RESUMO
This study reported that all three human BolA proteins (hBolA1, hBolA2, and hBolA3) are novel non-classical secreted proteins identified with bioinformatics and molecular biology experiments. The three BolA fusion proteins with c-Myc tag could be secreted into the culture medium of the transfected Cos-7 cells, although they could not be colocalized with Golgi apparatus. And the secretion of three BolA proteins could not be inhibited after BFA treatment. Furthermore, the secretion was not dependent on its predicted signal peptide. All the experiment results suggested that the secretion was a non-classical export. Phylogenetic analysis showed that the human BolAs belong to three different groups with functional divergence of BolA subfamily, where the different helix-turn-helix motif among hBolA1, hBolA2, and hBolA3 could be responsible for their functional divergence. Our data provided a basis for functional studies of BolA protein family.
Assuntos
Variação Genética , Proteínas/metabolismo , Sequência de Aminoácidos , Animais , Células COS , Chlorocebus aethiops , Biologia Computacional , Células Eucarióticas/metabolismo , Evolução Molecular , Humanos , Proteínas Mitocondriais , Dados de Sequência Molecular , Proteínas Mutantes/metabolismo , Filogenia , Sinais Direcionadores de Proteínas , Transporte Proteico , Proteínas/química , Proteínas Recombinantes de Fusão/metabolismo , Frações Subcelulares/metabolismoRESUMO
Here we reported a novel human secreted protein named as hZG16, with a Jacalin domain. Evolution analysis through comparing with the orthologs of other organisms suggested that ZG16 is a conserved gene under the purifying selection (d(N)/d(s)<1) in the evolution. Interestingly, Northern and dot blot analyses showed that hZG16 were highly expressed in adult liver, not in fetal liver, and moderately in gut, including jejunum, ileum, and colon, in which the tissue expression pattern of hZG16 was significantly dissimilar to that of mouse and rat orthologs that were uniquely expressed in spleen and pancreas, respectively. Unexpectedly, hZG16 was markedly down-regulated in hepatocellular carcinoma (HCC) as indicated by RT-PCR, Northern blot analysis and immunohistochemistry staining. However, the tunicamicin treatment and pulse-chase experiments showed that hZG16 protein had a similar molecular function with rZG16 that take part in glycoproteins' secretion in a bus mode.
