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Showing 1–23 of 23 results
Advanced filters: Author: Matthias Hebrok Clear advanced filters

  • Sox9 is a well-known transcriptional regulator of embryonic pancreas and endocrine cell development. Here, the authors show that loss of Sox9 in mature beta cells disrupts alternative splicing patterns and impairs insulin secretion, with significant implications for cellular function.

    • Sapna Puri
    • Hasna Maachi
    • Matthias Hebrok
    ResearchOpen Access
    Nature Communications
    Volume: 15, P: 1-17

  • Clinical and genetic phenotyping of consanguineous family cases of neonatal syndromic diabetes and type 2 diabetes, combined with in-depth functional studies in pluripotent stem cells, reveals a role for genetic variants of ONECUT1 in monogenic and multifactorial diabetes.

    • Anne Philippi
    • Sandra Heller
    • Alexander Kleger
    Research
    Nature Medicine
    Volume: 27, P: 1928-1940

  • Effectively targeting deregulated KRAS signaling remains an unmet clinical need, as current approaches commonly lead to the development of chemoresistance in clinical settings. ADAM9-mediated lysosomal KRAS degradation is now shown to counteract PDAC chemoresistance independently of mutational status.

    • Laura Leonhardt
    • Matthias Hebrok
    News & Views
    Nature Cancer
    Volume: 5, P: 375-377

  • The debut of stem cell-derived islets in the clinic for glycaemic control in patients with type 1 diabetes mellitus has garnered much excitement. Ongoing research in this field guarantees to be transformative for modern treatment of diabetes mellitus.

    • Veronica A. Cochrane
    • Matthias Hebrok
    Comments & Opinion
    Nature Reviews Endocrinology
    Volume: 19, P: 681-682

  • Adult beta cells, which are highly specialised insulin-secreting cells, rarely replicate. Puri et al. demonstrate that beta cell proliferative capacity is inversely correlated with their functionality and differentiation state, by inducing proliferation of adult cells with ectopic overexpression of the cell cycle regulator c-Myc.

    • Sapna Puri
    • Nilotpal Roy
    • Matthias Hebrok
    ResearchOpen Access
    Nature Communications
    Volume: 9, P: 1-12

  • Insulin-producing pancreatic beta cells, generatedin vitro, could lead to new anti-diabetic therapies. Here, Zhu et al. convert human fibroblasts into endodermal progenitors that differentiate in vitrointo glucose-responsive beta-like cells that, following transplantation in mice, protect from diabetes.

    • Saiyong Zhu
    • Holger A. Russ
    • Sheng Ding
    ResearchOpen Access
    Nature Communications
    Volume: 7, P: 1-13

  • A genetic analysis of patients with permanent neonatal diabetes mellitus has revealed functional conservation of transcription factors critical for β-cell development in both mouse and man. This finding supports the use of mice for modelling human disease but also highlights the need for additional human-specific studies of β-cell function.

    • Alexandra E. Folias
    • Matthias Hebrok
    News & Views
    Nature Reviews Endocrinology
    Volume: 10, P: 253-255

  • Pancreatic ductal adenocarcinoma (PDAC) is characterized by near-universal mutations in KRAS and frequent deregulation of the Hedgehog (Hh) and Wnt–β-catenin pathways. This Review examines the central part that KRAS plays in the biology of PDAC, and how the timing and ___location of Hh and Wnt–β-catenin signalling dictate the specification and oncogenic properties of PDAC.

    • John P. Morris IV
    • Sam C. Wang
    • Matthias Hebrok
    Reviews
    Nature Reviews Cancer
    Volume: 10, P: 683-695

  • This Review highlights the research advances, advantages and challenges in several different strategies for generating functional β-cells for therapeutic use in diabetes mellitus. In addition, scalable bioengineering processes are also discussed for the realization of the therapeutic potential of derived β-cells.

    • Gopika G. Nair
    • Emmanuel S. Tzanakakis
    • Matthias Hebrok
    Reviews
    Nature Reviews Endocrinology
    Volume: 16, P: 506-518

  • Dysfunction or loss of insulin-secreting β cells in the pancreas is a hallmark of diabetes. Here, Dorrell et al.identify four subpopulations of β cells in humans, which differ in gene expression and insulin secretion kinetics, and the abundance of which is altered in patients with type 2 diabetes.

    • Craig Dorrell
    • Jonathan Schug
    • Markus Grompe
    ResearchOpen Access
    Nature Communications
    Volume: 7, P: 1-9

  • Diabetes is a substantial and increasing health concern. In this Review, Lickert and colleagues discuss the progress made in developing insulin-producing islets using in vitro methods, including which aspects need to be improved in order to use these islets as transplants. Using these islets in laboratory settings could further our understanding of pancreatic function and the mechanisms underlying diabetes.

    • Johanna Siehler
    • Anna Karolina Blöchinger
    • Heiko Lickert
    Reviews
    Nature Reviews Drug Discovery
    Volume: 20, P: 920-940

  • A systematic comparison shows that differential DNA methylation accounts for some of the differences in somatic gene expression between induced pluripotent stem cells (iPSCs) and embryonic stem cells. The somatic genes that have persistent expression in iPSCs tend to be isolated from other genes that undergo silencing during reprogramming. This may explain the observed delay in recruitment of the DNA methylation machinery and in the genes being silenced.

    • Yuki Ohi
    • Han Qin
    • Miguel Ramalho-Santos
    Research
    Nature Cell Biology
    Volume: 13, P: 541-549

  • Heller et al analyze transcriptomic and epigenetic datasets from human PSCs differentiating into pancreatic progenitors to elucidate the regulatory mechanisms behind pancreatic development. The authors report that the transcription factor ONECUT1 is expressed specifically in pancreatic development and associates with other key TFs (such as FOXA2, GATA6, PDX1) during endocrine specification.

    • Sandra Heller
    • Zhijian Li
    • Ivan G. Costa
    ResearchOpen Access
    Communications Biology
    Volume: 4, P: 1-12