ArticleProceedings of the National Academy of Sciences of the United States of America2025
Understanding TAK1 deficiency in microglia: Dual mechanisms for photoreceptor protection in a mouse model of retinitis pigmentosa.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Targeting the CCL7-STAT1 axis attenuates microglial neurotoxicity and photoreceptor degeneration in retinitis pigmentosa.Journal of neuroinflammation · 2026Article
- Exploring retinal microglia: development, degeneration, and iPSC-derived model systems.Brain structure & function · 2026Review
- Dual-targeting CSF1R signaling attenuates neurotoxic myeloid activation and preserves photoreceptors in retinitis pigmentosa.Journal of neuroinflammation · 2025Article
- Understanding TAK1 deficiency in microglia: Dual mechanisms for photoreceptor protection in a mouse model of retinitis pigmentosa.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Multifaceted disruption of AMPA receptor signaling byComputational and structural biotechnology journal · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Retinitis pigmentosa (RP) is a group of inherited retinal diseases characterized by the progressive loss of photoreceptors. Neuroinflammation has been implicated in the pathophysiology of RP and its progression. Previous studies have suggested that the transforming growth factor-beta-activated kinase 1 (TAK1) plays a pivotal role in regulating acute and chronic neuroinflammation. However, the functional role of TAK1 in neuroinflammation remains unclear in RP. Here, we observed TAK1 upregulation in activated microglia of the rd10 mouse model of RP. To create the conditional deletion of TAK1 in microglia, we backcrossed Cx3cr1
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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.