ArticleCell death discovery2026
FKBP5 isoforms shape immune pathways related to tumor tolerance.
Article in Cell death discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
FKBP51 is a multifunctional immunophilin that regulates key cellular pathways, including NF-κB signaling, AKT activation, and steroid receptor trafficking. Alternative splicing of the FKBP5 gene generates a shorter isoform, FKBP51s, lacking the C-terminal TPR domain mediating protein‒protein interactions. Previous studies support the hypothesis that splicing of the FKBP5 gene underpins the mechanisms crucial for establishing control over T lymphocyte expansion and that the balance between the canonical and spliced isoforms could be pivotal in the immune system's capacity to finely tune the intensity and span of the immune response.To investigate the impact of FKBP51 splicing, we generated a knock-in mouse model (huFKBP5) expressing only the full-length human FKBP51 isoform, thereby ablating all splice variants. While the heterozygous animals were viable and fertile, the homozygous huFKBP5
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