Molecular turnover, the H3.3 dilemma and organismal aging (hypothesis)
Author:
Affiliation:
1. Faculty of Public Health Lebanese University LU Beirut Lebanon
2. Institute Gustave Roussy University Paris SUD 114, rue Edouard Vaillant Villejuif 94805France
Publisher
Wiley
Subject
Cell Biology,Ageing
Link
https://onlinelibrary.wiley.com/doi/pdf/10.1111/acel.12332
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1. Chemokine Signaling via the CXCR2 Receptor Reinforces Senescence
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3. Structural basis for the recognition and cleavage of histone H3 by cathepsin L
4. The Histone Variant H3.3 Marks Active Chromatin by Replication-Independent Nucleosome Assembly
5. H3F3A K27M mutations in thalamic gliomas from young adult patients
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