Abstract
Golgi phosphoprotein 2 (GOLPH2, also termed GP73 and GOLM1) is a type II transmembrane protein residing in the cis and medial-Golgi cisternae. GOLPH2 is predominantly expressed in the epithelial cells of many human tissues. Under poorly defined circumstances, GOLPH2 can be cleaved and released to the extracellular space. Despite of its relatively “young age” since the first description in 2000, the physiological and pathological roles of GOLPH2 have been the subject that has attracted considerable amount of attention in recent years. Here, we review the history of GOLPH2’s discovery and the multitude of studies by many groups around the world aimed at understanding its molecular, cellular, physiological, and pathogenic activities in various settings.
Highlights
Golgi phosphoprotein 2 (GOLPH2, termed GP73 and GOLM1) is a type II transmembrane protein residing in the cis and medial-Golgi cisternae
The GOLPH2 gene The 73 kDa protein is coded by the gene GOLM1 located on human chromosome 9q21.33 and was originally cloned by differential screening of a cDNA library derived from liver tissue of a patient with adult giant-cell hepatitis [1], a rare form of hepatitis with suspected viral etiology
The closest human homologue to GOLPH2 is the cancer susceptibility candidate gene 4 (CASC4) protein (Swiss-Prot Q6P4E1), a single-pass type II membrane protein that co-localizes with GOLPH2, the increased expression level of which is associated with HER-2/neu proto-oncogene overexpression [3]
Summary
Golgi phosphoprotein 2 (GOLPH2, termed GP73 and GOLM1) is a type II transmembrane protein residing in the cis and medial-Golgi cisternae. * Correspondence: peng_tao@gibh.ac.cn; xim2002@med.cornell.edu 5State Key Laboratory of Respiratory Disease, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China 1Department of Microbiology and Immunology, 1300 York Avenue, New York, NY 10065, USA Full list of author information is available at the end of the article and contains exons 1, and 3 to 11.
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