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In most cases the specificity of TFs are inferred from collections of binding sites.
Collections of binding sites are obtained in simulation experiments where the true model for the transcription factor is known and various sampling procedures are employed.
Collections of binding sites for the γ/β- and the α-Proteobacteria were derived from experimental data from E. coli and several α-Proteobacteria species as described previously [ 43, 64].
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Comparison of VIPs for a collection of binding motifs to sequences determined experimentally indicates that the prediction algorithm is accurate and applicable to a diverse range of structures.
Much more commonly a small collection of binding sites is obtained and from them a model for the TF's binding specificity is determined.
Regardless of how the collection of binding sites is obtained, and especially important for the use of motif discovery methods, a model for the TF's specificity must be used, and usually it is some form of PWM.
This degeneracy allows a motif to model a collection of binding sites.
Since this hypothesis was proposed, a collection of binding proteins have been identified using several toxic snake venom sPLA2 [ 31].
The method takes as input a collection of binding interactions and returns groups of factors sharing a conspicuous number of mRNA targets.
Hence, discovering unknown motifs (i.e., a collection of binding sites) in co-expressed genes or finding de novo binding sites associated with a known TF is crucial to understand the gene regulatory mechanisms [ 2- 4].
Importantly, the M-type receptors also bind with several mammalian sPLA2 [ 31, 36], suggesting that these proteins are the endogenous ligands for these receptors, and possibly for the collection of binding proteins initially identified with venom sPLA2.
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