What is he best known for?
The fields of study he is best known for:
- Gene
- Internal medicine
- Enzyme
Michael R. Blackburn spends much of his time researching Immunology, Adenosine, Adenosine receptor, Adenosine deaminase and Lung.
His studies in Immunology integrate themes in fields like Fibrosis and Mucin.
Michael R. Blackburn combines subjects such as Signal transduction, Purinergic signalling and Pathogenesis with his study of Adenosine.
His Purinergic signalling research integrates issues from Adenosine A3 receptor and Cell biology.
His biological study spans a wide range of topics, including Molecular biology and Cellular differentiation.
His biological study deals with issues like Immunodeficiency, which deal with fields such as Spleen and Deficient mouse.
His most cited work include:
- Muc5b is required for airway defence (407 citations)
- Adenosine receptors in regulation of dendritic cell differentiation and function (246 citations)
- Mucin Is Produced by Clara Cells in the Proximal Airways of Antigen-Challenged Mice (233 citations)
What are the main themes of his work throughout his whole career to date?
His main research concerns Adenosine, Immunology, Adenosine deaminase, Adenosine receptor and Internal medicine.
His study in Adenosine is interdisciplinary in nature, drawing from both Adenosine A3 receptor, Receptor, Signal transduction, Purinergic signalling and Adenosine A2B receptor.
His research in Immunology focuses on subjects like Lung, which are connected to Fibrosis and Pathology.
As part of the same scientific family, Michael R. Blackburn usually focuses on Adenosine deaminase, concentrating on Molecular biology and intersecting with Thymocyte.
The study incorporates disciplines such as Pharmacology and Nucleoside in addition to Adenosine receptor.
His study looks at the intersection of Internal medicine and topics like Endocrinology with Decidua.
He most often published in these fields:
- Adenosine (59.43%)
- Immunology (40.98%)
- Adenosine deaminase (34.84%)
What were the highlights of his more recent work (between 2015-2021)?
- Adenosine (59.43%)
- Fibrosis (17.62%)
- Cancer research (14.75%)
In recent papers he was focusing on the following fields of study:
Michael R. Blackburn mainly investigates Adenosine, Fibrosis, Cancer research, Adenosine A2B receptor and Lung.
Michael R. Blackburn works in the field of Adenosine, focusing on Adenosine deaminase in particular.
His work deals with themes such as Idiopathic pulmonary fibrosis and Pathogenesis, which intersect with Fibrosis.
His Adenosine A2B receptor research includes themes of Hypoxia and Pulmonary edema.
The Lung study combines topics in areas such as Nucleotidase, Immunology and Pathology.
Michael R. Blackburn specializes in Immunology, namely Inflammation.
Between 2015 and 2021, his most popular works were:
- Neutrophil transfer of miR-223 to lung epithelial cells dampens acute lung injury in mice (82 citations)
- STAT-3 contributes to pulmonary fibrosis through epithelial injury and fibroblast-myofibroblast differentiation (73 citations)
- Beneficial Role of Erythrocyte Adenosine A2B Receptor–Mediated AMP-Activated Protein Kinase Activation in High-Altitude Hypoxia (66 citations)
In his most recent research, the most cited papers focused on:
- Gene
- Internal medicine
- Enzyme
The scientist’s investigation covers issues in Adenosine, Lung, Inflammation, Adenosine A2B receptor and Pulmonary fibrosis.
His work on Adenosine deaminase as part of his general Adenosine study is frequently connected to Nucleoside transporter, thereby bridging the divide between different branches of science.
The subject of his Inflammation research is within the realm of Immunology.
His Immunology study combines topics from a wide range of disciplines, such as Cell signaling and Inosine.
The concepts of his Adenosine A2B receptor study are interwoven with issues in Adenosine A3 receptor, Endocrinology, Hypoxia and Signal transduction.
In his work, Cancer research and Fibroblast is strongly intertwined with Idiopathic pulmonary fibrosis, which is a subfield of Pulmonary fibrosis.
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