• Animal Bioscience
• /
• v.36 no.10
• /
• pp.1584-1595
• /
• 2023

Objective: This study was conducted to evaluate the effect of a low-protein diet on growth performance, carcass traits, nutrient digestibility, blood profiles, and odor emissions in growing-finishing pigs. Methods: A total of 126 crossbred pigs ([Yorkshire×Landrace]×Duroc) with an average body weight (BW) of 38.56±0.53 kg were used for a 14-week feeding trial. Experimental pigs were allotted to one of 6 treatments in 3 replicates of 7 pigs per pen in a randomized complete block design. Pigs were fed each treatment diet with different levels of crude protein (CP). Phase 1 (early growing): 14%, 15%, 16%, 17%, 18%, 19%; phase 2 (late growing): 13%, 14%, 15%, 16%, 17%, 18%; phase 3 (early finishing): 12%, 13%, 14%, 15%, 16%, 17%; phase 4 (late finishing): 11%, 12%, 13%, 14%, 15%, 16%. All experimental diets in each phase were contained the same concentration of lysine (Lys), methionine (Met), threonine (Thr), and tryptophan (Trp). Results: Over the entire experimental period, there was no significant difference in BW, average daily feed intake, and gain-to-feed ratio among all treatments (p>0.05), but a quadratic effect (p = 0.04) was observed in average daily gain (ADG) during the late finishing phase with higher ADG in Group D. Blood urea nitrogen concentration linearly increased with an increase in dietary CP levels (p<0.01). Regarding nutrient digestibility, excreted nitrogen in urine and feces and nitrogen retention linearly increased as the CP level increased (p<0.01). A linear effect was observed with increasing CP levels in amines, ammonia, and hydrogen sulfide in odor emissions (p<0.01). No significant effects were observed in the measurements of carcass traits and meat characteristics (p>0.05). Conclusion: In phase feeding, reducing the CP level to 14% in early-growing pigs, 13% in late-growing pigs, 12% in early-finishing pigs, and 11% in late-finishing pigs is recommended.

• Molecules and Cells
• /
• v.41 no.4
• /
• pp.362-372
• /
• 2018

High mobility group box 2 (HMGB2) is an abundant, chromatin-associated, non-histone protein involved in transcription, chromatin remodeling, and recombination. Recently, the HMGB2 gene was found to be significantly downregulated during senescence and shown to regulate the expression of senescent-associated secretory proteins. Here, we demonstrate that HMGB2 transcription is repressed by p21 during radiation-induced senescence through the ATM-p53-p21 DNA damage signaling cascade. The loss of p21 abolished the downregulation of HMGB2 caused by ionizing radiation, and the conditional induction of p21 was sufficient to repress the transcription of HMGB2. We also showed that the p21 protein binds to the HMGB2 promoter region, leading to sequestration of RNA polymerase and transcription factors E2F1, Sp1, and p300. In contrast, NF-Y, a CCAAT box-binding protein complex, is required for the expression of HMGB2, but NF-Y binding to the HMGB2 promoter was unaffected by either radiation or p21 induction. A proximity ligation assay results confirmed that the chromosome binding of E2F1 and Sp1 was inhibited by p21 induction. As HMGB2 have been shown to regulate premature senescence by IR, targeting the p21-mediated repression of HMGB2 could be a strategy to overcome the detrimental effects of radiation-induced senescence.

• Animal cells and systems
• /
• v.8 no.3
• /
• pp.205-212
• /
• 2004

The tumor suppressor protein p53 is stabilized by the herpes-virus-associated ubiquitin-specific protease (HAUSP), a deubiquitinating enzyme. We previously isolated and characterized a mouse orthologue of HAUSP, mHAUSP. mHAUSP cDNA consisted of 3,312 bp encodes 1,103 amino acids with a molecular weight of approximately 135 kDa containing highly conserved Cys, Asp (I), His, and Asn/Asp (II) domains. In this study, we carried out site-directed mutagenesis of 6 conserved amino acids (Cys224, Gln231, Asp296, His457, His465, and Asp482) in Cys box, QQD box, and His box. Interestingly, the conserved Gln 231 was not essential for the catalytic activity of mHAUSP. However, the other conserved amino acids were required for deubiquitinating activity of mHAUSP. We performed isopeptidase assay and confirmed that mHAUSP is able to remove ubiquitin from ubiquitinated substrates. In addition, we observed that mHAUSP induces apoptosis in HeLa cells.

• Korean Journal of Pharmacognosy
• /
• v.40 no.2
• /
• pp.118-122
• /
• 2009

Methanol extracts of Orostachys japonicus A. Berger (OAB) were found to exhibit apoptosis induction of HL60 human acute promyelocytic leukemia cells. Treatment of OAB exerted strong cytotoxicity against HL60 cells. OAB induced DNA fragmentation of HL60 cells in a dose dependent manner. Nitric oxide production were also increased in OAB-treated RAW264.7 macrophage cell lines. Treatment of OAB increased the expression of p53 and iNOS gene and the expression of p53, $NF-{\kappa}B$ and iNOS protein in cultured HL60 and RAW264.7 cells. These results suggest that OAB are effective on strong anti-cancer properties and can be useful as a chemo-preventive agents.

• The Journal of the Korean bone and joint tumor society
• /
• v.20 no.2
• /
• pp.99-103
• /
• 2014

Li-Fraumeni syndrome (LFS) is an autosomal dominant hereditary disorder characterised by a variety of different tumor types in children and young adults. That contains with a germline mutation in the tumor suppressor gene Tumor Protein p53 (TP53). That is extremely rare. Furthermore, this is sometimes overlooked. Here, we report a case of LFS which was confirmed by mutational analysis of the p53 gene. Also, literature review is intended to improve understanding of this disease entity.

• Proceedings of the Korean Society of Life Science Conference
• /
• 2003.05a
• /
• pp.143-143
• /
• 2003

• Proceedings of the Korean Society of Life Science Conference
• /
• 2001.09a
• /
• pp.106-106
• /
• 2001

• YAKHAK HOEJI
• /
• v.46 no.1
• /
• pp.18-23
• /
• 2002

Ailanthus altissima has been used to settle an upset stomach, to alleviate a fever and as an insecticide. We reported that the water extract of A. altissima induced apoptotic cell death in Jurkat T-acute Iymphoblastic leukemia cells. Here, we showed the dose-dependent inhibitions of cell viability by the extract, as measured by cell morphology. The cell cycle control genes are considered to play important roles in tumorigenesis. The purpose of the present study is also to investigate the effect of A. altissima on cell cycle progression and its molecular mechanism in the cells. The level of p21 protein was increased after treatment of the extract, whereas both Bcl-2 and Bax protein levels were not changed. These results suggest that A. altissima induces apoptotic cell death via p21-dependent signaling pathway in Jurkat cells which delete wild type p53. Gl checkpoint related gene products tested (cyclin D3, cyclin dependent kinase 4, retinoblastoma, E2Fl) were decreased in their protein levels in a dose-dependent manner after treatment of the extract Taken together, these results indicate that the increase of apoptotic cell death by A. altissima may be due to the inhibition of cell cycle in Jurkat cells.

• Journal of Ginseng Research
• /
• v.23 no.3 s.55
• /
• pp.190-197
• /
• 1999

In this study, the molecular mechanism of the growth inhibitory effect of panaxynol was investigated in a human malignant melanoma cell line, SK-MEL-l. In the cell cycle analysis, panaxynol arrested cell cycle progression of SK-MEL-I at the G1 phase. Immunoblot analysis demonstrated that panaxynol increased $p21^{WAF1}$ and decreased cdc2 expression. Protein levels of pl6, p27, E2F-1, Rb, and p53 were not changed. Thus, the changes in expression levels of $p21^{WAF1}$ and cdc2 apparently mediate the cell cycle arrest caused by panaxynol. In addition, cycloheximide (CHX) partially reversed the growth inhibition by panaxynol, which suggested that new protein synthesis was required. On the other hand, LLnL, a proteasome inhibitor, increased antiproliferative effect of panaxynol. This may be due to stabilization of the protein(s) responsible for the growth inhibition such as $p21^{WAF1}$. In summary, these results demonstrate that panaxynol inhibits proliferation of SK-MEL-I by inducing cell cycle arrest at the G1 phase and the inhibitory effect is mediated by the increased level of $p21^{WAF1}$ as well as decreased cdc2 expression.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.17 no.1
• /
• pp.213-219
• /
• 2003

We investigated the effects of Insamsapye-tang (ISSPT) water extract on the cell proliferation of human lung carcinoma A549 cells. ISSPT treatment resulted in the inhibition of cell proliferation in a concentration-dependent manner. This anti-proliferative effect of A549 cells by ISSSPT treatment was associated with morphological changes such as membrane shrinking and cell rounding up. DNA flow cytometric histograms showed that population of G1 phase of the cell cycle was increased by ISSPT treatment in a concentration-dependent manner. ISSPT treatment induced the levels of tumor suppressor p53 protein and cyclin-dependent kinase (Cdk) inhibitor p27 without significant alteration of cyclins and Cdks expression. In addition, ISSPT treatment resulted in down-regulation of phosphorylated retinoblastoma protein (pRB). However, the levels of p130, the pRB family protein, and transcription factors. E2F-1 and E2F-4. were remained unchanged. The present results indicated that ISSPT-induced inhibition of lung cancer cell proliferation is associated with the blockage of G1/S progression and the induction of apoptosis, and we suggest that ISSPT will be an effective therapeutic agent on human lung cancer.