ReviewZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences2018
[Research progress on receptor interacting proteins in inflammation].
Review in Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed, 1 citations in OpenAlex.
- Ubiquitination in hepatocellular carcinoma immunity.Journal of translational medicine · 2025Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Receptor interacting proteins (RIPs) are a group of threonine/serine protein kinases, which have relatively conserved kinase domains and different non-kinase domains, and are involved in physiological and pathological processes including innate immune response and inflammation. In recent years, many studies have shown that RIPs mediate cell necroptosis and triggers inflammatory responses by participating in the formation of necrotic complexes, and RIP1 and RIP3 are particularly closely related to cell necrosis. Cell necroptosis is a well-regulated way of cell death. The death signal that transmit through the TNF signaling pathway and the Toll-like receptor signaling pathway can recruit and phosphorylate mixed lineage kinase domain-like protein (MLKL), and eventually leading to disintegration and death of cells, and the release of cells intercellular material after cell disintegration can trigger an inflammatory reaction. This review mainly focuses on the major signaling pathways and molecular mechanisms that are involved in the mediation of necrosis and inflammation by RIPs. It also highlights the importance of RIPs in the development of inflammatory diseases and their potentials as therapeutic targets for inflammatory diseases.
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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.