Academic Journal

Loss of Kat2b impairs intraflagellar transport and the Hedgehog signaling pathway in primary cilia

التفاصيل البيبلوغرافية
العنوان: Loss of Kat2b impairs intraflagellar transport and the Hedgehog signaling pathway in primary cilia
المؤلفون: Jae Hee Jun, Hwayeon Cha, Je Yeong Ko, Ho-Shik Kim, Kyung Hyun Yoo, Jong Hoon Park
المصدر: Scientific Reports, Vol 15, Iss 1, Pp 1-15 (2025)
بيانات النشر: Nature Portfolio, 2025.
سنة النشر: 2025
المجموعة: LCC:Medicine
LCC:Science
مصطلحات موضوعية: Acetylation, Ciliogenesis, Intraflagellar transport, Kat2b, Primary cilia, Medicine, Science
الوصف: Abstract Primary cilia are sensory organelles that regulate various signaling pathways. When microtubules are compared to a highway, motor proteins carry and transport cargo proteins, which are tuned by post-translational modifications, such as acetylation. However, the role of acetylation in primary cilia regulation remains unclear. In this study, histone K (lysine) acetyltransferase 2 B (Kat2b) was identified as a novel regulator of primary cilia. Kat2b, which mainly regulates transcription as a p300/CBP associated factor, is localized to the cytosol, centrosome, and cilium basal body. In addition, basal Kat2b expression gradually increased during ciliogenesis. Kat2b regulates the rate of cilia assembly, particularly in the early stages, and loss of Kat2b reduces the recruitment of intraflagellar transport (IFT) components to the ciliary axoneme and impairs Hedgehog (Hh) signaling activation. In addition, Kat2b-knockout mice showed mild abnormalities and ciliary IFT defects in the kidneys. These results establish a link between acetylation regulated by Kat2b and its relevance to ciliary assembly and function.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 2045-2322
Relation: https://doaj.org/toc/2045-2322
DOI: 10.1038/s41598-025-86292-5
URL الوصول: https://doaj.org/article/3593b02cec0c44ebaedc73a3deec60e7
رقم الانضمام: edsdoj.3593b02cec0c44ebaedc73a3deec60e7
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:20452322
DOI:10.1038/s41598-025-86292-5