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. 2021 Nov 6;297(6):101381. doi: 10.1016/j.jbc.2021.101381

Figure 4.

Figure 4

DNA binding of TCF4 homo and heterodimers is impaired by mutations associated with PTHS.A, Western blot analysis of in vitro-translated WT or disease-associated missense variations or mutations containing TCF4-B¯ proteins. Molecular mass marker is shown on the right. B–D, EMSA to study the binding of in vitro-translated WT or mutant TCF4-B¯ proteins to the 32P-labeled μE5 E-box (CACCTG) containing oligonucleotide as (B) homodimers (TCF4-B:TCF4-B), (C) intra-TCF4 heterodimers consisting of one WT or mutant TCF4-B¯ and one WT VP16-bHLH subunit (TCF4-B:VP16-bHLH), and (D) heterodimers with ASCL1 (TCF4-B:ASCL1). The unlabeled WT (μE5) or mutated (μE5m) E-box oligonucleotides were added to the binding mixture for competition where indicated in italics. The uncropped EMSA images can be found in Figure S1. bHLH, basic helix-loop-helix; kDa, kilodalton; MMID, Mild-to-moderate intellectual disability; PTHS, Pitt-Hopkins syndrome; RTT-like, Rett-like syndrome; SCZ, Schizophrenia; TCF4, transcription factor 4; WB, Western Blot.