ArticleCell death and differentiation2020
SIRT1 modulates cell cycle progression by regulating CHK2 acetylation-phosphorylation.
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Article in Cell death and differentiation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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59 citing papers in PubMed, 85 citations in OpenAlex.
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- Paligenosis: dual potential of mature cell plasticity in regeneration and tumorigenesis.MedScience · 2026Review
- From modification to malignancy: Bridging acetylation mechanisms and therapeutic innovations in melanoma (Review).Oncology reports · 2026Review
- Iron regulation by Sirtuins 1 & 2 and their therapeutic modulation by Sirtinol.Frontiers in pharmacology · 2026Review
- Regulation of stem cell aging and cellular proliferation by Klotho-Sirt1 pathways in heart, kidney and small intestine.npj aging · 2025Article
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- MiR-148a-3p/SIRT7 axis promotes glioma progression and regulates temozolomide chemosensitivity.Journal of neuro-oncology · 2025Article
- Therapeutic applications of exercise in neurodegenerative diseases: focusing on the mechanism of SIRT1.Molecular and cellular biochemistry · 2025Review
- SIRT1 as a masterful reciprocal regulator of molecular mechanisms and signaling pathways involved in tumor growth and expansion.Clinical and experimental medicine · 2025Review
- Investigating postbiotics as innovative adjuvants: deciphering the gut-breast connection in breast Cancer therapy, from gut microbiome to personalized medicine.Molecular biology reports · 2025Review
- Bromodomain and extraterminal protein inhibitor JQ1 induces maturation arrest and disrupts the cytoplasmic organization in mouse oocytes under in vitro conditions.Scientific reports · 2025Article
- Sirtuin 2 exacerbates renal tubule injury and inflammation in diabetic mice via deacetylation of c-Jun/c-Fos.Cellular and molecular life sciences : CMLS · 2025Article
- Lipin3 deficiency aggravates cisplatin induced acute kidney injury via activating Sirt1-p21-Caspase 3-GSDME pyroptosis pathway.International journal of biological sciences · 2025Article
- The role of circulating anti-aging αKlotho in cardiac aging.Cell signaling · 2025Article
- Wenyang Jiedu Tongluo formula ameliorates diabetic kidney disease by regulating JAML/SIRT1 signaling to improve lipid metabolism in db/db mice.Frontiers in pharmacology · 2025Article
- Klotho enhances diastolic function in aged hearts through Sirt1-mediated pathways.GeroScience · 2024Article
- Dynamics and necessity of SIRT1 for maternal-zygotic transition.Scientific reports · 2024Article
- Mitochondrial Morphology and Function Abnormality in Ovarian Granulosa Cells of Patients with Diminished Ovarian Reserve.Reproductive sciences (Thousand Oaks, Calif.) · 2024Article
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Authors and funding
18 authors at 6 institutions in 5 countries.
Wenyu ZhangInstitute of Translational Medicine, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, China Medical University, No. 77, Puhe Road, Shenyang North New Area, Shenyang, 110122, Liaoning, China.
Yanling FengInstitute of Translational Medicine, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, China Medical University, No. 77, Puhe Road, Shenyang North New Area, Shenyang, 110122, Liaoning, China.
Qiqiang GuoInstitute of Translational Medicine, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, China Medical University, No. 77, Puhe Road, Shenyang North New Area, Shenyang, 110122, Liaoning, China.
Wendong GuoInstitute of Translational Medicine, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, China Medical University, No. 77, Puhe Road, Shenyang North New Area, Shenyang, 110122, Liaoning, China.
Hongde XuInstitute of Translational Medicine, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, China Medical University, No. 77, Puhe Road, Shenyang North New Area, Shenyang, 110122, Liaoning, China.
Xiaoman LiInstitute of Translational Medicine, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, China Medical University, No. 77, Puhe Road, Shenyang North New Area, Shenyang, 110122, Liaoning, China.
Fei YiInstitute of Translational Medicine, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, China Medical University, No. 77, Puhe Road, Shenyang North New Area, Shenyang, 110122, Liaoning, China.
Yi GuanInstitute of Translational Medicine, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, China Medical University, No. 77, Puhe Road, Shenyang North New Area, Shenyang, 110122, Liaoning, China.
Nanxi GengDepartment of Cell Biology, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, China Medical University, No. 77, Puhe Road, Shenyang North New Area, Shenyang, 110122, Liaoning, China.
Pingyuan WangCenter for Molecular Medicine, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Longyue CaoDepartment of Medicine (Cardiology), Wilf Family Cardiovascular Research Institute, Albert Einstein College of Medicine, Bronx, NY, 10461, USA.
Brian P O'RourkeDepartment of Physiology and Biophysics, Albert Einstein College of Medicine, Bronx, NY, 10461, USA.
Juhyeon JoDepartment of Life Science, College of Natural Science Office #106, Science building C, Ewha Womans University 52, Ewhayeodae-gil, Seodaemun-gu, Seoul, 03760, South Korea.
Jiyun KwonDepartment of Life Science, College of Natural Science Office #106, Science building C, Ewha Womans University 52, Ewhayeodae-gil, Seodaemun-gu, Seoul, 03760, South Korea.
Ruihong WangFaculty of Health Science, University of Macau, Macau, China.
Xiaoyu SongInstitute of Translational Medicine, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, China Medical University, No. 77, Puhe Road, Shenyang North New Area, Shenyang, 110122, Liaoning, China. xysong@cmu.edu.cn.
In Hye LeeDepartment of Life Science, College of Natural Science Office #106, Science building C, Ewha Womans University 52, Ewhayeodae-gil, Seodaemun-gu, Seoul, 03760, South Korea. lih3026@ewha.ac.kr.ORCID http://orcid.org/0000-0003-2334-3594
Liu CaoInstitute of Translational Medicine, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, China Medical University, No. 77, Puhe Road, Shenyang North New Area, Shenyang, 110122, Liaoning, China. lcao@cmu.edu.cn.
China Medical University · CNAlbert Einstein College of Medicine · USEwha Womans University · KRMinistry of Education · KNNational Institutes of Health · USUniversity of Macau · MO
Funding
No grant is acknowledged in the PubMed record.
Abstract
Both the stress-response protein, SIRT1, and the cell cycle checkpoint kinase, CHK2, play critical roles in aging and cancer via the modulation of cellular homeostasis and the maintenance of genomic integrity. However, the underlying mechanism linking the two pathways remains elusive. Here, we show that SIRT1 functions as a modifier of CHK2 in cell cycle control. Specifically, SIRT1 interacts with CHK2 and deacetylates it at lysine 520 residue, which suppresses CHK2 phosphorylation, dimerization, and thus activation. SIRT1 depletion induces CHK2 hyperactivation-mediated cell cycle arrest and subsequent cell death. In vivo, genetic deletion of Chk2 rescues the neonatal lethality of Sirt1
Indexed as
AcetylationAnimalsCell CycleCells, CulturedCheckpoint Kinase 2HumansMiceMice, KnockoutPhosphorylationSirtuin 1Checkpoint Kinase 2Chek2 protein, mouseSirt1 protein, mouseSirtuin 1
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