“…Giantin knock-out or mutant animal models have revealed the cell-type specific function of Giantin (Katayama et al, 2011, 2018; Lan et al, 2016; Bergen et al, 2017; McGee et al, 2017; Stevenson et al, 2017). Moreover, Giantin gene mutations and pathogenic changes in Giantin levels have been reported in various diseases, including sickle cell disease (Alsultan et al, 2018; Amlie-Lefond et al, 2018), bipolar disorder (Kerner et al, 2013), hepatocellular carcinoma (Choi et al, 2017), leukemia (Troadec et al, 2017), pulmonary disease (Raparelli et al, 2018), and post-alcohol recovery (Casey et al, 2018). These various phenotypes might be caused by the expression of Giantin binding partners, including GCP60 (Sohda et al, 2001), RCAN2 (Stevenson et al, 2018), PRMT5 (Sohail et al, 2015), PLK3 (Ruan et al, 2004), Rab6, p115, and Rab1 (Beard et al, 2005).…”