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Stacey Fynch
Researcher at St. Vincent's Institute of Medical Research
Publications - 24
Citations - 676
Stacey Fynch is an academic researcher from St. Vincent's Institute of Medical Research. The author has contributed to research in topics: NOD mice & Insulitis. The author has an hindex of 13, co-authored 23 publications receiving 563 citations.
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Journal ArticleDOI
The proapoptotic BH3-only proteins Bim and Puma are downstream of endoplasmic reticulum and mitochondrial oxidative stress in pancreatic islets in response to glucotoxicity
Jibran Ja Wali,Dieter Rondas,Mark D. McKenzie,Yuxing Zhao,Lorraine Elkerbout,Stacey Fynch,Esteban Nicolas Gurzov,Shizuo Akira,Chantal Mathieu,Thomas W.H. Kay,Lut Overbergh,Andreas Strasser,Helen E. Thomas +12 more
TL;DR: The data demonstrate that high concentrations of glucose induce ER and oxidative stress, which causes cell death mediated by Bim and Puma, which indicates that inhibition of BIM and Pum, or their inducers, may prevent beta-cell destruction in type 2 diabetes.
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Liver‐specific suppressor of cytokine signaling‐3 deletion in mice enhances hepatic insulin sensitivity and lipogenesis resulting in fatty liver and obesity
Nirupa Sachithanandan,Barbara C Fam,Stacey Fynch,Nicolas Dzamko,Matthew J. Watt,Sam Wormald,Jane Honeyman,Sandra Galic,Joseph Proietto,Sofianos Andrikopoulos,Andrea L. Hevener,Thomas W.H. Kay,Gregory R. Steinberg,Gregory R. Steinberg +13 more
TL;DR: Deletion of SOCS3 in the liver increases liver insulin sensitivity in mice fed a control diet but paradoxically promotes lipogenesis, leading to the development of nonalcoholic fatty liver disease, inflammation, and obesity.
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Macrophage Deletion of SOCS1 Increases Sensitivity to LPS and Palmitic Acid and Results in Systemic Inflammation and Hepatic Insulin Resistance
Nirupa Sachithanandan,Kate L. Graham,Sandra Galic,Jane Honeyman,Stacey Fynch,Kimberly A. Hewitt,Gregory R. Steinberg,Thomas W.H. Kay +7 more
TL;DR: The expression of SOCS1 in hematopoietic cells protects mice against systemic inflammation and hepatic insulin resistance potentially by inhibiting LPS and palmitate-induced TLR4 signaling in macrophages.
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Repurposed JAK1/JAK2 inhibitor reverses established autoimmune insulitis in NOD mice
Prerak Trivedi,Kate L. Graham,Nicholas A. Scott,Misty R. Jenkins,Suktilang Majaw,Robyn M. Sutherland,Robyn M. Sutherland,Stacey Fynch,Andrew M. Lew,Christopher J. Burns,Balasubramanian Krishnamurthy,Thomas C. Brodnicki,Stuart I. Mannering,Thomas W.H. Kay,Helen E. Thomas +14 more
TL;DR: The JAK1/JAK2 inhibitor AZD1480 blocked the effect of cytokines on mouse and human β-cells by inhibiting MHC class I upregulation, and prevented the direct interaction between CD8+ T cells and β- cells, and reduced immune cell infiltration into islets.
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Islet β-Cells Deficient in Bcl-xL Develop but Are Abnormally Sensitive to Apoptotic Stimuli
Emma M. Carrington,Mark D. McKenzie,Elisa S. Jansen,Michelle Myers,Stacey Fynch,Cameron Kos,Andreas Strasser,Thomas W.H. Kay,Clare L. Scott,Janette Allison +9 more
TL;DR: Bcl-xL expression at physiological levels may partially protect β-cells from apoptotic stimuli, including apoptosis because of mediators implicated in type 1 diabetes and death or degeneration of transplanted islets.