| Autor: |
Abu Alhaija, Abed Alkarem, Lone, Imtiaz Nisar, Sekeroglu, Esin Ozkuru, Batur, Tugce, Angelov, Dimitar, Dimitrov, Stefan, Hamiche, Ali, Firat Karalar, Elif Nur, Ercan, Muhammed Erdem, Yagci, Tamer, Alotaibi, Hani, Diril, Muhammed Kasim |
| Předmět: |
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| Zdroj: |
FEBS Open Bio; Feb2024, Vol. 14 Issue 2, p309-321, 13p |
| Abstrakt: |
The linker histone H1 C‐terminal domain (CTD) plays a pivotal role in chromatin condensation. De novo frameshift mutations within the CTD coding region of H1.4 have recently been reported to be associated with Rahman syndrome, a neurological disease that causes intellectual disability and overgrowth. To investigate the mechanisms and pathogenesis of Rahman syndrome, we developed a cellular model using murine embryonic stem cells (mESCs) and CRISPR/Cas9 genome engineering. Our engineered mES cells facilitate detailed investigations, such as H1‐4 dynamics, immunoprecipitation, and nuclear localization; in addition, we tagged the mutant H1‐4 with a photoactivatable GFP (PA‐GFP) and an HA tag to facilitate pulldown assays. We anticipate that these engineered cells could also be used for the development of a mouse model to study the in vivo role of the H1‐4 protein. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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