Michael R. Blackburn

Affiliations: 
The University of Texas Graduate School of Biomedical Sciences at Houston 
Area:
Pathology, Biochemistry
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"Michael Blackburn"
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Publications

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Wang W, Chen NY, Ren D, et al. (2021) Enhancing Extracellular Adenosine Levels Restores Barrier Function in Acute Lung Injury Through Expression of Focal Adhesion Proteins. Frontiers in Molecular Biosciences. 8: 636678
Chambers ED, White A, Vang A, et al. (2020) Blockade of equilibrative nucleoside transporter 1/2 protects against Pseudomonas aeruginosa-induced acute lung injury and NLRP3 inflammasome activation. Faseb Journal : Official Publication of the Federation of American Societies For Experimental Biology. 34: 1516-1531
Weng T, Huang J, Wagner EJ, et al. (2019) Downregulation of CFIm25 amplifies dermal fibrosis through alternative polyadenylation. The Journal of Experimental Medicine
Ko J, Mills T, Huang J, et al. (2019) Transforming growth factor beta 1 alters the 3'UTR of mRNA to promote lung fibrosis. The Journal of Biological Chemistry
Wu M, Skaug B, Bi X, et al. (2019) Interferon regulatory factor 7 (IRF7) represents a link between inflammation and fibrosis in the pathogenesis of systemic sclerosis. Annals of the Rheumatic Diseases
Collum SD, Molina JG, Hanmandlu A, et al. (2019) Adenosine and hyaluronan modulate lung fibrosis and pulmonary hypertension in combined pulmonary fibrosis and emphysema (CPFE). Disease Models & Mechanisms
Huang C, Xiao X, Yang Y, et al. (2019) Correction: MicroRNA-101 attenuates pulmonary fibrosis by inhibiting fibroblast proliferation and activation. The Journal of Biological Chemistry. 294: 6694
Weng T, Ko J, Masamha CP, et al. (2019) Cleavage factor 25 deregulation contributes to pulmonary fibrosis through alternative polyadenylation. The Journal of Clinical Investigation. 130
Aherne CM, Collins CB, Rapp CR, et al. (2018) Coordination of ENT2-dependent adenosine transport and signaling dampens mucosal inflammation. Jci Insight. 3
Liu H, Adebiyi M, Liu RR, et al. (2018) Elevated ecto-5'-nucleotidase: a missing pathogenic factor and new therapeutic target for sickle cell disease. Blood Advances. 2: 1957-1968
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