Abstract
The main methods used to screen transcription factors are RNA-seq, promoter analysis, and chromatin immunoprecipitation (ChIP). Previous studies have constructed transcription factor action models, but some crucial questions remain unresolved. The information obtained from mRNA profiling is inadequate for predicting the activities of transcription factors at the proteomic scale, and ChIP-seq produces only limited transcription factor data at a time because of the constraints on experimental throughput. How can transcription factors be effectively screened and identified at the proteome level? A concatenated tandem array of transcription factor response elements (catTFREs) pulldown technique can be used to identify and assess the binding activities of transcription factors to DNA at the proteomic scale. In this chapter, the determination of the transcription factor responses to Yersinia pestis infection with a catTFRE pulldown technique is described.
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References
Vaquerizas JM, Kummerfeld SK, Teichmann SA, Luscombe NM (2009) A census of human transcription factors: function, expression and evolution. Nat Rev Genet 10(4):252–263
Kadonaga JT (2004) Regulation of RNA polymerase II transcription by sequence-specific DNA binding factors. Cell 116(2):247–257
Ding C, Chan DW, Liu W, Liu M, Li D, Song L, Li C, Jin J, Malovannaya A, Jung SY et al (2013) Proteome-wide profiling of activated transcription factors with a concatenated tandem array of transcription factor response elements. Proc Natl Acad Sci U S A 110(17):6771–6776
Lund ME, To J, O'Brien BA, Donnelly S (2016) The choice of phorbol 12-myristate 13-acetate differentiation protocol influences the response of THP-1 macrophages to a pro-inflammatory stimulus. J Immunol Methods 430:64–70
Kohro T, Tanaka T, Murakami T, Wada Y, Aburatani H, Hamakubo T, Kodama T (2004) A comparison of differences in the gene expression profiles of phorbol 12-myristate 13-acetate differentiated THP-1 cells and human monocyte-derived macrophage. J Atheroscler Thromb 11(2):88–97
Park EK, Jung HS, Yang HI, Yoo MC, Kim C, Kim KS (2007) Optimized THP-1 differentiation is required for the detection of responses to weak stimuli. Inflamm Res: Off J Eur Histamine Res Soc 56(1):45–50
Daigneault M, Preston JA, Marriott HM, Whyte MK, Dockrell DH (2010) The identification of markers of macrophage differentiation in PMA-stimulated THP-1 cells and monocyte-derived macrophages. PLoS One 5(1):e8668
Yang H, Wang T, Tian G, Zhang Q, Wu X, Xin Y, Yan Y, Tan Y, Cao S, Liu W et al (2017) Host transcriptomic responses to pneumonic plague reveal that Yersinia pestis inhibits both the initial adaptive and innate immune responses in mice. Int J Med Microbiol: IJMM 307(1):64–74
Zhou Q, Liu M, Xia X, Gong T, Feng J, Liu W, Liu Y, Zhen B, Wang Y, Ding C et al (2017) A mouse tissue transcription factor atlas. Nat Commun 8:15089
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Jing, C. (2018). Screening of Regulator Responses to Yersinia pestis Infection with a Concatenated Tandem Array of Transcription Factor Response Element (catTFRE) Pulldown. In: Yang, R. (eds) Yersinia Pestis Protocols. Springer Protocols Handbooks. Springer, Singapore. https://doi.org/10.1007/978-981-10-7947-4_25
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DOI: https://doi.org/10.1007/978-981-10-7947-4_25
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