Park SW

References (15)

Title : Evaluation of the clinical usefulness of pancreatic alpha amylase as a novel biomarker in dogs with acute pancreatitis: a pilot study - Kim_2024_Vet.Q_44_1
Author(s) : Kim K , Kim HH , Joo JB , Kim OK , Park SW , Suh GH , Ro WB , Lee CM
Ref : Vet Q , 44 :1 , 2024
Abstract : Pancreatic alpha amylase (P-AMY) is used as a biomarker of acute pancreatitis (AP) in human medicine. To our knowledge, there are no studies evaluating the usefulness of P-AMY in dogs with AP. In this study, we evaluated the diagnostic value of P-AMY, currently not verified in veterinary medicine. The AP group (n = 40) consisted of dogs with AP diagnosed using clinical signs and laboratory examinations, including abnormal canine pancreatic lipase (cPL) concentration, and compatible abdominal ultrasound examination at first presentation. Evaluation of the canine AP severity (CAPS) score was performed. The control group (n = 38) was composed of normal dogs without any abnormalities in clinical findings, blood exams or diagnostic imaging. The correlation of P-AMY with cPL was confirmed by Pearson's correlation analysis (r = 0.564, p < .001). The sensitivity and specificity for the most appropriate cut-off values of P-AMY were recorded similar to the values of DGGR. The dogs with AP and CAPS <=11 had significantly higher serum P-AMY (p = .016) contrary to DGGR lipase and cPL. Furthermore, there was a significant difference in the median P-AMY dependent on the presence of systemic inflammatory response syndrome (p = .001). P-AMY showed similar level of diagnostic accuracy along with sensitivity and specificity compared to DGGR lipase. In addition, P-AMY showed a significant association with CAPS score, contrary to cPL and DGGR lipase. Along with other biomarkers associated with AP, P-AMY has the potential of usefulness as a supportive diagnostic and prognostic biomarker of AP in dogs.
ESTHER : Kim_2024_Vet.Q_44_1
PubMedSearch : Kim_2024_Vet.Q_44_1
PubMedID: 38497337

Title : Analysis of treatment pattern of anti-dementia medications in newly diagnosed Alzheimer's dementia using OMOP CDM - Byun_2022_Sci.Rep_12_4451
Author(s) : Byun J , Lee DY , Jeong CW , Kim Y , Rhee HY , Moon KW , Heo J , Hong Y , Kim WJ , Nam SJ , Choi HS , Park JI , Chun IK , Bak SH , Lee K , Byeon GH , Kim KL , Kim JA , Park YJ , Kim JH , Lee EJ , Lee SA , Kwon SO , Park SW , Kasani PH , Kim JK , Kim S , Jang JW
Ref : Sci Rep , 12 :4451 , 2022
Abstract : Anti-dementia medications are widely prescribed to patients with Alzheimer's dementia (AD) in South Korea. This study investigated the pattern of medical management in newly diagnosed patients with AD using a standardized data format-the Observational Medical Outcome Partnership Common Data Model from five hospitals. We examined the anti-dementia treatment patterns from datasets that comprise > 5 million patients during 2009-2019. The medication utility information was analyzed with respect to treatment trends and persistence across 11 years. Among the 8653 patients with newly diagnosed AD, donepezil was the most commonly prescribed anti-dementia medication (4218; 48.75%), followed by memantine (1565; 18.09%), rivastigmine (1777; 8.98%), and galantamine (494; 5.71%). The rising prescription trend during observation period was found only with donepezil. The treatment pathways for the three cholinesterase inhibitors combined with N-methyl-D-aspartate receptor antagonist were different according to the drugs (19.6%; donepezil; 28.1%; rivastigmine, and 17.2%; galantamine). A 12-month persistence analysis showed values of approximately 50% for donepezil and memantine and approximately 40% for rivastigmine and galantamine. There were differences in the prescribing pattern and persistence among anti-dementia medications from database using the Observational Medical Outcome Partnership Common Data Model on the Federated E-health Big Data for Evidence Renovation Network platform in Korea.
ESTHER : Byun_2022_Sci.Rep_12_4451
PubMedSearch : Byun_2022_Sci.Rep_12_4451
PubMedID: 35292697

Title : Acetylcholinesterase activity in the brain of wild birds in Korea-2014 to 2016 - Bang_2019_J.Vet.Sci_20_e9
Author(s) : Bang JH , Ku HO , Kang HG , Kim H , Kim S , Park SW , Kim YS , Jang I , Bae YC , Woo GH , Yi H
Ref : J Vet Sci , 20 :e9 , 2019
Abstract : Acetylcholinesterase (AChE) activity level can be used as a diagnostic marker for anticholinesterase pesticide poisoning. In this study, we aimed to establish a baseline level of normal brain AChE activity in wild birds. AChE activity was measured in the brains of 87dead wild birds (26 species). The level of AChE activity ranged from 6.40 to 15.9 micromol/min/g of brain tissue in normal wild birds. However, the brain tissue AChE activity level in wild birds exposed to organophosphate (OP) pesticide was 48.0%-96.3% of that in the normal birds. These results may serve as reference values to facilitate routine diagnosis and monitoring of OP-poisoned wild birds.
ESTHER : Bang_2019_J.Vet.Sci_20_e9
PubMedSearch : Bang_2019_J.Vet.Sci_20_e9
PubMedID: 30944532

Title : Sequential Emergence and Wide Spread of Neutralization Escape Middle East Respiratory Syndrome Coronavirus Mutants, South Korea, 2015 - Kim_2019_Emerg.Infect.Dis_25_1161
Author(s) : Kim YS , Aigerim A , Park U , Kim Y , Rhee JY , Choi JP , Park WB , Park SW , Lim DG , Inn KS , Hwang ES , Choi MS , Shin HS , Cho NH
Ref : Emerg Infect Dis , 25 :1161 , 2019
Abstract : The unexpectedly large outbreak of Middle East respiratory syndrome in South Korea in 2015 was initiated by an infected traveler and amplified by several "superspreading" events. Previously, we reported the emergence and spread of mutant Middle East respiratory syndrome coronavirus bearing spike mutations (I529T or D510G) with reduced affinity to human receptor CD26 during the outbreak. To assess the potential association of spike mutations with superspreading events, we collected virus genetic information reported during the outbreak and systemically analyzed the relationship of spike sequences and epidemiology. We found sequential emergence of the spike mutations in 2 superspreaders. In vivo virulence of the mutant viruses seems to decline in human patients, as assessed by fever duration in affected persons. In addition, neutralizing activity against these 2 mutant viruses in serum samples from mice immunized with wild-type spike antigen were gradually reduced, suggesting emergence and wide spread of neutralization escapers during the outbreak.
ESTHER : Kim_2019_Emerg.Infect.Dis_25_1161
PubMedSearch : Kim_2019_Emerg.Infect.Dis_25_1161
PubMedID: 30900977

Title : Efficacy and safety of evogliptin monotherapy in patients with type 2 diabetes and moderately elevated glycated haemoglobin levels after diet and exercise - Park_2017_Diabetes.Obes.Metab_19_1681
Author(s) : Park J , Park SW , Yoon KH , Kim SR , Ahn KJ , Lee JH , Mok JO , Chung CH , Han KA , Koh GP , Kang JG , Lee CB , Kim SH , Kwon NY , Kim DM
Ref : Diabetes Obes Metab , 19 :1681 , 2017
Abstract : AIMS: To evaluate the efficacy and safety of evogliptin, a newly developed dipeptidyl peptidase-4 inhibitor, in patients with type 2 diabetes (T2D) inadequately controlled by diet and exercise. MATERIALS AND METHODS: In this randomized, double-blind, placebo-controlled, parallel-group, multicentre, phase III study, 160 patients with T2D were assigned to either evogliptin 5 mg or placebo for 24 weeks. The primary endpoint was the mean change in glycated haemoglobin (HbA1c) from baseline to week 24. RESULTS: The mean baseline HbA1c levels were similar in the evogliptin and the placebo groups (7.20% +/- 0.56% vs 7.20% +/- 0.63%, respectively). At week 24, evogliptin significantly reduced HbA1c levels from baseline compared with placebo (-0.23% vs 0.05%, respectively, P < .0001). Additionally, the proportion of patients achieving HbA1c <6.5% was significantly higher in the evogliptin group than in the placebo group (33.3% vs 15.2%; P = .008). The overall incidence of adverse events, including hypoglycaemia, was similar in the 2 groups. CONCLUSIONS: In this 24-week study, once-daily evogliptin monotherapy significantly improved glycaemic control and was well tolerated in patients with T2D.
ESTHER : Park_2017_Diabetes.Obes.Metab_19_1681
PubMedSearch : Park_2017_Diabetes.Obes.Metab_19_1681
PubMedID: 28448688

Title : Efficacy and safety of adding evogliptin versus sitagliptin for metformin-treated patients with type 2 diabetes: A 24-week randomized, controlled trial with open label extension - Hong_2017_Diabetes.Obes.Metab_19_654
Author(s) : Hong SM , Park CY , Hwang DM , Han KA , Lee CB , Chung CH , Yoon KH , Mok JO , Park KS , Park SW
Ref : Diabetes Obes Metab , 19 :654 , 2017
Abstract : AIMS: This trial consisted of a 24-week multicentre, randomized, double-blind, double-dummy, active-controlled study and a 52-week open label extension study to assess the efficacy and safety of evogliptin, a novel dipeptidyl peptidase-4 inhibitor, compared to sitagliptin in patients with type 2 diabetes who have inadequate glycaemic control with metformin alone.
METHODS: Adult patients with type 2 diabetes mellitus (N = 222) with HbA1c 6.5% to 11% who were receiving stable doses of metformin (>/=1000 mg/d) were randomized 1:1 to add-on evogliptin 5 mg (N = 112) or sitagliptin 100 mg (N = 110) once daily for 24 weeks. The primary efficacy analysis consisted of a comparison of the change from baseline HbA1c at week 24. Non-inferiority was concluded if the upper limit of the 2-sided 95% confidence interval for the HbA1c difference between treatments was <0.35%.
RESULTS: Mean changes in HbA1c following addition of evogliptin or sitagliptin were -0.59% and -0.65%, respectively. The between-group difference was 0.06% (2-sided 95% confidence interval, -0.10 to 0.22), demonstrating non-inferiority. After the 52-week treatment, evogliptin caused a persistently decreased level of HbA1c (-0.44% +/- 0.65%, P < .0001). In general, both treatments were well tolerated, with incidences and types of adverse events comparable between the two groups. Hypoglycaemic events, mostly mild, were reported in 0.9% of patients treated with evogliptin and in 2.8% of patients treated with sitagliptin for 24 weeks.
CONCLUSIONS: Evogliptin 5 mg added to metformin therapy effectively improved glycaemic control and was non-inferior to sitagliptin and well tolerated in patients with type 2 diabetes mellitus that was inadequately controlled by metformin alone.
ESTHER : Hong_2017_Diabetes.Obes.Metab_19_654
PubMedSearch : Hong_2017_Diabetes.Obes.Metab_19_654
PubMedID: 28058750

Title : Efficacy and tolerability of rivastigmine patch therapy in patients with mild-to-moderate Alzheimer's dementia associated with minimal and moderate ischemic white matter hyperintensities: A multicenter prospective open-label clinical trial - Park_2017_PLoS.One_12_e0182123
Author(s) : Park KW , Kim EJ , Han HJ , Shim YS , Kwon JC , Ku BD , Park KH , Yi HA , Kim KK , Yang DW , Lee HW , Kang H , Kwon OD , Kim S , Lee JH , Chung EJ , Park SW , Park MY , Yoon B , Kim BC , Seo SW , Choi SH
Ref : PLoS ONE , 12 :e0182123 , 2017
Abstract : BACKGROUND AND OBJECTIVE: Studies investigating the impact of white matter hyperintensities (WMHs) on the response of acetylcholinesterase inhibitors in patients with Alzheimer's disease (AD) have presented inconsistent results. We aimed to compare the effects of the rivastigmine patch between patients with AD with minimal WMHs and those with moderate WMHs.
METHODS: Three hundred patients with mild to moderate AD were enrolled in this multicenter prospective open-label study and divided into two groups. Group 1 comprised patients with AD with minimal WMHs and group 2 comprised those with moderate WMHs. The patients were treated with a rivastigmine patch for 24 weeks. Efficacy measures were obtained at baseline and after 24 weeks. The primary endpoint was the change in the AD Assessment Scale-Cognitive subscale (ADAS-Cog) from the baseline to the end of the study.
RESULTS: Of the 300 patients, there were 206 patients in group 1 and 94 patients in group 2. The intention-to-treat group comprised 198 patients (group 1, n = 136; group 2, n = 46) during the 24-week study period. Demographic factors did not differ between group 1 and group 2. There were no significant differences in change in ADAS-cog between group 1 (-0.62+/-5.70) and group 2 (-0.23+/-5.98) after the 24-week rivastigmine patch therapy (p = 0.378). The patients in group 1 had a 0.63-point improvement from baseline on the Frontal Assessment Battery, while group 2 had a 0.16-point decline compared to baseline at the end of the study (p = 0.037). The rates of adverse events (AEs) (42.6 vs. 40.3%) and discontinuation due to AEs (10.3% vs. 4.3%) did not differ between the groups.
CONCLUSIONS: Although the efficacy and tolerability of rivastigmine patch therapy were not associated with WMH severity in patients with AD, some improvement in frontal function was observed in those with minimal WMHs. TRIAL REGISTRATION: NCT01380288.
ESTHER : Park_2017_PLoS.One_12_e0182123
PubMedSearch : Park_2017_PLoS.One_12_e0182123
PubMedID: 28786987

Title : A randomized, placebo-controlled, double-blind, phase 3 trial to evaluate the efficacy and safety of anagliptin in drug-naive patients with type 2 diabetes - Yang_2015_Endocr.J_62_449
Author(s) : Yang HK , Min KW , Park SW , Chung CH , Park KS , Choi SH , Song KH , Kim DM , Lee MK , Sung YA , Baik SH , Kim IJ , Cha BS , Park JH , Ahn YB , Lee IK , Yoo SJ , Kim J , Park Ie B , Park TS , Yoon KH
Ref : Endocrine Journal , 62 :449 , 2015
Abstract : The aim of this study was to evaluate the efficacy and safety of anagliptin in drug-naive patients with type 2 diabetes in a double-blind randomized placebo-controlled study. A total of 109 patients were randomized to 100 mg (n=37) or 200 mg (n=33) anagliptin twice daily or placebo (n=39). The primary objective was to alter HbA1c levels from baseline at a 24-week endpoint. The overall baseline mean age and body mass index were 56.20 +/- 9.77 years and 25.01 +/- 2.97 kg/m(2), respectively, and the HbA1c level was of 7.14 +/- 0.69 %. Anagliptin at 100 mg and 200 mg produced significant reductions in HbA1c (-0.50 +/- 0.45 % and -0.51 +/- 0.55%, respectively), and the placebo treatment resulted in an increase in HbA1c by 0.23 +/- 0.62 %. Both doses of anagliptin produced significant decreases in fasting plasma glucose (-0.53 +/- 1.25 mmol/L and -0.72 +/- 1.25 mmol/L, respectively) and the proinsulin/insulin ratio (-0.04 +/- 0.15 and -0.07 +/- 0.18, respectively) compared with placebo. No meaningful body weight changes from baseline were observed in three groups. Plasma dipeptidyl peptidase (DPP)-4 activity was significantly inhibited after 24 weeks of anagliptin treatment, and >75% and >90% inhibitions were observed during the meal tolerance tests with 100 mg and 200 mg anagliptin, respectively. The incidences of adverse or serious adverse events were similar among the three study groups. Twice-daily anagliptin therapy effectively inhibited DPP-4 activity and improved glycemic control and was well-tolerated in patients with type 2 diabetes.
ESTHER : Yang_2015_Endocr.J_62_449
PubMedSearch : Yang_2015_Endocr.J_62_449
PubMedID: 25819061

Title : Effects of mood-stabilizing drugs on dendritic outgrowth and synaptic protein levels in primary hippocampal neurons - Park_2015_Bipolar.Disord_17_278
Author(s) : Park SW , Lee JG , Seo MK , Cho HY , Lee CH , Lee JH , Lee BJ , Baek JH , Seol W , Kim YH
Ref : Bipolar Disord , 17 :278 , 2015
Abstract : OBJECTIVES: Mood-stabilizing drugs, such as lithium (Li) and valproate (VPA), are widely used for the treatment of bipolar disorder, a disease marked by recurrent episodes of mania and depression. Growing evidence suggests that Li exerts neurotrophic and neuroprotective effects, leading to an increase in neural plasticity. The present study investigated whether other mood-stabilizing drugs produce similar effects in primary hippocampal neurons.
METHODS: The effects of the mood-stabilizing drugs Li, VPA, carbamazepine (CBZ), and lamotrigine (LTG) on hippocampal dendritic outgrowth were examined. Western blotting analysis was used to measure the expression of synaptic proteins - that is, brain-derived neurotrophic factor (BDNF), postsynaptic density protein-95 (PSD-95), neuroligin 1 (NLG1), beta-neurexin, and synaptophysin (SYP). To determine neuroprotective effects, we used a B27-deprivation cytotoxicity model which causes hippocampal cell death upon removal of B27 from the culture medium.
RESULTS: Li (0.5-2.0 mM), VPA (0.5-2.0 mM), CBZ (0.01-0.10 mM), and LTG (0.01-0.10 mM) significantly increased dendritic outgrowth. The neurotrophic effect of Li and VPA was blocked by inhibition of phosphatidylinositol 3-kinase, extracellular signal-regulated kinase, and protein kinase A signaling; the effects of CBZ and LTG were not affected by inhibition of these signaling pathways. Li, VPA, and CBZ prevented B27 deprivation-induced decreases in BDNF, PSD-95, NLG1, beta-neurexin, and SYP levels, whereas LTG did not.
CONCLUSIONS: These results suggest that Li, VPA, CBZ, and LTG exert neurotrophic effects by promoting dendritic outgrowth; however, the mechanism of action differs. Furthermore, certain mood-stabilizing drugs may exert neuroprotective effects by enhancing synaptic protein levels against cytotoxicity in hippocampal cultures.
ESTHER : Park_2015_Bipolar.Disord_17_278
PubMedSearch : Park_2015_Bipolar.Disord_17_278
PubMedID: 25307211

Title : Anagliptin and sitagliptin as add-ons to metformin for patients with type 2 diabetes: a 24-week, multicentre, randomized, double-blind, active-controlled, phase III clinical trial with a 28-week extension - Jin_2015_Diabetes.Obes.Metab_17_511
Author(s) : Jin SM , Park SW , Yoon KH , Min KW , Song KH , Park KS , Park JY , Park IB , Chung CH , Baik SH , Choi SH , Lee HW , Lee IK , Kim DM , Lee MK
Ref : Diabetes Obes Metab , 17 :511 , 2015
Abstract : We conducted a 24-week, multicentre, double-blind, randomized study with a 28-week extension to compare the efficacy and safety of anagliptin and sitagliptin as an add-on to metformin in patients with type 2 diabetes. Patients inadequately controlled on metformin were randomized to either anagliptin (100 mg twice daily, n = 92) or sitagliptin (100 mg once daily, n = 88). The primary endpoint was the change in glycated haemoglobin (HbA1c) from baseline to week 24. The mean changes in HbA1c were -0.85 +/- 0.70% (p < 0.0001) for anagliptin and -0.83 +/- 0.61% (p < 0.0001) for sitagliptin, with a mean difference of -0.02% (95% confidence interval of difference, -0.22 to 0.18%). In both groups, the fasting proinsulin : insulin ratio significantly decreased from baseline, with improved insulin secretion. Safety profiles were similar in each group. In conclusion, the non-inferiority of the efficacy of anagliptin to sitagliptin as an add-on therapy was established with regard to efficacy and safety.
ESTHER : Jin_2015_Diabetes.Obes.Metab_17_511
PubMedSearch : Jin_2015_Diabetes.Obes.Metab_17_511
PubMedID: 25523633

Title : Toxic effects of methylmercury, arsanilic acid and danofloxacin on the differentiation of mouse embryonic stem cells into neural cells - Kang_2014_J.Vet.Sci_15_61
Author(s) : Kang SJ , Jeong SH , Kim EJ , Park YI , Park SW , Shin HS , Son SW , Kang HG
Ref : J Vet Sci , 15 :61 , 2014
Abstract : This study was performed to assess the neurotoxic effects of methylmercury, arsanilic acid and danofloxacin by quantification of neural-specific proteins in vitro. Quantitation of the protein markers during 14 days of differentiation indicated that the mouse ESCs were completely differentiated into neural cells by Day 8. The cells were treated with non-cytotoxic concentrations of three chemicals during differentiation. Low levels of exposure to methylmercury decreased the expression of GABAA-R and Nestin during the differentiating stage, and Nestin during the differentiated stage. In contrast, GFAP, Tuj1, and MAP2 expression was affected only by relatively high doses during both stages. Arsanilic acid affected the levels of GABAA-R and GFAP during the differentiated stage while the changes of Nestin and Tuj1 were greater during the differentiating stage. For the neural markers (except Nestin) expressed during both stages, danofloxacin affected protein levels at lower concentrations in the differentiated stage than the differentiating stage. Acetylcholinesterase activity was inhibited by relatively low concentrations of methylmercury and arsanilic acid during the differentiating stage while this activity was inhibited only by more than 40 muM of danofloxacin in the differentiated stage. Our results provide useful information about the different toxicities of chemicals and the impact on neural development.
ESTHER : Kang_2014_J.Vet.Sci_15_61
PubMedSearch : Kang_2014_J.Vet.Sci_15_61
PubMedID: 24136205

Title : Butyrylcholinesterase K and Apolipoprotein epsilon4 Affect Cortical Thickness and Neuropsychiatric Symptoms in Alzheimer's Disease - Yoo_2014_Curr.Alzheimer.Res_11_137
Author(s) : Yoo HB , Lee HW , Shin S , Park SW , Choi JS , Jung HY , Cha J , Lee JM , Lee JY
Ref : Curr Alzheimer Res , 11 :137 , 2014
Abstract : Two major genotypes are known to affect the development and progression of Alzheimer's disease (AD) and its response to cholinesterase inhibitors: the apolipoprotein E (ApoE) and butyrylcholinesterase genes (BChE). This study analyzed the effects of the BChE and ApoE genotypes on the cortical thickness of patients with AD and examined how these genotypes affect the neuropsychiatric symptoms of AD. AD-drug-naive patients who met the probable AD criteria proposed by the National Institute of Neurological and Communicative Disorders and Stroke-Alzheimer's Disease and Related Disorders Association were recruited. Of 96 patients with AD, 65 were eligible for cortical thickness analysis. 3D T1-weighted images were acquired, and the cortical regions were segmented using the constrained Laplacian-based automated segmentation with proximities (CLASP) algorithm. Neuropsychiatric symptoms were measured by Neuropsychiatric Inventory (NPI) scores. BChE wild-type carriers (BChE-W) showed more thinning in the left dorsolateral prefrontal cortex, including the lateral premotor regions and anterior cingulate cortex, than did BChE-K variant carriers (BChE-K). ApoE-epsilon4 carriers had a thinner left medial prefrontal cortex, left superior frontal cortex, and left posterior cingulate cortex than did ApoE-epsilon4 non-carriers. Statistical analyses revealed that BChE-K carriers showed significantly less severe aberrant motor behavioral symptoms and that epsilon4 non-carriers showed less severe anxiety and indifference symptoms. The current findings show that, similar to ApoE-epsilon4 non-carriers, BChE-K carriers are protected from the pathological detriments of AD that affect frontal cortical thickness and neuropsychiatric symptoms. This study visually demonstrated the effects of the BChE-K and ApoE genotypes on the structural degeneration and complex aspects of the symptoms of AD.
ESTHER : Yoo_2014_Curr.Alzheimer.Res_11_137
PubMedSearch : Yoo_2014_Curr.Alzheimer.Res_11_137
PubMedID: 24479631

Title : Cloning and expression analysis of the duplicated genes for carbon monoxide dehydrogenase of Mycobacterium sp. strain JC1 DSM 3803 - Song_2010_Microbiology_156_999
Author(s) : Song T , Park SW , Park SJ , Kim JH , Yu JY , Oh JI , Kim YM
Ref : Microbiology , 156 :999 , 2010
Abstract : Carbon monoxide dehydrogenase (CO-DH) is an enzyme catalysing the oxidation of CO to carbon dioxide in Mycobacterium sp. strain JC1 DSM 3803. Cloning of the genes encoding CO-DH from the bacterium and sequencing of overlapping clones revealed the presence of duplicated sets of genes for three subunits of the enzyme, cutB1C1A1 and cutB2C2A2, in operons, and a cluster of genes encoding proteins that may be involved in CO metabolism, including a possible transcriptional regulator. Phylogenetic analysis based on the amino acid sequences of large subunits of CO-DH suggested that the CO-DHs of Mycobacterium sp. JC1 and other mycobacteria are distinct from those of other types of bacteria. The growth phenotype of mutant strains lacking cutA genes and of a corresponding complemented strain showed that both of the duplicated sets of CO-DH genes were functional in this bacterium. Transcriptional fusions of the cutB genes with lacZ revealed that the cutBCA operons were expressed regardless of the presence of CO and were further inducible by CO. Primer extension analysis indicated two promoters, one expressed in the absence of CO and the other induced in the presence of CO. This is believed to be the first report to show the presence of multiple copies of CO-DH genes with identical sequences and in close proximity in carboxydobacteria, and to present the genetic evidence for the function of the genes in mycobacteria.
ESTHER : Song_2010_Microbiology_156_999
PubMedSearch : Song_2010_Microbiology_156_999
PubMedID: 20035005
Gene_locus related to this paper: 9myco-d5g1y8

Title : Identification of likely orthologs of tobacco salicylic acid-binding protein 2 and their role in systemic acquired resistance in Arabidopsis thaliana - Vlot_2008_Plant.J_56_445
Author(s) : Vlot AC , Liu PP , Cameron RK , Park SW , Yang Y , Kumar D , Zhou F , Padukkavidana T , Gustafsson C , Pichersky E , Klessig DF
Ref : Plant J , 56 :445 , 2008
Abstract : Salicylic acid-binding protein 2 (SABP2) is essential for the establishment of systemic acquired resistance (SAR) in tobacco; SABP2's methyl salicylate (MeSA) esterase activity is required in healthy systemic tissues of infected plants to release the active defense phytohormone SA from MeSA, which serves as a long-distance signal for SAR. In the current study, we characterize a new gene family from Arabidopsis thaliana encoding 18 potentially active alpha/beta fold hydrolases that share 32-57% identity with SABP2. Of 14 recombinant AtMES (MES for methyl esterase) proteins tested, five showed preference for MeSA as a substrate and displayed SA inhibition of MeSA esterase activity in vitro (AtMES1, -2, -4, -7, and -9). The two genes encoding MeSA esterases with the greatest activity, AtMES1 and -9, as well as AtMES7 were transcriptionally upregulated during infection of Arabidopsis with avirulent Pseudomonas syringae. In addition, conditional expression of AtMES1, -7, or -9 complemented SAR deficiency in SABP2-silenced tobacco, suggesting that these three members of the AtMES family are SABP2 functional homologs (orthologs). Underexpression by knockout mutation and/or RNAi-mediated silencing of multiple AtMES genes, including AtMES1, -2, -7, and -9, compromised SAR in Arabidopsis and correlated with enhanced accumulation of MeSA in the systemic tissue of SAR-induced plants. Together, the data show that several members of the AtMES gene family are functionally homologous to SABP2 and redundant for MeSA hydrolysis and probably SAR. These data suggest that MeSA is a conserved SAR signal in Arabidopsis and tobacco.
ESTHER : Vlot_2008_Plant.J_56_445
PubMedSearch : Vlot_2008_Plant.J_56_445
PubMedID: 18643994
Gene_locus related to this paper: arath-MES1

Title : Structural and biochemical studies identify tobacco SABP2 as a methyl salicylate esterase and implicate it in plant innate immunity - Forouhar_2005_Proc.Natl.Acad.Sci.U.S.A_102_1773
Author(s) : Forouhar F , Yang Y , Kumar D , Chen Y , Fridman E , Park SW , Chiang Y , Acton TB , Montelione GT , Pichersky E , Klessig DF , Tong L
Ref : Proc Natl Acad Sci U S A , 102 :1773 , 2005
Abstract : Salicylic acid (SA) is a critical signal for the activation of plant defense responses against pathogen infections. We recently identified SA-binding protein 2 (SABP2) from tobacco as a protein that displays high affinity for SA and plays a crucial role in the activation of systemic acquired resistance to plant pathogens. Here we report the crystal structures of SABP2, alone and in complex with SA at up to 2.1-A resolution. The structures confirm that SABP2 is a member of the alpha/beta hydrolase superfamily of enzymes, with Ser-81, His-238, and Asp-210 as the catalytic triad. SA is bound in the active site and is completely shielded from the solvent, consistent with the high affinity of this compound for SABP2. Our biochemical studies reveal that SABP2 has strong esterase activity with methyl salicylate as the substrate, and that SA is a potent product inhibitor of this catalysis. Modeling of SABP2 with MeSA in the active site is consistent with all these biochemical observations. Our results suggest that SABP2 may be required to convert MeSA to SA as part of the signal transduction pathways that activate systemic acquired resistance and perhaps local defense responses as well.
ESTHER : Forouhar_2005_Proc.Natl.Acad.Sci.U.S.A_102_1773
PubMedSearch : Forouhar_2005_Proc.Natl.Acad.Sci.U.S.A_102_1773
PubMedID: 15668381
Gene_locus related to this paper: nicta-SABP2