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Showing 1–20 of 20 results
Advanced filters: Author: Kenneth S. Zaret Clear advanced filters

  • Most insulin-secreting pancreatic β-cells are irreplaceably lost in type 1 diabetes. In a mouse model, pancreatic α-cells seem to sacrifice their identity to replenish the low stock of β-cells1. Two experts discuss what this means for understanding the basic cell biology involved and its relevance to treating diabetes.boxed-text

    • Kenneth S. Zaret
    • Morris F. White
    News & Views
    Nature
    Volume: 464, P: 1132-1133

  • Upon physiological injury, hepatocytes transdifferentiate into biliary epithelial cells, a process involving molecular rewiring. Here, authors show that Sox4 organizes the early steps, acting as a pioneer factor to decommission hepatocyte enhancers and open chromatin around biliary genes.

    • Takeshi Katsuda
    • Jonathan H. Sussman
    • Ben Z. Stanger
    ResearchOpen Access
    Nature Communications
    Volume: 15, P: 1-20

  • Five leading researchers provide their perspectives on our current understanding of pioneer factors and their important gene regulatory roles in cell differentiation, cell fate determination and reprogramming.

    • Martha L. Bulyk
    • Jacques Drouin
    • Kenneth S. Zaret
    Reviews
    Nature Reviews Genetics
    Volume: 24, P: 809-815

  • Cell-tracing analysis reveals that a disperse group of cells in the mouse liver express the enzyme telomerase, which preserves chromosome ends. These cells contribute to liver maintenance and regeneration.

    • Kenneth S. Zaret
    News & Views
    Nature
    Volume: 556, P: 181-182

  • A previously under-appreciated subset of liver cells has been found to contribute to the day-to-day maintenance of liver mass in mice. The cells are induced and supported by signals from an adjacent vein. See Article p.180

    • Kenneth S. Zaret
    News & Views
    Nature
    Volume: 524, P: 165-166

  • New genomic analyses indicate that pioneer transcription factors can sample a diverse repertoire of common binding sites among different cell types and become enriched where they cooperate with other factors specific to each cell. Pioneer-factor binding is mechanistically separate from, and is necessary for, subsequent phenomena of chromatin opening and epigenetic memory in vivo.

    • Kenneth S. Zaret
    News & Views
    Nature Genetics
    Volume: 50, P: 167-169

  • Newly specified hepatic and pancreatic progenitors, which originate from common endodermal domains, are able to reverse their course and develop into gut progenitors. Understanding what underlies such programming reversal and intrinsic regenerative capacities should illuminate the basis of cellular plasticity and facilitate targeted programming of stem cells.

    • Kenneth S. Zaret
    Reviews
    Nature Reviews Genetics
    Volume: 9, P: 329-340

  • An inflammatory profile is associated with aging and senescence. Here, Hao et al. show that TXNRD1 drives the senescence-associated secretory phenotype through the cGAS–STING pathway, independently of its enzymatic activity, during senescence and that the TXNRD1–cGAS interaction may be a target for selectively suppressing inflammaging.

    • Xue Hao
    • Bo Zhao
    • Rugang Zhang
    Research
    Nature Aging
    Volume: 4, P: 185-197

  • Recent data indicate that various transcription factors and RNA polymerase II bind to mitotic chromatin and that thousands of genes remain transcriptionally active in mitosis, contradicting the view that mitotic cells are transcriptionally silenced. These mechanisms provide mitotic transcriptional memory, which allows re-establishment of cell-type-specific gene expression following division.

    • Katherine C. Palozola
    • Jonathan Lerner
    • Kenneth S. Zaret
    Reviews
    Nature Reviews Molecular Cell Biology
    Volume: 20, P: 55-64

  • In a new paper in Cell Research, Ji et al. find that transcription factor-instigated opening of chromatin, during cell reprogramming, can be sensed by the Baf60b-containing chromatin remodeling complex, which then activates the ATM-p53 pathway, leading to cell death. These findings from reprogramming studies unveil what I term a “chromatin remodeling checkpoint” whereby extensive, inappropriate chromatin opening events lead to cell elimination, thus preventing cell fate conversion that might occur upon tissue damage; if unchecked, such conversion could lead to metaplasia and cancer.

    • Kenneth S Zaret
    Research Highlights
    Cell Research
    Volume: 27, P: 598-599