Blake J. Cochran
University of New South Wales
55 Papers
77 Citations
Blake J. Cochran is an academic researcher from University of New South Wales. The author has contributed to research in topics: Medicine & Internal medicine. The author has an hindex of 12, co-authored 34 publications. Previous affiliations of Blake J. Cochran include University of Wollongong & Imperial College London.
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Papers
Targeting GLP-1 receptor trafficking to improve agonist efficacy.
Ben Jones,Teresa Buenaventura,N Kanda,Pauline Chabosseau,Bryn M. Owen,Rebecca Scott,Robert D. Goldin,N. Angkathunyakul,N. Angkathunyakul,Ivan R. Corrêa,Domenico Bosco,Paul Johnson,Lorenzo Piemonti,Piero Marchetti,A. M. James Shapiro,Blake J. Cochran,Blake J. Cochran,Aylin C. Hanyaloglu,Asuka Inoue,Tricia Tan,Guy A. Rutter,Alejandra Tomas,Stephen R. Bloom +22 more
TL;DR: It is shown that a longer plasma membrane retention time of GLP-1R results in greater long-term insulin release, which is dependent on a reduction in β-arrestin recruitment and faster agonist dissociation rates.
APOA1: a Protein with Multiple Therapeutic Functions
TL;DR: In this article, the main apolipoprotein of plasma high-density lipoproteins (HDLs), APO A1, has several well documented cardioprotective functions.
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Colchicine Inhibits Neutrophil Extracellular Trap Formation in Patients With Acute Coronary Syndrome After Percutaneous Coronary Intervention.
Kaivan Vaidya,Bradley Tucker,Bradley Tucker,R. Kurup,R. Kurup,Chinmay Khandkar,Elvis Pandzic,Jennifer Y. Barraclough,Jennifer Y. Barraclough,Joshua Machet,Ashish Misra,Mary M. Kavurma,Gonzalo Martínez,Kerry-Anne Rye,Blake J. Cochran,Sanjay Patel,Sanjay Patel,Sanjay Patel +17 more
TL;DR: In this paper, the neutrophil extracellular traps (NETs) after percutaneous coronary intervention (PCI) in acute coronary syndrome (ACS) is associated with periprocedural myocardial infarction.
90
Apolipoprotein A-I Increases Insulin Secretion and Production From Pancreatic β-Cells via a G-Protein-cAMP-PKA-FoxO1–Dependent Mechanism
Blake J. Cochran,R. Bisoendial,Liming Hou,Elias N. Glaros,Jérémie Rossy,Shane R. Thomas,Philip J. Barter,Kerry-Anne Rye,Kerry-Anne Rye,Kerry-Anne Rye +9 more
TL;DR: ApoA-I increases insulin synthesis and secretion via a heterotrimeric G-protein-cAMP-protein kinase A-FoxO1–dependent mechanism that involves transmembrane adenylyl cyclases and increased transcription of key insulin response and &bgr;-cell survival genes.
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Apolipoprotein A-I enhances insulin-dependent and insulin-independent glucose uptake by skeletal muscle.
Shudi Tang,Fatiha Tabet,Blake J. Cochran,Luisa F. Cuesta Torres,Ben J. Wu,Philip J. Barter,Kerry-Anne Rye +6 more
TL;DR: Results establish that apoA-I increases glucose disposal in skeletal muscle by activating the IR/IRS-1/PI3K/Akt/AS160 signal transduction pathway, and suggest that therapeutic agents that increase apo A-I levels may improve glycemic control in people with type 2 diabetes.