This decommissioned ERA site remains active temporarily to support our final migration steps to https://ualberta.scholaris.ca, ERA's new home. All new collections and items, including Spring 2025 theses, are at that site. For assistance, please contact erahelp@ualberta.ca.
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Spring 2017
ADP-ribosylation factors (Arfs) play a central role in the regulation of vesicular trafficking through the Golgi. Arfs are activated on cis-Golgi membranes exclusively by the guanine nucleotide exchange factor (GEF) Golgi-specific BFA resistance factor 1 (GBF1), upon recruitment from cytosol....
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Spring 2010
Anion Exchanger 1, AE1, is a membrane glycoprotein that functions as a dimer in the red blood cells (RBC) as well the kidney. It functions to exchange Cl- for HCO3- in an electroneutral manner, with the RBC AE1 having an additional function in maintaining its biconcave shape. Mutations in AE1...
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Fall 2014
Fungal pathogens are recognized by Dectin-1, a pattern recognition receptor expressed on mammalian innate immune cells. Dectin-1 detects β-glucans, which are polymers of glucose that are a main component of the fungal cell wall. While purified, soluble β-glucans have been used in the clinic as...
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Fall 2019
Cilia are microtubule-based structures that project from nearly every cell in the vertebrate body. While cilia in different contexts can have either sensory or motile functions, all cilia rely upon a core set of genes. When these genes are mutated either singly or in various combinations, a...
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Spring 2016
Equilibrative nucleoside transporter 1 (ENT1) is an ubiquitously expressed membrane transporter in mammalian cells responsible for the transmembrane flux of endogenous nucleosides such as adenosine, as well as chemotherapeutic, anti-viral, and anti-parasitic nucleoside analogues. The present...
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Fall 2012
The kidney anion exchanger 1 (kAE1) is crucial in the regulation of physiological pH by facilitating Cl-/HCO3- exchange. Inability to do so results in distal renal tubular acidosis (dRTA), which is more often due to mutations leading to mis-localization of kAE1, rather than complete abolishment...