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Apoptosis

  • RESEARCH ARTICLE
    Myh6-driven Cre recombinase activates the DNA damage response and the cell cycle in the myocardium in the absence of loxP sites
    Xinrui Wang, Amelia Lauth, Tina C. Wan, John W. Lough, John A. Auchampach
    Disease Models & Mechanisms 2020 13: dmm046375 doi: 10.1242/dmm.046375 Published 18 December 2020

    Summary: The presence of tamoxifen-induced Cre recombinase (merCremer) in the nucleus of cardiomyocytes induces DNA damage and unscheduled cell-cycle activation, indicating the requirement for appropriate controls when using Cre-loxP models for cardiac regeneration studies.

  • RESEARCH ARTICLE
    Progenitor death drives retinal dysplasia and neuronal degeneration in a mouse model of ATRIP-Seckel syndrome
    Gabriel E. Matos-Rodrigues, Pedro B. Tan, Maurício Rocha-Martins, Clara F. Charlier, Anielle L. Gomes, Felipe Cabral-Miranda, Paulius Grigaravicius, Thomas G. Hofmann, Pierre-Olivier Frappart, Rodrigo A. P. Martins
    Disease Models & Mechanisms 2020 13: dmm045807 doi: 10.1242/dmm.045807 Published 30 October 2020

    Summary: Retinopathies have been reported in primordial dwarfism syndromes. We show that the loss of Atrip, a gene mutated in Seckel syndrome, causes photoreceptor degeneration owing to p53-dependent apoptosis of retinal progenitors during development.

  • RESEARCH ARTICLE
    A Drosophila model to study retinitis pigmentosa pathology associated with mutations in the core splicing factor Prp8
    Dimitrije Stanković, Ann-Katrin Claudius, Thomas Schertel, Tina Bresser, Mirka Uhlirova
    Disease Models & Mechanisms 2020 13: dmm043174 doi: 10.1242/dmm.043174 Published 26 June 2020

    Summary: A Drosophila melanogaster disease model of retinitis pigmentosa type 13 to study the mechanisms underlying the loss of tissue homeostasis and degeneration caused by mutations in the core component of the spliceosome Prp8.

  • RESEARCH ARTICLE
    Adenoviral TMBIM6 vector attenuates ER-stress-induced apoptosis in a neonatal hypoxic-ischemic rat model
    Desislava Doycheva, Ningbo Xu, Harpreet Kaur, Jay Malaguit, Devin William McBride, Jiping Tang, John H. Zhang
    Disease Models & Mechanisms 2019 12: dmm040352 doi: 10.1242/dmm.040352 Published 22 November 2019

    Summary: Elucidating the role of Bax inhibitor 1 (BI-1) and its mechanisms in the pathophysiology of hypoxic ischemic encephalopathy may help provide a basis for BI-1 as a potential therapeutic target in clinics.

  • RESEARCH ARTICLE
    Perturbed development of cranial neural crest cells in association with reduced sonic hedgehog signaling underlies the pathogenesis of retinoic-acid-induced cleft palate
    Qi Wang, Hiroshi Kurosaka, Masataka Kikuchi, Akihiro Nakaya, Paul A. Trainor, Takashi Yamashiro
    Disease Models & Mechanisms 2019 12: dmm040279 doi: 10.1242/dmm.040279 Published 4 October 2019

    Editor's choice: The RA-Shh signaling pathway is revealed to be critical during cranial neural crest development, which impacts secondary palate development.

  • RESEARCH ARTICLE
    Disruption of asxl1 results in myeloproliferative neoplasms in zebrafish
    Evisa Gjini, Chang-Bin Jing, Ashley T. Nguyen, Deepak Reyon, Emma Gans, Michiel Kesarsing, Joshua Peterson, Olga Pozdnyakova, Scott J. Rodig, Marc R. Mansour, Keith Joung, A. Thomas Look
    Disease Models & Mechanisms 2019 12: dmm035790 doi: 10.1242/dmm.035790 Published 7 May 2019

    Summary: Homozygous loss of asxl1 in zebrafish leads to apoptosis of newly formed HSCs by upregulation of bim and bid. Half of the asxl1+/− zebrafish had MPNs by 5 months of age.

  • RESEARCH ARTICLE
    Spliceosomal components protect embryonic neurons from R-loop-mediated DNA damage and apoptosis
    Shelly Sorrells, Sara Nik, Mattie J. Casey, Rosannah C. Cameron, Harold Truong, Cristhian Toruno, Michelle Gulfo, Albert Lowe, Cicely Jette, Rodney A. Stewart, Teresa V. Bowman
    Disease Models & Mechanisms 2018 11: dmm031583 doi: 10.1242/dmm.031583 Published 26 February 2018

    Summary: Loss of RNA splicing factors causes R-loop accumulation and DNA damage in embryonic neurons, sensitizing them to radiation-induced cell death. These findings suggest that diseased cells with mutations in splicing factors are vulnerable to radiotherapy.

  • RESEARCH ARTICLE
    Activation of the Nkx2.5–Calr–p53 signaling pathway by hyperglycemia induces cardiac remodeling and dysfunction in adult zebrafish
    Yanyi Sun, Qiuyun Wang, Yuehua Fang, Chunfang Wu, Guoping Lu, Zhenyue Chen
    Disease Models & Mechanisms 2017 10: 1217-1227; doi: 10.1242/dmm.026781

    Summary: Induction of hyperglycemia gives rise to cardiac apoptosis and dysfunction in adult zebrafish via the Nkx2.5–Calr–p53 signaling pathway, resulting in adult cardiomyopathy.

  • RESOURCE ARTICLE
    Bar-coding neurodegeneration: identifying subcellular effects of human neurodegenerative disease proteins using Drosophila leg neurons
    Josefin Fernius, Annika Starkenberg, Stefan Thor
    Disease Models & Mechanisms 2017 10: 1027-1038; doi: 10.1242/dmm.029637

    Summary: Toxic effects of neurodegenerative disease proteins on neuronal function and morphology can be addressed using an array of transgenic fluorescent reporters in the adult Drosophila leg.

  • RESEARCH ARTICLE
    (CCUG)n RNA toxicity in a Drosophila model of myotonic dystrophy type 2 (DM2) activates apoptosis
    Vildan Betul Yenigun, Mario Sirito, Alla Amcheslavky, Tomek Czernuszewicz, Jordi Colonques-Bellmunt, Irma García-Alcover, Marzena Wojciechowska, Clare Bolduc, Zhihong Chen, Arturo López Castel, Ralf Krahe, Andreas Bergmann
    Disease Models & Mechanisms 2017 10: 993-1003; doi: 10.1242/dmm.026179

    Summary: A Drosophila model of myotonic dystrophy type 2 (DM2) recapitulates several features of the human disease, identifies apoptosis as a contributing factor to DM2, and is likely to provide a convenient tool for drug screening.

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