• Journal of Life Science
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• v.21 no.4
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• pp.613-615
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• 2011

ERp29 is a endoplasmic reticulum (ER) lumenal resident protein that shows sequence similarity to the protein disulfide isomerase family. Its biological function is thought to play a role in the processing of secretory proteins within the ER, possibly by participating in the folding of proteins in the ER. Although some data on ERp29 have been reported, its normal functions are still unclear. To gain insights into the function of ERp29, we identified ARF5 protein as a protein that interacts with ERp29 using yeast two-hybrid screening and GST pull-down assay. Interaction between ERp29 and ARF5 was detected under normal cell conditions but not under ER stress conditions. This result may provide a clue for understanding ERp29 biological functions.

• Journal of Life Science
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• v.10 no.2
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• pp.150-156
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• 2000

This experiment was performed to evaluate the effect of TSH (thyroid-stimulating) on the ERp29 (endoplasmic reticulum resident 29 kDa protein) gene expression in the rat thyrocytes of FRTL-5 cells. Although ERp29 mRNA was constantly expressed, its expression began to increase remarkably from 10-9 M TSH. and its maximum expression was at 5×10-9 M TSH (about 3.5 fold). On the other hand, the effect of TSH on the abundance of ERp29 mRNA started within 6 h, and peaked at 8 h (about 2.5 fold). Actinomycin D (transcription inhibitor) strongly blocked this effect while cycloheximide (translation inhibitor) did not. The half-life of ERp29 mRNA was about 4.5 h in the presence or absence of TSH that was not affected by the stability of ERp29 mRNA. The effect of TSH on the ERp29 gene expression was specific, while other growth factors (transfferin, insulin, and hydrocortisone) did not alter its expression. Our data indicate for the first time that the expression of ERp29 is regulated transcriptionally by TSH in the thyrocytes.

• Journal of Life Science
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• v.31 no.6
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• pp.568-573
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• 2021

This study identified genomic factors associated with endoplasmic reticulum protein (ERp)29 gene expression in a genome-wide association study (GWAS) of genetic variants, including single-nucleotide polymorphisms (SNPs). In total, 373 European genes from the 1000 Genomes Project were analyzed. SNPs with an allelic frequency of less than or more than 5% were removed, resulting in 5,913,563 SNPs including in the analysis. The following expression quantitative trait loci (eQTL) from the long noncoding RNA LOC105372577 were strongly associated with ERp29 expression: rs6138266 (p<4.172e10), rs62193420 (p<1.173e10), and rs6138267 (p<2.041e10). These were strongly expressed in the testis and in the brain. The three eQTL were identified through a transcriptome-wide association study (TWAS) and showed a significant association with ERp29 and osteosarcoma amplified 9 (OS9) expression. Upstream sequences of rs6138266 were recognized by ChIP-seq data, while HaploReg was used to demonstrate how its regulatory DNA binds upstream of transcription factor 1 (USF1). There were no changes in the expression of OS9 or USF1 following ER stress.

• Journal of Life Science
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• v.20 no.12
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• pp.1820-1828
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• 2010

Cobalt(II) chloride, a chemical compound with the formula$CoCl_2$, has been widely used in the treatment of anemia, as a chemical agent for the induction of hypoxia in cell cultures, and is known to activate hypoxic signaling. However, excessive exposure to cobalt is associated with several clinical conditions, including asthma, pneumonia, and hematological abnormalities, and can lead to tissue and cellular toxicity. It is also known to induce apoptosis. One of the questions was that of whether $CoCl_2$ might induce apoptosis via endoplasmic reticulum (ER) stress in neurons. To address this question, first, the level of DNA fragmentation was measured for assay of apoptotic rates using $CoCl_2$ with neuron PC12 cells. After confirmation of apoptosis inductions, under the same conditions, the expression levels of ER stress associated factors [ER chaperones Bip, calnexin, ERp72, ERp29, PDI, and ER membrane kinases (IRE1, ATF6, PERK)] were examined by RT-PCR and Western blotting. These results indicated that apoptosis is induced through activation of ER membrane kinases via ER stress. In conclusion, during induction of apoptosis through $CoCl_2$-induced hypoxia in neuron PC12 cells, ER membrane kinase of IRE1 was dominantly up-expressed, and, consecutively, TRAF2, which has been suggested to be one of the links connecting apoptosis and ER stress, was strongly up-expressed.