ArticleNature communications2025
Structural insights into a highly flexible zinc finger module unravel INSM1 function in transcription regulation.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
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.
Who cites it
5 citing papers in PubMed.
- Zinc Fingers as Programmable Metalloprotein Scaffolds for Altering Pathogenic Biomolecular Phase Transitions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Systematic analysis of hippo pathway signaling identifies TEAD1 as a transcriptional regulator of neuroendocrine prostate cancer.Neoplasia (New York, N.Y.) · 2026Article
- TEAD1 Enhances Exosome Secretion and Promotes Exosome-Mediated Tissue Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Insulinoma-associated 1 promotes neurogenic proliferation of cortical basal progenitors but is largely dispensable for projection neuron production.bioRxiv : the preprint server for biology · 2026Article
- AlphaFold 3-Assisted Deciphering of the DNA Recognition by DREB1 Transcription Factors in Rice.International journal of molecular sciences · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
Orderly development of neuroendocrine and nervous system of mammals requires INSM1, a key regulator for cell differentiation. Ectopic expression of INSM1 is closely correlated with human neuroendocrine tumorigenesis, which makes INSM1 a reliable diagnostic biomarker and potential therapeutic target. To date, INSM1 is known as a transcription repressor binding to GGGG-contained DNA element and TEAD1 using its five zinc fingers (ZFs), while the binding mechanism remains unknown. Here, we reveal highly variable conformations of the whole structure of the five ZFs, among which ZF1 adopts an unusual CCHC-fold. ZF1 binds to the TEAD domain of TEAD1 through hydrophobic interactions, and forms a ternary complex with TEAD1 and TEAD1-targeted DNA. Based on this, INSM1 cooperates with TEAD1 to repress the transcription of TEAD1-targeted genes. ZF2 and ZF3 of INSM1 can bind to DNA but have no specificity to the GGGG-contained element due to long flexible interdomain linker. Instead, INSM1 collaborates with CTCF to target genome loci having the GGGG-contained element and regulate the expression of adjacent genes. This study defines a functional mode of INSM1 by cooperating with diverse DNA-binding proteins for targeting specific genome loci in transcription regulation, and provides structural information for designing INSM1-related therapeutic drugs and diagnostic probes.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.