgen response genes in prostate cancer cells by coupling chromatin immunoprecipitation and genomic microarray analysis

“…This scanning successfully identified 10 bona fide in vivo ARBSs with a Po1e-5. Notably, all of the 10 ARBSs included ARE sequences as determined by the sequence analysis utilities based on TRANSFAC or JASPER transcription factor-binding profiles (Matys et al, 2003;Sandelin et al, 2004), and ChIP-PCR validation confirmed that those ARBSs had abilities to recruit AR ligand dependently. Our ChIPchip approach is a powerful high-throughput method that can be applied to the whole genome-wide screen of ARBSs.…”

“…Using a weighted matrix-based finder TRANSFAC (Matys et al, 2003) with the matrix conservation >75% or a sequence analysis utility of JASPER with the relative profile score threshold >70% (Sandelin et al, 2004), we identified canonical ARE sequences in all of the ARBSs (Table 2).…”

“…ChIP analyses for acetylated histone H3/H4 (AcH3/H4) and RNA PolII were performed on the 10 ARBS regions in LNCaP cells (Figure 4). The AREs in PSA promoter and enhancer were used as positive ARE sequences were primarily determined by a position-weighted matrix method TRANSFAC with the matrix conservation >75% (Matys et al, 2003). If no ARE was predicted by the first criteria, alternative ARE sequences (indicated as *) were determined by a sequence analysis utility of JASPER with the relative profile score threshold >70% (Sandelin et al, 2004).…”

WS5, a direct target of oncogenic transcription factor Myc, is related to human melanoma glycoprotein genes and has oncogenic potential

“…The cluster of Myc-binding sites contains three canonical (CACGTG or CATGTG) and one noncanonical (CACATG) sequence motives (Blackwell et al, 1993). The C/EBPa site perfectly conforms to the consensus TTNNNNAA and is detected with a high score by the AliBaba and TFSEARCH algorithms (Grabe, 2002;Matys et al, 2003). Sequence comparison of the promoter regions of WS5 and of the presumed chicken ortholog Mmp115 (Gallus gallus linkage group E22C19W28 genomic contig, NW_100947.1, nt 3231-2972) revealed conservation of the putative Myc-and C/EBPa-binding sites (Figure 2d).…”

A highly conserved proapoptotic gene, IKIP, located next to the APAF1 gene locus, is regulated by p53

“…The presence of potential transcription factor binding sites was determined using MatInspector professional in combination with the TRANSFAC database. 17 With classical TATA and CCAAT boxes being absent, the promoter 'backbone' is mainly built by a series of SP-1 sites. From the variety of potential transcription factor binding sites (see Figure 7a), p53 and E2F-1 have been found to be functional and lead to increased APAF1 expression.…”