ArticleScientific reports2020
Latexin deficiency in mice up-regulates inflammation and aggravates colitis through HECTD1/Rps3/NF-κB pathway.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- DHA Supplementation Attenuates Inflammation-Associated Gene Expression in the Mammary Gland of Lactating Mothers Who Deliver Preterm.The Journal of nutrition · 2022Trial
- APOA1, DEFB103A_DEFB103B and DSG3 Are Novel Circulating Biomarkers of Psoriasis.International journal of molecular sciences · 2026Article
- HECT ubiquitin ligases as regulators of inflammatory signalling.Cell death and differentiation · 2026Review
- Genetic associations of LXN polymorphisms with toxicities of platinum-based concurrent chemoradiotherapy of nasopharyngeal carcinoma.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2026Article
- Retinoic acid promotes expression of inflammatory factors in proliferative adult human heart cells.American journal of physiology. Cell physiology · 2026Article
- The role of HECT-type E3 ubiquitin ligases in inflammation.Frontiers in immunology · 2026Review
- HECTD1-mediated SFTPB overexpression in fibrotic lung induced by silica.Biochemistry and biophysics reports · 2025Article
- Sequence variants in HECTD1 result in a variable neurodevelopmental disorder.American journal of human genetics · 2025Article
- Ribosomal proteins: the missing piece in the inflammation puzzle?Molecular and cellular biochemistry · 2025Review
- Premature renal epithelial cell senescence promoted by LXN/Rps3/p53 signaling pathway activation increases calcium oxalate crystal deposition by altering macrophage polarization.Frontiers in immunology · 2025Article
- SEC14L3 knockdown inhibited clear cell renal cell carcinoma proliferation, metastasis and sunitinib resistance through an SEC14L3/RPS3/NFκB positive feedback loop.Journal of experimental & clinical cancer research : CR · 2024Article
- Latexin deficiency limits foam cell formation and ameliorates atherosclerosis by promoting macrophage phenotype differentiation.Cell death & disease · 2024Article
- Huaiyu pill alleviates inflammatory bowel disease in mice blocking toll like receptor 4/ myeloid differentiation primary response gene 88/ nuclear factor kappa B subunit 1 pathway.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2024Article
- ABLIM1, a novel ubiquitin E3 ligase, promotes growth and metastasis of colorectal cancer through targeting IĸBα ubiquitination and activating NF-ĸB signaling.Cell death and differentiation · 2024Article
- Identification and Functional Analysis of Rare HECTD1 Missense Variants in Human Neural Tube Defects.Research square · 2024Article
- Investigation of targets and anticancer mechanisms of covalently acting natural products by functional proteomics.Acta pharmacologica Sinica · 2023Article
- Latexin regulates sex dimorphism in hematopoiesis via gender-specific differential expression of microRNA 98-3p and thrombospondin 1.Cell reports · 2023Article
- Circ_0002715 promotes the development of osteoarthritis through regulating LXN by sponging miR-127-5p.Journal of orthopaedic surgery and research · 2023Article
- Article
- Loss of LXN promotes macrophage M2 polarization and PD-L2 expression contributing cancer immune-escape in mice.Cell death discovery · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The function of Latexin (LXN) in inflammation has attracted attention. However, no data are available regarding its role in colitis. We report that LXN is a suppressor of colitis. LXN deficiency leads to the severity of colitis in DSS-induced mice, and LXN is required for the therapeutic effect of retinoic acid on colitis. Using a proteomics approach, we demonstrate that LXN interacts and forms a functional complex with HECTD1 (an E3 ubiquitin ligase) and ribosomal protein subunit3 (Rps3). IκBα is one of the substrates of HECTD1. Ectopic expression of LXN leads to IκBα accumulation in intestinal epithelial cells, however, LXN knockdown enhances the interaction of HECTD1 and Rps3, contributing to the ubiquitination degradation of IκBα, and subsequently enhances inflammatory response. Thus, our findings provided a novel mechanism underlying LXN modulates colitis via HECTD1/Rps3/NF-κB pathway and significant implications for the development of novel strategies for the treatment of colitis by targeting LXN.
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