ArticleNature communications2025
PEAK1 maintains tight junctions in intestinal epithelial cells and resists colitis by inhibiting autophagy-mediated ZO-1 degradation.
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 18 papers.
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Who cites it
18 citing papers in PubMed.
- Trichinella spiralis galectin disrupts gut epithelial integrity and mediates larval invasion via acting MUC13- ROCK2/MAPK pathway.PLoS neglected tropical diseases · 2026Article
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- Senkyunolide I Inhibits mtDNA-cGAS-STING Signaling in Macrophages via Targeting VDAC1 Oligomerization to Attenuate Ulcerative Colitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Curcumin-loaded tetrahedral framework nucleic acids reshape intestinal homeostasis in ulcerative colitis by coordinating barrier repair, microbiota reconstruction, and immune modulation.Materials today. Bio · 2026Article
- Neoagarotetraose from Marine Red Algae Ameliorates UVB-Induced Skin Barrier Damage in Mice and HaCaT Keratinocytes.Marine biotechnology (New York, N.Y.) · 2026Article
- Treatment of heterotopic ossification via inhibiting the MMP-2/CDH5 axis through oral delivery of network pharmacology-predicted Chinese medicine.Materials today. Bio · 2026Article
- Dietary dimethylglycine sodium salt improves growth performance, liver function, and meat quality of broilers exposed to heat stress.Poultry science · 2026Article
- Chinese bayberry exosome-like nanoparticles attenuate DSS-induced colitis via immunomodulation, barrier restoration, and microbiota remodeling.NPJ science of food · 2026Article
- The ubiquitin-like protein FAT10 enhances the autophagy-mediated degradation of ZO-1 by stabilizing ATG3 to promote the lung metastasis of colon cancer.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Transfer factor alleviates bovine mastitis and protects mammary epithelial barrier via the TAK1/NF-κB/MLCK signaling axis.Journal of animal science · 2026Article
- Microbiota metabolite butyrate alleviates intestinal inflammation associated with enhanced autophagy-related signaling in DSS-induced colitis.Frontiers in immunology · 2026Article
- Carbon dots derived fromFrontiers in molecular biosciences · 2026Article
- Huangjin Shuangshen decoction alleviates chronic atrophic gastritis by suppressing TNF/NF-κB signaling and promoting CFTR-associated gastric mucosal barrier repair.Frontiers in immunology · 2026Article
- Effects ofFrontiers in microbiology · 2026Article
- A "One-Stone-Three-Birds" Inspired Nanoplatform for Multitargeted Ulcerative Colitis Therapy via Combined Aryl Hydrocarbon Receptor Activation and Reactive Oxygen Species Scavenging.Biomaterials research · 2026Article
- Probiotics as eco-friendlybio-preservatives: In vivo mechanisms of mycotoxin inhibition and emerging applications for food safety and human health.Mycotoxin research · 2025Review
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13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tight junctions are crucial for maintaining intestinal barrier homeostasis, but how organisms modulate these junctions remain unclear. Here, we show a role for PEAK1 at cell-cell contact sites, where it interacts with ZO-1 via a conserved region spanning amino acids 714-731. This interaction masks the LC3-interacting region on ZO-1, preventing autophagy-mediated ZO-1 degradation and preserving the integrity of tight junctions in intestinal epithelial cells. Src-mediated phosphorylation of PEAK1 at Y724 promotes the binding between PEAK1 and ZO-1 to stabilize ZO-1 in intestinal epithelial cells. Additionally, PEAK1 binds to CSK to positively regulate Src activity. Loss of PEAK1 in intestinal epithelial cells leads to decreased Src activity and lower ZO-1 protein levels, resulting in disrupted tight junctions, both in vitro and in vivo. In mice, Peak1 deficiency increases intestinal epithelium permeability and exacerbates inflammation in experimentally induced colitis models. Our findings reveal PEAK1's critical role in maintaining tight junction integrity and resistance to intestinal inflammation, extending its known function from promoting tumor cell proliferation and migration to essential physiological processes. These insights refine our understanding of the mechanisms regulating tight junctions and offer potential therapeutic targets for enhancing epithelial barrier function and treating related diseases.
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