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Characterization of a variant of ERGIC2 protein
Author(s) -
Kwok Simon Chun Man,
Kumar Sudhanshu,
Dai Guoli
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.784.6
Subject(s) - biology , endoplasmic reticulum , transfection , wild type , microbiology and biotechnology , fusion protein , golgi apparatus , signal transduction , complementary dna , gene , cell growth , genetics , mutant , recombinant dna
ERGIC2 is a gene identified in our laboratory as a potential tumor suppressor. Because of its high sequence homology with the yeast chaperone protein, Erv41p, it was suggested that ERGIC2 protein may be involved in protein trafficking between endoplasmic reticulum (ER) and cis‐Golgi. However, over‐expression of ERGIC2 in prostate cancer cell line, PC‐3 cells, induced cell growth arrest and senescence, suppressed colony formation in soft agar, and decreased invasive potential in invasive chamber assay. Therefore, ERGIC2 protein may also be involved in yet unknown signal transduction pathways. Recently, we isolated a cDNA encoding a variant of ERGIC2 that has a 4‐base deletion after codon #189. As a result of this frame‐shift mutation, a truncated protein of 215 residues is predicted as compared to the 377‐residue wild‐type protein. This effectively abrogates its function as ER‐Golgi transport shuttle. The objective of this study is to investigate the functions of this ERGIC2‐variant. Expression construct of the ERGIC2‐variant was transiently transfected into PC‐3 cells, and its effect on cell growth was studied. A protein with a size distinct from wild‐type ERGIC2 was detected by Western blot. However, when the cells were selected for stable expression, complete loss of the fusion‐protein was resulted, suggesting that the variant can also arrest cell growth as the wild‐type ERGIC2.