Publications (13)31.59 Total impact
-
Article: Breast cancer metastasis suppressor 1 (BRMS1) is destabilized by the Cul3-SPOP E3 ubiquitin ligase complex.
[show abstract] [hide abstract]
ABSTRACT: Breast cancer metastasis suppressor 1 (BRMS1) suppresses metastasis without affecting primary tumorigenesis. The regulatory mechanism of BRMS1 at the protein level has not been revealed until recently. Here, we found that cullin 3 (Cul3), a component of E3 ubiquitin ligase, is a new binding partner of BRMS1 and the interaction between BRMS1 and Cul3 is mediated by the SPOP adaptor protein. Intriguingly, BRMS1 turns out to be a potent substrate that is ubiquitinated by the Cul3-SPOP complex. Knockdown of SPOP increases the level of BRMS1 protein and represses the expression of BRMS1 repressive target genes such as OPN and uPA in breast cancer cells. These results suggest that the novel regulatory mechanism of BRMS1 by Cul3-SPOP complex is important for breast cancer progression.Biochemical and Biophysical Research Communications 11/2011; 415(4):720-6. · 2.48 Impact Factor -
Article: Highly selectively monitoring heavy and transition metal ions by a fluorescent sensor based on dipeptide.
[show abstract] [hide abstract]
ABSTRACT: Fluorescent sensor (DMH) based on dipeptide was efficiently synthesized in solid phase synthesis. The dipeptide sensor shows sensitive response to Ag(I), Hg(II), and Cu(II) among 14 metal ions in 100% aqueous solution. The fluorescent sensor differentiates three heavy metal ions by response type; turn on response to Ag(I), ratiometric response to Hg(II), and turn off detection of Cu(II). The detection limits of the sensor for Ag(I) and Cu(II) were much lower than the EPA's drinking water maximum contaminant levels (MCL). Specially, DMH penetrated live cells and detected intracellular Ag(+) by turn on response. We described the fluorescent change, binding affinity, detection limit for the metal ions. The study of a heavy metal-responsive sensor based on dipeptide demonstrates its potential utility in the environment field.Talanta 09/2011; 85(3):1566-74. · 3.79 Impact Factor -
Article: UCH-L1 promotes cancer metastasis in prostate cancer cells through EMT induction.
[show abstract] [hide abstract]
ABSTRACT: Ubiquitin C-terminal hydrolse-L1 (UCH-L1) is a deubiquitinating enzyme (DUB) that cleaves the ubiquitin (ub) moiety from ub precursors or protein substrates. The correlation between UCH-L1 and cancer has been reported in various tissues, but the role of UCH-L1 in prostate cancer has not been thoroughly researched. Here we found that UCH-L1 is specifically highly expressed in the metastatic DU145 prostate cancer cell line, but not in the benign or weakly metastatic prostate cancer cells. To determine the role of UCH-L1 in prostate cancer metastasis, we constructed UCH-L1-knockdown DU145 and UCH-L1 or the active site mutant form of UCH-L1 (UCH-L1 C90S) expressing RWPE1 stable cells. Notably, the expression of UCH-L1 in RWPE1 cells promotes epithelial-to-mesenchymal transition (EMT), and this is an important process for cancer cell invasion and metastasis. On the contrary, knockdown of UCH-L1 in DU145 cells induces MET, the reverse program of EMT. Furthermore, the change of EMT status caused by altering the UCH-L1 level affects the migration and invasiveness of prostate cancer cells. Our results indicate that UCH-L1 promotes prostate cancer metastasis through EMT induction and UCH-L1 could be a novel diagnostic and therapeutic target for prostate cancer treatment.Cancer letters 03/2011; 302(2):128-35. · 4.86 Impact Factor -
Article: Different antiulcer activities of pantoprazole in stress, alcohol and pylorus ligation-induced ulcer models.
[show abstract] [hide abstract]
ABSTRACT: Antiulcer effects of pantoprazole, a proton-pump inhibitor, on water-immersion restraint stress (WIRS)-, alcohol (ethanol)- and pylorus ligation-induced gastric ulcers were investigated in male rats. Rats were orally administered with pantoprazole 30 min prior to exposure to various types of ulcer inducers. In stress-induced ulcer model, rats were subjected to WIRS at 22℃ for 4 hours, and the degree of ulcer (in mm) was evaluated. In alcohol-induced ulcer model, rats were orally administered with pure (100%) ethanol (1 mL/kg), and the ulcer lesions were measured 1 hour after ethanol challenge. In pylorus ligation-induced ulcer model, rats were subjected to pylorus ligation, and the degree of erosions and ulcers was scored 17 hours after the operation. Pantoprazole attenuated the ulcer lesions induced by WIRS in a dose-dependent manner, exhibiting a median effective dose (ED(50)) value of 0.78 mg/kg. By comparison, pantoprazole was effective at relatively-high doses for the improvement of ethanol-induced ulcers, showing an ED(50) value of 20.5 mg/kg. Notably, pantoprazole was practically ineffective (ED(50)>50.0) in pylorus ligation model. Taken together, it was confirmed that pantoprazole showed inhibitory activity on gastric ulcers induced by stress and alcohol, but was ineffective on pylorus ligation-induced ulcer. Therefore, the results indicate that proton-pump inhibitors including pantoprazole might reveal highly-different effects according to the type of ulcer inducers, and that the prescription of antiulcer agents should be carefully selected.Laboratory animal research. 03/2011; 27(1):47-52. -
Article: Anti-inflammatory effects of a Houttuynia cordata supercritical extract.
[show abstract] [hide abstract]
ABSTRACT: Anti-inflammatory effects of Houttuynia cordata supercritical extract (HSE) were investigated in a carrageenan-air pouch model. HSE (200 mg/kg, oral) suppressed exudation and albumin leakage, as well as inflammatory cell infiltration. Dexamethasone (2 mg/kg, i.p.) only decreased exudation and cell infiltration, while indomethacin (2 mg/kg, i.p.) reduced exudate volume and albumin content. HSE lowered tumor-necrosis factor (TNF)-alpha and nitric oxide (NO), as well as prostaglandin E(2) (PGE(2)). Dexamethasone only reduced TNF-alpha and NO, while indomethacin decreased TNF-alpha and PGE(2). The suppressive activity of HSE on NO and PGE(2) production was confirmed in RAW 264.7. These results demonstrate that HSE exerts anti-inflammatory effects by inhibiting both TNF-alpha-NO and cyclooxygenase II-PGE(2) pathways.Journal of veterinary science (Suwŏn-si, Korea) 09/2010; 11(3):273-5. · 0.89 Impact Factor -
Article: Comparative antihypertensive activities of losartan and HM70186 in rats with hepatic dysfunction.
[show abstract] [hide abstract]
ABSTRACT: HM70186, a medoxomil ester of EXP3174 which is an active metabolite of angiotensin II receptor blocker losartan, was synthesized, and its antihypertensive efficacy was evaluated in rats with hepatic dysfunction. Male Wistar rats were intraperitoneally injected with 0.5 mL/kg of carbon tetrachloride to cause hepatic injury, and implanted with an osmotic minipump containing angiotensin II (0.4 mg/kg/day) to induce hypertension. After confirmation of both hepatic damage and hypertension, the rats were orally administered losartan or HM70186, and then blood pressure and heart rate were monitored for 24 h. In normal animals, angiotensin II-induced hypertension was lowered by losartan, resulting in an ED(-30 mmHg) of 9.05 mg/kg. HM70186 also immediately decreased the blood pressure in a dose-dependent manner, exhibiting an ED(-30 mmHg) of 0.89 ng/kg (10,000 times the potency observed with losartan). Moreover, HM70186 (3 ng/kg) exerted a strong antihypertensive effect even in rats with hepatic injury, while losartan (10 microg/kg) was ineffective. These results suggest that HM70186 could be a promising candidate for the treatment of hypertension accompanied by hepatic dysfunction.Archives of Pharmacal Research 08/2009; 32(7):1005-11. · 1.59 Impact Factor -
Article: Green tea extract increases cyclophosphamide-induced teratogenesis by modulating the expression of cytochrome P-450 mRNA.
[show abstract] [hide abstract]
ABSTRACT: The effects of green tea extract (GTE) on the fetal development and external, visceral and skeletal abnormalities induced by cyclophosphamide were investigated in rats. Pregnant rats were daily administered GTE (100mg/kg) by gavage for 7 d, from the 6th to 12th day of gestation, and intraperitoneally administered with cyclophosphamide (11mg/kg) 1h after the final treatment. On the 20th day of gestation, maternal and fetal abnormalities were determined by Cesarian section. Cyclophosphamide was found to reduce fetal and placental weights without increasing resorption or death. In addition, it induced malformations in live fetuses; 94.6%, 41.5% and 100% of the external (skull and limb defects), visceral (cleft palate and ureteric dilatation) and skeletal (acrania, vertebral/costal malformations and delayed ossification) abnormalities. When pre-treated with GTE, cyclophosphamide-induced body weight loss and abnormalities of fetuses were remarkably aggravated. Moreover, repeated treatment with GTE greatly increased mRNA expression and activity of hepatic cytochrome P-450 (CYP) 2B, which metabolizes cyclophosphamide into teratogenic acrolein and cytotoxic phosphoramide mustard, while reducing CYP3A expression (a detoxifying enzyme). The results suggest that repeated intake of GTE may aggravate cyclophosphamide-induced body weight loss and malformations of fetuses by modulating CYP2B and CYP3A.Reproductive Toxicology 01/2009; 27(1):79-84. · 3.23 Impact Factor -
Article: trans-Resveratrol relaxes the corpus cavernosum ex vivo and enhances testosterone levels and sperm quality in vivo.
[show abstract] [hide abstract]
ABSTRACT: We examined the effects of trans-resveratrol on male reproductive functions; ex-vivo penile erection and in-vivo sperm counts and quality. For the ex-vivo study, the relaxation effects of resveratrol on isolated New Zealand white rabbit corpus cavernosum, precontracted by phenylephrine (5x10(-5) M) were measured. The in-vivo study measured reproductive organ weights, blood testosterone levels, testicular histopathology, sperm counts, as well as the epididymal sperm motility and deformity of male ICR mice given an oral dose of resveratrol (50 mg/ kg) for 28 days. Resveratrol elicited a concentration-dependent relaxing effect on corpus cavernosum, leading to a median effective concentration (EC50) of 0.29 mg/mL. Repeated treatment with resveratrol (50 mg/kg) did not cause an increase in body weight, reproductive organ weight or testicular microscopic findings; however, resveratrol did elicit an increase in blood testosterone concentration, testicular sperm counts and epididymal sperm motility by 51.6%, 15.8% and 23.3%, respectively, without influence on sperm deformity. In conclusion, we propose that resveratrol has a positive effect on male reproductive function by triggering a penile erection, as well as enhancing blood testosterone levels, testicular sperm counts, and epididymal sperm motility.Archives of Pharmacal Research 02/2008; 31(1):83-7. · 1.59 Impact Factor -
Article: PURIFICATION AND CHARACTERIZATION OF A CATALASE FROM THE LIVER OF BULLFROG, RANA CATESBEIANA SHAW
[show abstract] [hide abstract]
ABSTRACT: ABSTRACTA catalase was purified from the liver of bullfrog, Rana catesbeiana Shaw, after extraction, ammonium sulfate precipitations, DEAE-Sephadex A-50 chromatography, gel filtration chromatography on a Sephadex G-150 column, ion exchange chromatography on a DEAE-Sephacel column and Sephacryl S-300 column. The yield and purification from the starting crude extract were 0.25% and 73.57-fold, respectively. The purified catalase with an apparent molecular mass of 186 kDa was shown to be composed of four identical subunits of apparent molecular mass of 47.7 kDa. The purified catalase is active over a broad pH range of 6.0–10.0, and it has an isoelectric point of 6.3. The enzyme showed a Kmfor H2O2of 20 mM and an apparent Vmaxof 51.91 U/mg, and its maximum absorption was at 408 nm in the visible portion of the spectrum. In addition, the purified enzyme was markedly inhibited by azide, cyanide and hydroxylamine.Journal of Food Biochemistry 03/2005; 28(6):435 - 448. · 0.81 Impact Factor -
Article: Differential expression of dendritic cell markers by all-trans retinoic acid on human acute promyelocytic leukemic cell line.
[show abstract] [hide abstract]
ABSTRACT: Dendritic cells (DCs) are the most potent antigen-presenting cells (APCs) for naive T cells and play an important role in cancer immunology. All-trans retinoic acid (ATRA) is known to be a differentiating agent in the treatment of acute promyelocytic leukemia (APL). In this study, we investigated whether ATRA can differentiate the retinoic acid (RA)-sensitive promyelocytic leukemic cell line, NB4, to DC-like cells and whether these differentiated cells can activate T cells. NB4 cells were differentiated to myeloid cells by 4, 6, and 8 days of ATRA treatment. NB4 cells up-regulated markers found in DCs, including HLA-DR, costimulatory molecules (CD80 and CD86), adhesion molecules (CD40), and chemokine receptors (CCR6) when cultured for 8 days in the presence of 1 microM ATRA. Upregulation of CD83 was also detected on the surface of ATRA-treated NB4 cells versus untreated cells. The addition of cytokines alone, such as GM-CSF or CD40 ligand, did not affect the expression of CD83 in untreated NB4 cells but they up-regulated CD83 in ATRA-treated cells. CD11b was coexpressed with CD80, CD83, and CD86 in ATRA-treated NB4 cells. In a functional assay, ATRA-treated NB4 cells stimulated T cell proliferation when challenged with Staphylococcus enterotoxin B. These results suggest that the differentiation of NB4 cells by ATRA causes the cells to express DC markers, and that ATRA-differentiated NB4 cells are able to present antigens to T cells.International Immunopharmacology 01/2005; 4(13):1587-601. · 2.38 Impact Factor -
Article: Phosphatidic acid and tumor necrosis factor-alpha induce the expression of CD83 through mitogen activated protein kinase pathway in a CD34+ hematopoietic progenitor cell line, KG1.
[show abstract] [hide abstract]
ABSTRACT: To elucidate the signaling pathways involved in the expression of CD83, which is linked to the differentiation and maturation states of dendritic cells, we examined the effect of phosphatidic acid (PA) on the expression of CD83 in KG1, a CD34(+) hematopoietic progenitor cell. In the presence of tumor necrosis factor (TNF)-alpha, PA but not lyso-PA up-regulated CD83 on KG1 cells. Moreover, PA and TNF-alpha-induced expression of CD83 was slightly increased by propranolol, an inhibitor of PA phosphohydrolase but was unaffected by phospholipase A2 inhibitor. PA and TNF-alpha increased the phosphorylation of extracellular signal-regulated kinase (ERK)-1/2, p38-kinase, and c-Jun N-terminal kinase (JNK) by Western blotting. However, the up-regulation of CD83 by PA/TNF-alpha on KG1 was significantly abrogated by PD98059, a specific inhibitor of ERK kinase, but was enhanced by SP600125, a JNK inhibitor. Bis-indolylmaleimide, an inhibitor of protein kinase C, partially blocked the up-regulation of CD83 and ERK phosphorylation induced by PA and TNF-alpha. Moreover, the incubation of KG1 cells with phorbol ester and TNF-alpha for 5 days increased the protein level of phospholipase D. These results suggest that PA and TNF-alpha induce the up-regulation of CD83 and that their action is regulated by ERK and JNK.International Immunopharmacology 01/2005; 4(13):1603-13. · 2.38 Impact Factor -
Article: Anti-apoptotic mechanism and reduced expression of phospholipase D in spontaneous and Fas-stimulated apoptosis of human neutrophils.
[show abstract] [hide abstract]
ABSTRACT: Neutrophil apoptosis is a constitutive process that can be enhanced or delayed by signals triggered by various stimuli. In this work, we investigated the action mechanism of phospholipase D (PLD) and its expression in the inhibition of spontaneous and Fas-mediated apoptosis. Anti-Fas antibody-stimulated apoptosis of neutrophils was significantly blocked by the exogenous addition of bacterial PLD from Streptomyces chromofuscus (scPLD), and neutrophils cultured for 24 h in the presence of anti-Fas antibody showed lower agonist-stimulated PLD activity compared to untreated cells. The amount of PLD1a protein reduced time-dependently in cultured neutrophils, but was recovered by treating with LPS or GM-CSF. The reduction in PLD1a protein level was blocked by caspase inhibitors. The exogenous addition of scPLD blocked the up-regulation of Fas-associated death domain expression, mitochondrial permeability, and the cleavages of procaspase-8, procaspase-3, and protein kinase C-delta. We also found that the protein level of apoptosis-inducing factor was increased in cultured neutrophils but its expression was reduced by scPLD. However, sulfasalazine-induced apoptosis and change of protein expression were not blocked by scPLD. Taken together, the activity and protein levels of PLD play a role as an anti-apoptotic factor by acting at multiple levels of the apoptotic cascade in neutrophils.European Journal of Immunology 11/2004; 34(10):2760-70. · 5.10 Impact Factor -
Article: Phosphorylation of phospholipase D1 and the modulation of its interaction with RhoA by cAMP-dependent protein kinase.
[show abstract] [hide abstract]
ABSTRACT: Agents that elevate cellular cAMP are known to inhibit the activation of phospholipase D (PLD). We investigated whether PLD can be phosphorylated by cAMP-dependent protein kinase (PKA) and PKA-mediated phosphorylation affects the interaction between PLD and RhoA, a membrane regulator of PLD. PLD1, but not PLD2 was found to be phosphorylated in vivo by the treatment of dibutyryl cAMP (dbcAMP) and in vitro by PKA. PKA inhibitor (KT5720) abolished the dbcAMP-induced phosphorylation of PLD1, but dibutyryl cGMP (dbcGMP) failed to phosphorylate PLD1. The association between PLD1 and Val14RhoA in an immunoprecipitation assay was abolished by both dbcAMP and dbcGMP. Moreover, RhoA but not PLD1 was dissociated from the membrane to the cytosolic fraction in dbcAMP-treated cells. These results suggest that both PLD1 and RhoA are phosphorylated by PKA and the interaction between PLD1 and RhoA is inhibited by the phosphorylation of RhoA rather than by the phosphorylation of PLD1.Experimental and Molecular Medicine 05/2004; 36(2):172-8. · 2.48 Impact Factor
Top co-authors
Top Journals
Institutions
-
2011
-
Inha University
- Department of Biological Sciences
Seoul, Seoul, South Korea
-
-
2008–2011
-
Chungbuk National University
- College of Veterinary Medicine
Tyundyu, North Chungcheong, South Korea
-
-
2005
-
Pukyong National University
- Department of Chemistry
Pusan, Busan, South Korea
-
-
2004–2005
-
Dong-A University
Pusan, Busan, South Korea
-
