Evidence map›Paper›PMID 40766474›Full record

ArticlebioRxiv : the preprint server for biology2025

A SWI/SNF-specific Ig-like domain, SWIFT, is a transcription factor binding platform.

Siddhant U Jain, Kaylyn E Williamson, Alexander W Ying, Ruidong Jerry Jiang, Aasha M Turner, Kevin So, Maxwell P Allison, Akshay Sankar, Daniel D Sáme Guerra, Nazar Mashtalir and 6 more

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors.

Siddhant U JainDepartment of Pediatric Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02215, USA.ORCID 0000-0002-7390-6757
Kaylyn E WilliamsonDepartment of Pediatric Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02215, USA.ORCID 0000-0002-3252-5050
Alexander W YingDepartment of Pediatric Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02215, USA.
Ruidong Jerry JiangDepartment of Chemistry, Washington University in St. Louis, St. Louis, MO 63105, USA.
Aasha M TurnerDepartment of Pediatric Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02215, USA.
Kevin SoDepartment of Pediatric Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02215, USA.
Maxwell P AllisonDepartment of Pediatric Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02215, USA.
Akshay SankarDepartment of Pediatric Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02215, USA.
Daniel D Sáme GuerraDepartment of Pediatric Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02215, USA.
Nazar MashtalirDepartment of Pediatric Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02215, USA.
Henry W RohrsDepartment of Chemistry, Washington University in St. Louis, St. Louis, MO 63105, USA.
Cheryl F LichtiDepartments of Pathology and Immunology, School of Medicine, Washington University in St. Louis, St. Louis, MO 63110.
Steven P GygiDepartment of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.ORCID 0000-0001-7626-0034
Joao A PauloDepartment of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.ORCID 0000-0002-4291-413X
Michael L GrossDepartment of Chemistry, Washington University in St. Louis, St. Louis, MO 63105, USA.
Cigall KadochDepartment of Pediatric Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02215, USA.ORCID 0000-0002-4058-5985

Funding

New Sample Multiplexing Technologies to Identify Chemical Probes and Illuminate Ubiquitin BiologyR01GM067945 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI GYGI, STEVEN P · 2003 to 2024
$10.5M
Structure-activity relationships governing mammalian SWI/SNF chromatin remodeling activity as a function of chromatin stateR01CA259365 · NCI · DANA-FARBER CANCER INST · PI Cigall Kadoch, Tom Muir · 2021 to 2026
$4.2M
Reversing Oncogenic BAF Complex Structure & Function: New Therapeutic ApproachesDP2CA195762 · NCI · DANA-FARBER CANCER INST · PI KADOCH, CIGALL · 2014 to 2014
$2.6M
A Biomedical Mass Spectrometry Resource: Ongoing Driving Biomedical ProjectsR24GM136766 · NIGMS · WASHINGTON UNIVERSITY · PI GROSS, MICHAEL L · 2020 to 2022
$2.3M
Mass Spectrometry-Based Protein Footprinting: A New Tool for Amyloid Protein AggregationR01AG079283 · NIA · WASHINGTON UNIVERSITY · PI MICHAEL L GROSS · 2024 to 2026
$2.2M
Advancing Multiplexed Isobaric Tag-based Strategies for Proteome ProfilingR01GM132129 · NIGMS · HARVARD MEDICAL SCHOOL · PI PAULO, JOAO A · 2019 to 2023
$1.7M
Developing proteomics pipelines to improve depth, throughput, and accuracyR35GM156406 · NIGMS · HARVARD MEDICAL SCHOOL · PI Joao A Paulo · 2025 to 2026
$878k
Structure and Function of ATP-Dependent Chromatin Remodeling Complexes in Human CancerK99CA237855 · NCI · DANA-FARBER CANCER INST · PI MASHTALIR, NAZAR · 2019 to 2020
$278k
NCI NIH HHS DP2 CA195762NCI NIH HHS K99 CA237855NCI NIH HHS R01 CA259365NIA NIH HHS R01 AG079283NIGMS NIH HHS R01 GM067945NIGMS NIH HHS R01 GM132129NIGMS NIH HHS R24 GM136766NIGMS NIH HHS R35 GM156406
6 · The paper itself

Abstract

Mammalian SWI/SNF (BAF) chromatin remodeling complexes modulate DNA accessibility and gene expression, however, the mechanisms by which these master regulatory complexes are targeted on chromatin remain incompletely understood. Here, we define SWIFT (SWI/SNF Ig-Fold for Transcription Factor Interactions) found on the SMARCD family of subunits within the core module as a transcription factor (TF) binding platform. We demonstrate that SWIFT is necessary and sufficient for direct interaction with the transactivation domain of a lineage-specific TF, PU.1, in vitro and in cells. A single amino acid mutation in SWIFT disrupts the PU.1-mSWI/SNF interaction, inhibits site-specific complex targeting and activity, and attenuates oncogenic gene expression and proliferation of PU.1-dependent AML cells. Dominant expression of SWIFT in isolation sequesters mSWI/SNF-interacting TFs and poisons TF-addicted cancer cells. Finally, we present SWIFT as an evolutionarily conserved domain that serves as a universal binding platform for diverse TFs, suggesting approaches for modulation of cell type and disease-specific transcription.

Identifiers

PMID40766474
PMCPMC12324477

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.