ArticlePloS one2013
Alternative splicing of the RAGE cytoplasmic domain regulates cell signaling and function.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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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.
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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.
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Who cites it
33 citing papers in PubMed, 55 citations in OpenAlex.
- Accumulation of amyloid beta in human glioblastomas.Clinical and experimental immunology · 2020Trial
- RAGE phosphorylation by CK2 in human epithelial cell model: Modulation of connexin 43 expression.iScience · 2026Article
- RAGE Signalling in Acute Inflammatory Disorders: Therapeutic Potential of Natural Products.Biomolecules · 2026Review
- Investigating the Cellular and Tissue Response to Herbal Glucose/Cellulose-based Mesoporous Graphene Frameworks in a Rat Diabetic Wounds Model.Cell biochemistry and biophysics · 2026Article
- Modulation of Aging Diseases via RAGE Targets: A Dietary Intervention Review.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Targeting the AGEs-RAGE axis: pathogenic mechanisms and therapeutic interventions in diabetic wound healing.Frontiers in medicine · 2025Review
- Advanced Glycation End Products in Neurodegenerative Diseases.Journal of molecular neuroscience : MN · 2024Review
- Binding of RAGE and RIPK1 induces cognitive deficits in chronic hyperglycemia-derived neuroinflammation.CNS neuroscience & therapeutics · 2024Article
- Article
- RAGE inhibitor TTP488 (Azeliragon) suppresses metastasis in triple-negative breast cancer.NPJ breast cancer · 2023Article
- Accelerated AGEing: The Impact of Advanced Glycation End Products on the Prognosis of Chronic Kidney Disease.Antioxidants (Basel, Switzerland) · 2023Review
- Therapeutic potential of targeting the receptor for advanced glycation end products (RAGE) by small molecule inhibitors.Drug development research · 2022Review
- Co-expression of High-mobility group box 1 protein (HMGB1) and receptor for advanced glycation end products (RAGE) in the prognosis of esophageal squamous cell carcinoma.Discover oncology · 2022Article
- Review
- Peptidomic Analysis on Mouse Lung Tissue Reveals AGDP as a Potential Bioactive Peptide against Pseudorabies Virus Infection.International journal of molecular sciences · 2022Article
- Article
- Soluble receptor for advanced glycation end products protects from ischemia- and reperfusion-induced acute kidney injury.Biology open · 2022Article
- Role and Therapeutic Potential of RAGE Signaling in Neurodegeneration.Current drug targets · 2022Article
- Neurodegenerative diseases: a hotbed for splicing defects and the potential therapies.Translational neurodegeneration · 2021Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Receptor for Advanced Glycation End-products (RAGE) is a multi-ligand receptor present on most cell types. Upregulation of RAGE is seen in a number of pathological states including, inflammatory and vascular disease, dementia, diabetes and various cancers. We previously demonstrated that alternative splicing of the RAGE gene is an important mechanism which regulates RAGE signaling through the production of soluble ligand decoy isoforms. However, no studies have identified any alternative splice variants within the intracellular region of RAGE, a region critical for RAGE signaling. Herein, we have cloned and characterized a novel splice variant of RAGE that has a truncated intracellular domain (RAGEΔICD). RAGEΔICD is prevalent in both human and mouse tissues including lung, brain, heart and kidney. Expression of RAGEΔICD in C6 glioma cells impaired RAGE-ligand induced signaling through various MAP kinase pathways including ERK1/2, p38 and SAPK/JNK. Moreover, RAGEΔICD significantly affected tumor cell properties through altering cell migration, invasion, adhesion and viability in C6 glioma cells. Furthermore, C6 glioma cells expressing RAGEΔICD exhibited drastic inhibition on tumorigenesis in soft agar assays. Taken together, these data indicate that RAGEΔICD represents a novel endogenous mechanism to regulate RAGE signaling. Significantly, RAGEΔICD could play an important role in RAGE related disease states through down regulation of RAGE signaling.
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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.