Michael R. Blackburn
University of Texas Health Science Center at Houston
211 Papers
2.8K Citations
Michael R. Blackburn is an academic researcher from University of Texas Health Science Center at Houston. The author has contributed to research in topics: Adenosine & Adenosine deaminase. The author has an hindex of 63, co-authored 205 publications. Previous affiliations of Michael R. Blackburn include University of Texas at Austin & Thomas Jefferson University.
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Papers
Animal Models of Airway Diseases
TL;DR: This chapter provides an in-depth description of each in vivo study, and a critical view of the therapeutic potentials for the treatment of airway diseases.
Maternal high-fat diet modifies epigenetic marks H3K27me3 and H3K27ac in bone to regulate offspring osteoblastogenesis in mice
Jin-Ran Chen,Perry C Caviness,Haijun Zhao,Beau Belcher,Umesh D. Wankhade,Kartik Shankar,Michael R. Blackburn,Oxana P. Lazarenko +7 more
TL;DR: Findings indicate that chronic maternal HFD changes histone trimethylation and acetylation epigenetic marks to regulate expression of genes controlling osteoblastogenesis.
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MicroRNA-98 reduces nerve growth factor expression in nicotine-induced airway remodeling
Cherry Wongtrakool,Junsuk Ko,Andrew J. Jang,Kora Grooms,Sarah Chang,Cory Sylber,Beata Kosmider,Karim Bahmed,Michael R. Blackburn,Roy L. Sutliff,C. Michael Hart,Changwon Park,Toru Nyunoya,Michael J. Passineau,Qing Lu,Bum-Yong Kang +15 more
TL;DR: Findings demonstrate that nicotine-induced increases in NGF and other markers of airway remodeling are negatively regulated by miR-98.
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Further Differentiation of Murine Double-Positive Thymocytes Is Inhibited in Adenosine Deaminase-Deficient Murine Fetal Thymic Organ Culture
C. Justin Van De Wiele,Michelle L. Joachims,Amy M. Fesler,James G. Vaughn,Michael R. Blackburn,Stephanie T. McGee,Linda F. Thompson,Linda F. Thompson +7 more
TL;DR: The data suggest that ADA deficiency leads to the induction of mitochondria-dependent apoptosis as a consequence of the accumulation of dATP derived from thymocytes failing the positive/negative selection checkpoint.
Adenosine deaminase-deficient mice: models for the study of lymphocyte development and adenosine signaling.
TL;DR: PEG-ADA treatment of ADA-deficient mice will serve as a useful in vivo system to biochemically manipulate adenosine levels and signaling to influence the eosinophilia, elevated IgE levels, alveolar defects, and severe inflammation and damage seen in the lungs of the mice.
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