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91.
Crott JW Liu Z Keyes MK Choi SW Jang H Moyer MP Mason JB 《The Journal of nutritional biochemistry》2008,19(5):328-335
Folate deficiency may affect gene expression by disrupting DNA methylation patterns or by inducing base substitution, DNA breaks, gene deletions and gene amplification. Changes in expression may explain the inverse relationship observed between folate status and risk of colorectal cancer. Three cell lines derived from the normal human colon, HCEC, NCM356 and NCM460, were grown for 32–34 days in media containing 25, 50, 75 or 150 nM folic acid, and the expression of genes involved in cell-cycle checkpoints, intracellular signaling, folate uptake and cell adhesion and migration was determined. Expression of Folate Receptor 1 was increased with decreasing media folate in all cell lines, as was p53, p21, p16 and β-catenin. With decreasing folate, the expression of both E-cadherin and SMAD-4 was decreased in NCM356. APC was elevated in NCM356 but unchanged in the other lines. No changes in global methylation were detected. A significant increase in p53 exon 7–8 strand breaks was observed with decreasing folate in NCM460 cells. The changes observed are consistent with DNA damage-induced activation of cell-cycle checkpoints and cellular adaptation to folate depletion. Folate-depletion-induced changes in the Wnt/APC pathway as well as in genes involved in cell adhesion, migration and invasion may underlie observed relationships between folate status and cancer risk. 相似文献
92.
Choi IG Shin DH Brandsen J Jancarik J Busso D Yokota H Kim R Kim SH 《Journal of structural and functional genomics》2003,4(1):31-34
Journal of Structural and Functional Genomics - 相似文献
93.
Kalthoum Tizaoui Jae Won Yang Keum Hwa Lee Ji Hong Kim Minseok Kim Sojung Yoon Yeonwoo Jung Joon Beom Park Kitae An Hyeok Choi Donggyu Song HyunTaek Jung Seongmin Ahn Taeho Yuh Hee Min Choi Jae Ha Ahn Younjuong Kim Sanghyun Jee Hyeongsun Lee Soohwa Jin Jun-Gu Kang Bohyun Koo Joo Yeop Lee Kyoung Min Min Wonseok Yoo Hyeong Jun Rhyu Yeonjung Yoon Min Ho Lee Sung Eun Kim Jimin Hwang Ai Koyanagi Louis Jacob Seoyeon Park Jae Il Shin Lee Smith 《International journal of biological sciences》2022,18(9):3731
YKL-40, a chitinase-3-like protein 1 (CHI3L1) or human cartilage glycoprotein 39 (HC gp-39), is expressed and secreted by various cell-types including macrophages, chondrocytes, fibroblast-like synovial cells and vascular smooth muscle cells. Its biological function is not well elucidated, but it is speculated to have some connection with inflammatory reactions and autoimmune diseases. Although having important biological roles in autoimmunity, there were only attempts to elucidate relationships of YKL-40 with a single or couple of diseases in the literature. Therefore, in order to analyze the relationship between YKL-40 and the overall diseases, we reviewed 51 articles that discussed the association of YKL-40 with rheumatoid arthritis, psoriasis, systemic lupus erythematosus, Behçet disease and inflammatory bowel disease. Several studies showed that YKL-40 could be assumed as a marker for disease diagnosis, prognosis, disease activity and severity. It is also shown to be involved in response to disease treatment. However, other studies showed controversial results particularly in the case of Behçet disease activity. Therefore, further studies are needed to elucidate the exact role of YKL-40 in autoimmunity and to investigate its potential in therapeutics. 相似文献
94.
Tae Hyuk Kim Ji Young Joung Mira Kang Sun Kyu Choi Kyunga Kim Ju Young Jang Yoon Young Cho Yong-Ki Min Jae Hoon Chung Sun Wook Kim 《PloS one》2015,10(12)
Background
The independent skeletal effect of thyrotropin (thyroid stimulating hormone, TSH) has been suggested in animal studies. However, clinical data on the association between bone loss and variations in TSH levels is inconsistent. This study aimed to investigate the relationship between TSH levels and bone mineral density (BMD).Methods
We conducted a cross-sectional study with 37,431 subjects (33,052 cases with euthyroidism and 4,379 cases with subclinical thyroid dysfunction) aged over 35 years. We performed thyroid function tests and measured BMD at the lumbar spine, femur neck, and total hip.Results
Levels of TSH and T3 were positively correlated in women (r = 0.076, P = 0.001) and uncorrelated in men. In both men and women, TSH levels correlated positively and T3 levels correlated negatively with BMD at all skeletal sites in age and body mass index adjusted analyses. BMD increased steadily with TSH levels from the subclinical hyperthyroid to subclinical hypothyroid range in subjects with T3 levels in the highest tertile (119.5–200.0 ng/dL), but was no longer significant in subjects with lower plasma T3 levels.Conclusions
The variations in TSH levels within the euthyroid and subclinical range were positively correlated with BMD in healthy men and women. The negative effect of T3 on BMD appears to be compensated for by increased TSH in subjects with plasma T3 levels in the upper normal range. 相似文献95.
Moon Woo Chun Sung Pil Choi Myong Jung Kim Chol Joon Bae Hyung Ryong Moon Hee-Doo Kim 《Nucleosides, nucleotides & nucleic acids》2013,32(4-5):615-616
Abstract Novel 1,3-oxathiolanyl pyrimidine nucleosides with 5-hydroxymethyl substituent were synthesized starting from d-mannose and evaluated for antiviral activities against HIV-1, HSV type 1,2 and HCMV. 相似文献
96.
97.
Samil Jung Davaajargal Myagmarjav Taeyeon Jo Soonduk Lee Songyi Han Nguyen Thi Ngoc Quynh Nguyen Hai Anh Son Hai Vu Yeongseon Choi Myeong-Sok Lee 《International journal of biological sciences》2022,18(9):3859
Chemotherapy has been widely used as a clinical treatment for cancer over the years. However, its effectiveness is limited because of resistance of cancer cells to programmed cell death (PCD) after treatment with anticancer drugs. To elucidate the resistance mechanism, we initially focused on cancer cell-specific mitophagy, an autophagic degradation of damaged mitochondria. This is because mitophagy has been reported to provide cancer cells with high resistance to anticancer drugs. Our data showed that TRIP-Br1 oncoprotein level was greatly increased in the mitochondria of breast cancer cells after treatment with various anticancer drugs including staurosporine (STS), the main focus of this study. STS treatment increased cellular ROS generation in cancer cells, which triggered mitochondrial translocation of TRIP-Br1 from the cytosol via dephosphorylation of TRIP-Br1 by protein phosphatase 2A (PP2A). Up-regulated mitochondrial TRIP-Br1 suppressed cellular ROS levels. In addition, TRIP-Br1 rapidly removed STS-mediated damaged mitochondria by activating mitophagy. It eventually suppressed STS-mediated PCD via degradation of VDACI, TOMM20, and TIMM23 mitochondrial membrane proteins. TRIP-Br1 enhanced mitophagy by increasing expression levels of two crucial lysosomal proteases, cathepsins B and D. In conclusion, TRIP-Br1 can suppress the sensitivity of breast cancer cells to anticancer drugs by activating autophagy/mitophagy, eventually promoting cancer cell survival. 相似文献
98.
The transposons Tn501(Hg) and Tn1721(Tc) are related 总被引:6,自引:0,他引:6
99.