ArticleNature communications2022
Tousled-like kinase 2 targets ASF1 histone chaperones through client mimicry.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- ASF1A: A versatile histone chaperone bridging chromatin dynamics, disease mechanisms and clinical potential (Review).Experimental and therapeutic medicine · 2026Review
- Co-Phosphoregulatory Network Underlying Functional Coherence of TLK1 and TLK2 Kinase Paralogs.International journal of molecular sciences · 2026Article
- Computational Innovations in Cancer Research and How Computing is Transforming Drug Discovery and Development: A Review.Mini reviews in medicinal chemistry · 2026Review
- Investigation of Genetic Aetiology in Intellectual Developmental Disorder with Trio-Whole Exome Sequencing Approach.Noro psikiyatri arsivi · 2026Article
- Mechanism of ASF1 engagement by CDAN1.Nature communications · 2025Article
- CODANIN-1 sequesters ASF1 by using a histone H3 mimic helix to regulate the histone supply.Nature communications · 2025Article
- Autophosphorylation of the Tousled-like kinases TLK1 and TLK2 regulates recruitment to damaged chromatin via PCNA interaction.Nucleic acids research · 2025Article
- Genome-wide association analysis of body conformation traits in Chinese Holstein Cattle.BMC genomics · 2024Article
- Mechanism of ASF1 Inhibition by CDAN1.bioRxiv : the preprint server for biology · 2024Article
- The TLK-ASF1 histone chaperone pathway plays a critical role in IL-1β-mediated AML progression.Blood · 2024Article
- Article
- Autophosphorylation of the Tousled-like kinases TLK1 and TLK2 regulates recruitment to damaged chromatin via PCNA interaction.bioRxiv : the preprint server for biology · 2024Article
- Illuminating the druggable genome: Pathways to progress.Drug discovery today · 2024Review
- Targeting Prostate Cancer, the 'Tousled Way'.International journal of molecular sciences · 2023Review
- Overexpression of tousled-like kinase 2 predicts poor prognosis in HBV-related hepatocellular carcinoma patients after radical resection.Frontiers in genetics · 2023Article
- Histone chaperone ASF1 mediates H3.3-H4 deposition in Arabidopsis.Nature communications · 2022Article
- Transcriptional Regulation of Endogenous Retroviruses and Their Misregulation in Human Diseases.International journal of molecular sciences · 2022Review
- Comprehensive analysis of transcriptome characteristics and identification ofFrontiers in genetics · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Tousled-like kinases (TLKs) are nuclear serine-threonine kinases essential for genome maintenance and proper cell division in animals and plants. A major function of TLKs is to phosphorylate the histone chaperone proteins ASF1a and ASF1b to facilitate DNA replication-coupled nucleosome assembly, but how TLKs selectively target these critical substrates is unknown. Here, we show that TLK2 selectivity towards ASF1 substrates is achieved in two ways. First, the TLK2 catalytic domain recognizes consensus phosphorylation site motifs in the ASF1 C-terminal tail. Second, a short sequence at the TLK2 N-terminus docks onto the ASF1a globular N-terminal domain in a manner that mimics its histone H3 client. Disrupting either catalytic or non-catalytic interactions through mutagenesis hampers ASF1 phosphorylation by TLK2 and cell growth. Our results suggest that the stringent selectivity of TLKs for ASF1 is enforced by an unusual interaction mode involving mutual recognition of a short sequence motifs by both kinase and substrate.
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Registered trials
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.