STK38 promotes ATM activation by acting as a reader of histone H4 ufmylation-Reference-Cited by-同舟云学术

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STK38 promotes ATM activation by acting as a reader of histone H4 ufmylation

Published:2020-06-05 Issue:23 Volume:6 Page:
ISSN:2375-2548
Container-title:Science Advances
language:en
Short-container-title:Sci. Adv.

Author:

Qin Bo¹²^ORCID,Yu Jia²^ORCID,Nowsheen Somaira¹³^ORCID,Zhao Fei¹,Wang Liewei²,Lou Zhenkun¹^ORCID

Affiliation:

1. Division of Oncology, Mayo Clinic, Rochester, MN 55905, USA.

2. Division of Clinical Pharmacology, Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN 55905, USA.

3. Mayo Medical Scientist Training Program, Mayo Medical School and Mayo Graduate School, Mayo Clinic, Rochester, MN 55905, USA.

Abstract

STK38, a reader of histone H4 ufmylation, regulates ATM activation.

Funder

National Institutes of Health

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

Reference44 articles.

1. The DNA-damage response in human biology and disease

2. Localization of an ataxia-telangiectasia gene to chromosome 11q22–23

3. A Single Ataxia Telangiectasia Gene with a Product Similar to PI-3 Kinase

4. The complete sequence of the coding region of the ATM gene reveals similarity to cell cycle regulators in different species

5. The ATRs, ATMs, and TORs Are Giant HEAT Repeat Proteins

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1. The emerging roles of UFMylation in the modulation of immune responses;Clinical and Translational Medicine;2024-09

2. Protein UFMylation regulates early events during ribosomal DNA-damage response;Cell Reports;2024-09

3. UFMylation: An integral post-translational modification for the regulation of proteostasis and cellular functions;Pharmacology & Therapeutics;2024-08

4. The silent guardian: unraveling the roles of H3K9me3 in genome maintenance;Genome Instability & Disease;2024-07-02

5. MUS81 UFMylation at K400 promotes cell survival in response to camptothecin-induced replication stress;Genome Instability & Disease;2024-07-01

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