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General Transcription Factors01:30

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Tissue-specific transcription factors contribute to diverse cellular functions in mammals. For example, the gene for beta globin, a major component of hemoglobin, is present in all cells of the body. However, it is only expressed in red blood cells because the transcription factors that can bind to the promoter sequences of the beta globin gene are only expressed in these cells. Tissue-specific transcription factors also ensure that mutations in these factors may impair only the function of...
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Transcriptional regulators bind to specific cis-regulatory sequences in the DNA to regulate gene transcription. These cis-regulatory sequences are very short, usually less than ten nucleotide pairs in length. The short length means that there is a high probability of the exact same sequence randomly occurring throughout the genome.  Since regulators can also bind to groups of similar sequences, this further increases the chances of random binding. Transcriptional regulators form...
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For successful DNA replication, the unwinding of double-stranded DNA must be accompanied by stabilization and protection of the separated single strands of the DNA. This crucial task is performed by single-strand DNA-binding (SSB) proteins. They bind to the DNA in a sequence-independent manner, which means that the nitrogenous bases of the DNA need not be present in a specific order for binding of SSB proteins to it. The binding of SSB proteins straightens single-stranded DNA (ssDNA) and makes...
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Cis-regulatory sequences are short fragments of non-coding DNA that are present on the same chromosomes as the genes that they regulate. These fragments serve as binding sites for transcriptional regulators, proteins that are responsible for controlling gene transcription and differential gene expression across cell types in eukaryotes. Cis-regulatory sequences can be close to the gene of interest or thousands of bases away in the DNA sequence; however, those sequences that are further away are...
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Updated: Jan 7, 2026

CD Spectroscopy to Study DNA-Protein Interactions
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A SWI/SNF-specific Ig-like domain, SWIFT, is a transcription factor binding platform.

Siddhant U Jain1, Kaylyn E Williamson1, Alexander W Ying1,2

  • 1Department of Pediatric Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA, USA.

Science (New York, N.Y.)
|January 1, 2026
PubMed
Summary
This summary is machine-generated.

Researchers discovered SWIFT, a protein domain that guides SWI/SNF complexes to specific genes by binding transcription factors (TFs). This mechanism is crucial for targeting these complexes in various cell types and diseases, offering therapeutic potential.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Cancer Biology

Background:

  • Mammalian SWI/SNF complexes regulate DNA accessibility and gene expression.
  • The precise genomic targeting mechanisms of SWI/SNF complexes are not fully understood.

Purpose of the Study:

  • To identify the mechanism by which SWI/SNF complexes are targeted to specific genomic locations.
  • To investigate the role of TF interactions in SWI/SNF targeting and function.

Main Methods:

  • Identification and characterization of the SWIFT domain.
  • Analysis of SWIFT domain interactions with transcription factors, particularly PU.1.
  • Mutation studies to assess the impact on complex binding and cellular function.
  • In vitro and in vivo assays to evaluate the role of SWIFT in cancer cells.

Main Results:

  • The SWIFT domain on SMARCD subunits acts as a TF binding platform.
  • SWIFT directly binds the transactivation domain of PU.1.
  • A single amino acid mutation in SWIFT disrupts PU.1-SWI/SNF binding, impairing targeting and reducing proliferation in cancer cells.
  • Isolated SWIFT domain expression inhibits TF-addicted cancer cells by sequestering TFs.
  • Diverse TFs interact with SMARCD paralog-specific SWIFT domains.

Conclusions:

  • SWIFT mediates cell type- and disease-specific targeting of SWI/SNF complexes through TF interactions.
  • This mechanism provides a new understanding of SWI/SNF regulation.
  • Targeting SWIFT interactions offers a potential therapeutic strategy for TF-addicted cancers.