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Daniela Nasteska and David J Hodson

-dependent periodic activation of a Ca2+-activated K+ conductance in glucose-stimulated pancreatic β-cells . Nature 353 849 – 852 . 10.1038/353849a0 Anisimova M García-Ortega LF Martínez O 2015 How many genes are expressed in a transcriptome

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Narudee Kashemsant and Catherine B Chan

homolog: a potential molecular mediator of human thermogenesis. Diabetes 46 900 –906. Goodge KA & Hutton JC 2000 Translational regulation of proinsulin biosynthesis and proinsulin conversion in the pancreatic β-cell

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Marloes Dekker Nitert, Cecilia L F Nagorny, Anna Wendt, Lena Eliasson and Hindrik Mulder

Introduction The β-cells of pancreatic islets secrete insulin in response to an increase in glucose. Glucose enters the cells and is metabolised, provoking a rise in the ATP:ADP ratio, which leads to closure of ATP-sensitive K + (K ATP ) channels

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Marija Trajkovic-Arsic, Evdokia Kalideris and Jens T Siveke

in pancreatic β cells creates an insulin secretory defect similar to that in type 2 diabetes . Cell 96 329 – 339 . ( doi:10.1016/S0092-8674(00)80546-2 ). Lankisch PG Manthey G Otto J Koop H Talaulicar M Willms B Creutzfeldt W 1982

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Sun-Ji Park, Tae-Shin Kim, Choon-Keun Park, Sang-Hee Lee, Jin-Man Kim, Kyu-Sun Lee, In-kyu Lee, Jeen-Woo Park, Mark A Lawson and Dong-Seok Lee

insulin-secreting pancreatic β-cells. As such, UPR signaling has been shown to regulate the production of specific proteins under homeostatic regulation ( Wu & Kaufman 2006 ). As Leydig cells require continuous steroidogenic enzyme synthesis for the

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Marie Schaeffer, David J Hodson, Chrystel Lafont and Patrice Mollard

turn, can modulate secretory activity and hormone output ( Gonzalez-Hernandez & Gonzalez 2000 ). In pancreatic islets, both endothelial cells and β-cells express NOS ( Corbett et al . 1992 a , b , Alm et al . 1999 ) and NO influences both regulation

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Carlos Larqué, Myrian Velasco, Francisco Barajas-Olmos, Neyvis García-Delgado, Juan Pablo Chávez-Maldonado, Jazmín García-Morales, Lorena Orozco and Marcia Hiriart

Introduction Pancreatic beta-cells secrete insulin in response to changes in extracellular glucose and other secretagogues and are considered a metabolic milestone involved in regulating not only glucose but also other nutrient levels such as

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Neil W Salter, Sudharsana R Ande, Hoa K Nguyen, B L Grégoire Nyomba and Suresh Mishra

evidences together suggest an important physiological role for TG2 in pancreatic β-cell function, though the actual mechanism involved is not understood. A well-known function of TG2 is calcium-dependent transamidation, which is also known as a ‘protein

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J Jason Collier, Tim E Sparer, Michael D Karlstad and Susan J Burke

, Wallberg & Cooke 2013 , Boldison & Wong 2016 ). Therefore, we will focus this review around pancreatic islet β-cell chemokine production with a discussion of two important chemokine receptor-signaling paradigms that fundamentally impact specific subsets of

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Chanchal Gupta and Kulbhushan Tikoo

). Hyperglycemia has been reported to promote pancreatic cancer in BxPC-3 and MIA PaCa-2 cells in a concentration-dependent manner ( Liu et al . 2011 a ). It has been reported that cancer-specific survival of patients with hyperglycemia was much less than that of