ArticleClinical immunology (Orlando, Fla.)2025
Calcium calmodulin kinase IV deficiency in podocytes prevents the development of lupus nephritis.
Article in Clinical immunology (Orlando, Fla.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- IgG Glycosylation-Dependent CLEC7A Signaling Drives Podocyte Dysfunction in Lupus Nephritis.Arthritis & rheumatology (Hoboken, N.J.) · 2026Article
- Cell-Targeted Inhibition of CaMK4 Suppresses Tertiary Lymphoid-like Structure Development in Lupus-Prone Mice.International journal of molecular sciences · 2026Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by widespread organ involvement including the kidney. Calcium/calmodulin-dependent protein kinase IV (CaMK4) has been shown to conrol immune cell nad podocyte function. To address the effect of genetic podocyte-specific CaMK4 deficiency on systemic autoimmunity and kidney pathology in lupus-prone mice we generated B6.lpr.Camk4
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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 Socratic graph.