ReviewJournal of leukocyte biology2013
RIP2 activity in inflammatory disease and implications for novel therapeutics.
Review in Journal of leukocyte biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 58 citations in OpenAlex.
- CMD-OPT model enables the discovery of a potent and selective RIPK2 inhibitor as preclinical candidate for the treatment of acute liver injury.Acta pharmaceutica Sinica. B · 2025Article
- A derivative of tanshinone IIA and salviadione, 15a, inhibits inflammation and alleviates DSS-induced colitis in mice by direct binding and inhibition of RIPK2.Acta pharmacologica Sinica · 2025Article
- ImmunoMet Oncogenesis: A New Concept to Understand the Molecular Drivers of Cancer.Journal of clinical medicine · 2025Review
- Dysregulation of Toll-Like Receptor Signaling-Associated Gene Expression in X-Linked Agammaglobulinemia: Implications for Correlations Genotype-Phenotype and Disease Expression.Journal of innate immunity · 2024Article
- Analysis of alternative splicing in chicken macrophages transfected with overexpression/knockdown ofAnimal biotechnology · 2023Article
- Receptor-interacting protein kinase 2 (RIPK2) profoundly contributes to post-stroke neuroinflammation and behavioral deficits with microglia as unique perpetrators.Journal of neuroinflammation · 2023Article
- Functions of the RIP kinase family members in the skin.Cellular and molecular life sciences : CMLS · 2023Review
- Novel Biomarkers for Inflammatory Bowel Disease and Colorectal Cancer: An Interplay between Metabolic Dysregulation and Excessive Inflammation.International journal of molecular sciences · 2023Article
- Recent advances in the development of RIPK2 modulators for the treatment of inflammatory diseases.Frontiers in pharmacology · 2023Review
- NOD/RIPK2 signalling pathway contributes to osteoarthritis susceptibility.Annals of the rheumatic diseases · 2022Article
- Application and prospect of targeting innate immune sensors in the treatment of autoimmune diseases.Cell & bioscience · 2022Review
- Pattern Recognition Receptor Signaling and Cytokine Networks in Microbial Defenses and Regulation of Intestinal Barriers: Implications for Inflammatory Bowel Disease.Gastroenterology · 2022Review
- Essential Role of the Innate Immune Adaptor RIP2 in the Response to Otitis Media.Frontiers in genetics · 2022Article
- Blau syndrome NOD2 mutations result in loss of NOD2 cross-regulatory function.Frontiers in immunology · 2022Article
- RIPK2 as a New Therapeutic Target in Inflammatory Bowel Diseases.Frontiers in pharmacology · 2021Review
- RICK/RIP2 is a NOD2-independent nodal point of gut inflammation.International immunology · 2019Article
- Multi-pathway Protective Effects of MicroRNAs on Human Chondrocytes in an In Vitro Model of Osteoarthritis.Molecular therapy. Nucleic acids · 2019Article
- Small molecule inhibitors reveal an indispensable scaffolding role of RIPK2 in NOD2 signaling.The EMBO journal · 2018Article
- A hyperactivating proinflammatory RIPK2 allele associated with early-onset osteoarthritis.Human molecular genetics · 2018Article
- CARD domain of rat RIP2 kinase: Refolding, solution structure, pH-dependent behavior and protein-protein interactions.PloS one · 2018Article
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 2 institutions in 1 country.
Funding
Abstract
The role of NOD2 and RIP2 in inflammatory disease has been paradoxical. Whereas loss-of-function NOD2 polymorphisms cause CD, a granulomatous disease of the gastrointestinal tract, gain-of-function mutations cause EOS-a granulomatous disease primarily affecting the skin, joints, and eyes. Thus, gain-of-function mutations and loss-of-function polymorphisms cause granulomatous inflammatory disease, only in different anatomic locations. The situation is complicated further by the fact that WT NOD2 and WT RIP2 activity has been implicated in diseases such as asthma, inflammatory arthritis and MS. This article reviews the role that the NOD2:RIP2 complex plays in inflammatory disease, with an emphasis on the inhibition of this signaling pathway as a novel pharmaceutical target in inflammatory disease.
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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.