ReviewCells2024
Updates on Inflammatory Molecular Pathways Mediated by ADAM17 in Autoimmunity.
Review in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed.
- Expression ofInternational journal of molecular sciences · 2026Article
- HDX-MS Detects Steric Protection and Trimeric Compaction of TNFα after It Binds Receptors or Antibodies.ACS omega · 2026Article
- NF1 Leucine Rich Domain-Derived Extracellular Vesicles Remodel the Glioblastoma Immune Microenvironment via an ADAM17-Associated Inflammatory Program.Journal of extracellular vesicles · 2026Article
- Inflammasomes in Sjögren's Disease: Exploring the Therapeutic Value.International journal of molecular sciences · 2026Review
- Global Adam17 Deficiency Preserves Renal Function and Modulates Integrated Pathogenic Responses in Experimental Diabetic Kidney Disease.International journal of molecular sciences · 2026Article
- Screening of autoinflammatory genes in patients with SARS-CoV-2-associated MIS-C.Human genomics · 2026Article
- Genetic variations in AAK1 and ADAM17 associated with circulatory cytokines changes influence COVID-19 susceptibility and severity.Human genomics · 2026Article
- Endurance training increases tmTNF-α and IL-6 levels in several vital organs in rats: relationship with hypoxia markers.Frontiers in molecular biosciences · 2026Article
- Engineering Single-Chain Antibody Fragment (scFv) Variants Targeting A Disintegrin and Metalloproteinase-17 (ADAM-17).Biomolecules · 2025Article
- Review
- ADAM17 as a promising therapeutic target: from structural basis to inhibitor discovery in human diseases.Frontiers in pharmacology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ADAM17 is a member of the disintegrin and metalloproteinase (ADAM) family of transmembrane proteases with immunoregulatory activity in multiple signaling pathways. The functional ADAM17 is involved in the shedding of the ectodomain characterizing many substrates belonging to growth factors, cytokines, receptors, and adhesion molecules. The ADAM17-dependent pathways are known to be crucial in tumor development and progression and in the modulation of many pathological and physiological processes. In the last decade, ADAM17 was considered the driver of several autoimmune pathologies, and numerous substrate-mediated signal transduction pathways were identified. However, the discoveries made to date have led researchers to try to clarify the multiple mechanisms in which ADAM17 is involved and to identify any molecular gaps between the different transductional cascades. In this review, we summarize the most recent updates on the multiple regulatory activities of ADAM17, focusing on reported data in the field of autoimmunity.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.