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  1. Article ; Online: Clinical application of facial aging clocks.

    Wang, Yiyang / Mao, Kehang / Zhai, Haotian / Jackie Han, Jing-Dong

    The Lancet regional health. Western Pacific

    2023  Volume 37, Page(s) 100858

    Language English
    Publishing date 2023-07-22
    Publishing country England
    Document type Journal Article
    ISSN 2666-6065
    ISSN (online) 2666-6065
    DOI 10.1016/j.lanwpc.2023.100858
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: An aging program at the systems level?

    Han, Jing-Dong Jackie

    Birth defects research. Part C, Embryo today : reviews

    2012  Volume 96, Issue 2, Page(s) 206–211

    Abstract: Many genes and pathways are known to modulate lifespan in various organisms, but it remains unclear whether there exists a common aging program, and how individual variations of lifespan can occur in an isogenic population. Recent studies on aging ... ...

    Abstract Many genes and pathways are known to modulate lifespan in various organisms, but it remains unclear whether there exists a common aging program, and how individual variations of lifespan can occur in an isogenic population. Recent studies on aging regulation at the systems and epigenetic levels point to the possibility of regulating and potentially reversing the aging epigenome and transcriptome, resulting in differential aging status and aging rate in different individuals. Here, the author summarize some of these findings and discuss the possibility of integrating multiple layers of aging regulation at the systems level, to identify an aging program that can explain lifespan variations introduced by environmental and developmental history.
    MeSH term(s) Aging/physiology ; Animals ; Caenorhabditis elegans/physiology ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/metabolism ; Epigenesis, Genetic ; Gene Expression Regulation, Developmental ; Humans ; Systems Biology
    Chemical Substances Caenorhabditis elegans Proteins
    Language English
    Publishing date 2012-06
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2104792-3
    ISSN 1542-9768 ; 1542-0752 ; 1542-9733 ; 1542-975X
    ISSN (online) 1542-9768
    ISSN 1542-0752 ; 1542-9733 ; 1542-975X
    DOI 10.1002/bdrc.21007
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Molecular and phenotypic biomarkers of aging.

    Xia, Xian / Chen, Weiyang / McDermott, Joseph / Han, Jing-Dong Jackie

    F1000Research

    2017  Volume 6, Page(s) 860

    Abstract: Individuals of the same age may not age at the same rate. Quantitative biomarkers of aging are valuable tools to measure physiological age, assess the extent of 'healthy aging', and potentially predict health span and life span for an individual. Given ... ...

    Abstract Individuals of the same age may not age at the same rate. Quantitative biomarkers of aging are valuable tools to measure physiological age, assess the extent of 'healthy aging', and potentially predict health span and life span for an individual. Given the complex nature of the aging process, the biomarkers of aging are multilayered and multifaceted. Here, we review the phenotypic and molecular biomarkers of aging. Identifying and using biomarkers of aging to improve human health, prevent age-associated diseases, and extend healthy life span are now facilitated by the fast-growing capacity of multilevel cross-sectional and longitudinal data acquisition, storage, and analysis, particularly for data related to general human populations. Combined with artificial intelligence and machine learning techniques, reliable panels of biomarkers of aging will have tremendous potential to improve human health in aging societies.
    Language English
    Publishing date 2017-06-09
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2699932-8
    ISSN 2046-1402
    ISSN 2046-1402
    DOI 10.12688/f1000research.10692.1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: A role for LSH in facilitating DNA methylation by DNMT1 through enhancing UHRF1 chromatin association.

    Han, Mengmeng / Li, Jialun / Cao, Yaqiang / Huang, Yuanyong / Li, Wen / Zhu, Haijun / Zhao, Qian / Han, Jing-Dong Jackie / Wu, Qihan / Li, Jiwen / Feng, Jing / Wong, Jiemin

    Nucleic acids research

    2021  Volume 48, Issue 21, Page(s) 12116–12134

    Abstract: LSH, a SNF2 family DNA helicase, is a key regulator of DNA methylation in mammals. How LSH facilitates DNA methylation is not well defined. While previous studies with mouse embryonic stem cells (mESc) and fibroblasts (MEFs) derived from Lsh knockout ... ...

    Abstract LSH, a SNF2 family DNA helicase, is a key regulator of DNA methylation in mammals. How LSH facilitates DNA methylation is not well defined. While previous studies with mouse embryonic stem cells (mESc) and fibroblasts (MEFs) derived from Lsh knockout mice have revealed a role of Lsh in de novo DNA methylation by Dnmt3a/3b, here we report that LSH contributes to DNA methylation in various cell lines primarily by promoting DNA methylation by DNMT1. We show that loss of LSH has a much bigger effect in DNA methylation than loss of DNMT3A and DNMT3B. Mechanistically, we demonstrate that LSH interacts with UHRF1 but not DNMT1 and facilitates UHRF1 chromatin association and UHRF1-catalyzed histone H3 ubiquitination in an ATPase activity-dependent manner, which in turn promotes DNMT1 recruitment to replication fork and DNA methylation. Notably, UHRF1 also enhances LSH association with the replication fork. Thus, our study identifies LSH as an essential factor for DNA methylation by DNMT1 and provides novel insight into how a feed-forward loop between LSH and UHRF1 facilitates DNMT1-mediated maintenance of DNA methylation in chromatin.
    MeSH term(s) Animals ; CCAAT-Enhancer-Binding Proteins/antagonists & inhibitors ; CCAAT-Enhancer-Binding Proteins/genetics ; CCAAT-Enhancer-Binding Proteins/metabolism ; Chromatin/chemistry ; Chromatin/metabolism ; DNA (Cytosine-5-)-Methyltransferase 1/antagonists & inhibitors ; DNA (Cytosine-5-)-Methyltransferase 1/genetics ; DNA (Cytosine-5-)-Methyltransferase 1/metabolism ; DNA (Cytosine-5-)-Methyltransferases/antagonists & inhibitors ; DNA (Cytosine-5-)-Methyltransferases/genetics ; DNA (Cytosine-5-)-Methyltransferases/metabolism ; DNA Helicases/antagonists & inhibitors ; DNA Helicases/genetics ; DNA Helicases/metabolism ; DNA Methylation ; DNA Methyltransferase 3A ; HCT116 Cells ; HEK293 Cells ; HeLa Cells ; Histones/genetics ; Histones/metabolism ; Humans ; Mice ; NIH 3T3 Cells ; Protein Processing, Post-Translational ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; Ubiquitin-Protein Ligases/antagonists & inhibitors ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitination ; DNA Methyltransferase 3B
    Chemical Substances CCAAT-Enhancer-Binding Proteins ; Chromatin ; DNMT3A protein, human ; Dnmt3a protein, mouse ; Histones ; RNA, Small Interfering ; DNA (Cytosine-5-)-Methyltransferase 1 (EC 2.1.1.37) ; DNA (Cytosine-5-)-Methyltransferases (EC 2.1.1.37) ; DNA Methyltransferase 3A (EC 2.1.1.37) ; DNMT1 protein, human (EC 2.1.1.37) ; UHRF1 protein, human (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; DNA Helicases (EC 3.6.4.-) ; HELLS protein, human (EC 5.99.-)
    Language English
    Publishing date 2021-01-20
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 186809-3
    ISSN 1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
    ISSN (online) 1362-4962 ; 1362-4954
    ISSN 0301-5610 ; 0305-1048
    DOI 10.1093/nar/gkaa1003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Understanding biological functions through molecular networks.

    Han, Jing-Dong Jackie

    Cell research

    2008  Volume 18, Issue 2, Page(s) 224–237

    Abstract: The completion of genome sequences and subsequent high-throughput mapping of molecular networks have allowed us to study biology from the network perspective. Experimental, statistical and mathematical modeling approaches have been employed to study the ... ...

    Abstract The completion of genome sequences and subsequent high-throughput mapping of molecular networks have allowed us to study biology from the network perspective. Experimental, statistical and mathematical modeling approaches have been employed to study the structure, function and dynamics of molecular networks, and begin to reveal important links of various network properties to the functions of the biological systems. In agreement with these functional links, evolutionary selection of a network is apparently based on the function, rather than directly on the structure of the network. Dynamic modularity is one of the prominent features of molecular networks. Taking advantage of such a feature may simplify network-based biological studies through construction of process-specific modular networks and provide functional and mechanistic insights linking genotypic variations to complex traits or diseases, which is likely to be a key approach in the next wave of understanding complex human diseases. With the development of ready-to-use network analysis and modeling tools the networks approaches will be infused into everyday biological research in the near future.
    MeSH term(s) Animals ; Cell Nucleus/genetics ; Evolution, Molecular ; Gene Expression Regulation/genetics ; Genetic Variation ; Genome, Human/genetics ; Genotype ; Humans ; Models, Genetic ; Quantitative Trait Loci/genetics
    Language English
    Publishing date 2008-02
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1319303-x
    ISSN 1748-7838 ; 1001-0602
    ISSN (online) 1748-7838
    ISSN 1001-0602
    DOI 10.1038/cr.2008.16
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Molecular and phenotypic biomarkers of aging [version 1; referees

    Xian Xia / Weiyang Chen / Joseph McDermott / Jing-Dong Jackie Han

    F1000Research, Vol

    3 approved]

    2017  Volume 6

    Abstract: Individuals of the same age may not age at the same rate. Quantitative biomarkers of aging are valuable tools to measure physiological age, assess the extent of ‘healthy aging’, and potentially predict health span and life span for an individual. Given ... ...

    Abstract Individuals of the same age may not age at the same rate. Quantitative biomarkers of aging are valuable tools to measure physiological age, assess the extent of ‘healthy aging’, and potentially predict health span and life span for an individual. Given the complex nature of the aging process, the biomarkers of aging are multilayered and multifaceted. Here, we review the phenotypic and molecular biomarkers of aging. Identifying and using biomarkers of aging to improve human health, prevent age-associated diseases, and extend healthy life span are now facilitated by the fast-growing capacity of multilevel cross-sectional and longitudinal data acquisition, storage, and analysis, particularly for data related to general human populations. Combined with artificial intelligence and machine learning techniques, reliable panels of biomarkers of aging will have tremendous potential to improve human health in aging societies.
    Keywords Aging ; Bioinformatics ; Cell Growth & Division ; Control of Gene Expression ; Developmental Molecular Mechanisms ; Membranes & Sorting ; Medicine ; R ; Science ; Q
    Subject code 612
    Language English
    Publishing date 2017-06-01T00:00:00Z
    Publisher F1000 Research Ltd
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: Biomarkers of aging for the identification and evaluation of longevity interventions.

    Moqri, Mahdi / Herzog, Chiara / Poganik, Jesse R / Justice, Jamie / Belsky, Daniel W / Higgins-Chen, Albert / Moskalev, Alexey / Fuellen, Georg / Cohen, Alan A / Bautmans, Ivan / Widschwendter, Martin / Ding, Jingzhong / Fleming, Alexander / Mannick, Joan / Han, Jing-Dong Jackie / Zhavoronkov, Alex / Barzilai, Nir / Kaeberlein, Matt / Cummings, Steven /
    Kennedy, Brian K / Ferrucci, Luigi / Horvath, Steve / Verdin, Eric / Maier, Andrea B / Snyder, Michael P / Sebastiano, Vittorio / Gladyshev, Vadim N

    Cell

    2023  Volume 186, Issue 18, Page(s) 3758–3775

    Abstract: With the rapid expansion of aging biology research, the identification and evaluation of longevity interventions in humans have become key goals of this field. Biomarkers of aging are critically important tools in achieving these objectives over ... ...

    Abstract With the rapid expansion of aging biology research, the identification and evaluation of longevity interventions in humans have become key goals of this field. Biomarkers of aging are critically important tools in achieving these objectives over realistic time frames. However, the current lack of standards and consensus on the properties of a reliable aging biomarker hinders their further development and validation for clinical applications. Here, we advance a framework for the terminology and characterization of biomarkers of aging, including classification and potential clinical use cases. We discuss validation steps and highlight ongoing challenges as potential areas in need of future research. This framework sets the stage for the development of valid biomarkers of aging and their ultimate utilization in clinical trials and practice.
    MeSH term(s) Humans ; Longevity ; Aging ; Biomarkers
    Chemical Substances Biomarkers
    Language English
    Publishing date 2023-08-09
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2023.08.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Accurate Drug Repositioning through Non-tissue-Specific Core Signatures from Cancer Transcriptomes.

    Xu, Chi / Ai, Daosheng / Shi, Dawei / Suo, Shengbao / Chen, Xingwei / Yan, Yizhen / Cao, Yaqiang / Zhang, Rui / Sun, Na / Chen, Weizhong / McDermott, Joseph / Zhang, Shiqiang / Zeng, Yingying / Han, Jing-Dong Jackie

    Cell reports

    2019  Volume 29, Issue 4, Page(s) 1055

    Language English
    Publishing date 2019-10-17
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2019.10.023
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Genome-wide analysis of histone acetylation dynamics during mouse embryonic stem cell neural differentiation.

    Liu, Pingyu / Dou, Xiaoyang / Peng, Guangdun / Han, Jing-Dong Jackie / Jing, Naihe

    Genomics data

    2015  Volume 5, Page(s) 15–16

    Abstract: Epigenetic modification as an intrinsic fine-tune program cooperates with key transcription factors to regulate the cell fate determination. The histone acetylation participating in neural differentiation of pluripotent stem cells is expected but not ... ...

    Abstract Epigenetic modification as an intrinsic fine-tune program cooperates with key transcription factors to regulate the cell fate determination. The histone acetylation participating in neural differentiation of pluripotent stem cells is expected but not well studied. Here, using acetylated histone H3 ChIP-sequencing (ChIP-seq), we demonstrate that the histone H3 acetylation level is gradually increased on the neural gene loci while decreased on the neural-inhibitory gene loci during mouse embryonic stem cell (mESC) neural differentiation. We further show that histone deacetylase 1 (HDAC1) is essential for neural commitment by targeting Nodal signaling. Thus, our study reveals a mechanism by which the epigenetic modification of histone acetylation/deacetylation interacts with extracellular signaling in mESC neural fate determination. Data were deposited in Gene Expression Omnibus (GEO) datasets under reference number GSE66025.
    Language English
    Publishing date 2015-05-09
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2751131-5
    ISSN 2213-5960
    ISSN 2213-5960
    DOI 10.1016/j.gdata.2015.05.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: Genome-wide ChIP-seq and RNA-seq analyses of Pou3f1 during mouse pluripotent stem cell neural fate commitment.

    Song, Lu / Sun, Na / Peng, Guangdun / Chen, Jun / Han, Jing-Dong Jackie / Jing, Naihe

    Genomics data

    2015  Volume 5, Page(s) 375–377

    Abstract: Appropriate neural initiation of the pluripotent stem cells in the early embryos is critical for the development of the central nervous system. This process is regulated by the coordination of extrinsic signals and intrinsic programs. However, how the ... ...

    Abstract Appropriate neural initiation of the pluripotent stem cells in the early embryos is critical for the development of the central nervous system. This process is regulated by the coordination of extrinsic signals and intrinsic programs. However, how the coordination is achieved to ensure proper neural fate commitment is largely unknown. Here, taking advantage of genome-wide ChIP-sequencing (ChIP-seq) and RNA-sequencing (RNA-seq) analyses, we demonstrate that the transcriptional factor Pou3f1 is an upstream activator of neural-promoting genes, and it is able to repress neural-inhibitory signals as well. Further studies revealed that Pou3f1 could directly bind neural lineage genes like Sox2 and downstream targets of neural inhibition signaling such as BMP and Wnt. Our results thus identify Pou3f1 as a critical dual-regulator of the intrinsic transcription factors and the extrinsic cellular signals during neural fate commitment. Data were deposited in Gene Expression Omnibus (GEO) datasets under reference number GSE69865.
    Language English
    Publishing date 2015-07-09
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2751131-5
    ISSN 2213-5960
    ISSN 2213-5960
    DOI 10.1016/j.gdata.2015.06.028
    Database MEDical Literature Analysis and Retrieval System OnLINE

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