• Title/Summary/Keyword: Protein phosphatase

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In vivo putative O-GlcNAcylation of human SCP1 and evidence for possible role of its N-terminal disordered structure

  • Koo, JaeHyung;Bahk, Young Yil
    • BMB Reports
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    • v.47 no.10
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    • pp.593-598
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    • 2014
  • RNA polymerase II carboxyl-terminal domain (RNAPII CTD) phosphatases are responsible for the dephosphorylation of the C-terminal domain of the small subunit of RNAPII in eukaryotes. Recently, we demonstrated the identification of several interacting partners with human small CTD phosphatase1 (hSCP1) and the substrate specificity to delineate an appearance of the dephosphorylation catalyzed by SCP1. In this study, using the established cells for inducibly expressing hSCP1 proteins, we monitored the modification of ${\beta}$-O-linked N-acetylglucosamine (O-GlcNAc). O-GlcNAcylation is one of the most common post-translational modifications (PTMs). To gain insight into the PTM of hSCP1, we used the Western blot, immunoprecipitation, succinylayed wheat germ agglutinin-precipitation, liquid chromatography-mass spectrometry analyses, and site-directed mutagenesis and identified the $Ser^{41}$ residue of hSCP1 as the O-GlcNAc modification site. These results suggest that hSCP1 may be an O-GlcNAcylated protein in vivo, and its N-terminus may function a possible role in the PTM, providing a scaffold for binding the protein(s).

Effects of Dokwhalgisaeng-tang Gamibang (DGG) Water Extract on Dexamethasone-treated Osteoblast (독활기생탕가미방이 Dexamethasone 처리 조골세포에 미치는 영향)

  • Baek, Seon-Eun;Jang, Sae-Byul;Yoo, Jeong-Eun;Yoo, Dong-Youl
    • The Journal of Korean Obstetrics and Gynecology
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    • v.29 no.2
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    • pp.1-14
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    • 2016
  • Objectives : In this study, the author aimed to evaluate the effects of water extract of Dokwhalgisaeng-tang Gamibang (DGG) on osteoblast proliferation in murine calvarial cells. Methods : The osteoblast separated from murine calvariae was cultivated and evaluated the cell function. After the addition of DGG on the culture medium, we determined the effect of DGG on the cell proliferation, protein synthesis, alkaline phosphatase activity, collagen synthesis, and cell viability of the cultivated osteoblast in the presence of dexamethasone. Results : DGG increased the survival rate, proliferation, alkaline phosphatase (ALP) activity, protein synthesis and collagen synthesis of rat calvarial osteoblast in the presence of dexamethasone. Conclusions : DGG might improve the osteoporosis resulted from augmentation of osteoblast proliferation.

Differential Responses of Rice Acid Phosphatase Activities and Isoforms to Phosphorus Deprivation

  • Lim, Jeong-Hyun;Chung, Ill-Min;Ryu, Sang-Soo;Park, Myoung-Ryoul;Yun, Song-Joong
    • BMB Reports
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    • v.36 no.6
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    • pp.597-602
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    • 2003
  • Acid phosphatases (APases) play a role in the release of phosphate in organic complexes in soil. We investigated tissue- and isoform-specific responses of APases to phosphorus (P) deficiency in three rice genotypes; Dasan-byeo, Sobi-byeo, and Palawan. The levels of shoot APase activity per protein were similar in the three genotypes. They significantly decreased with P deprivation that was longer than seven days. Root APase activity per protein was two- to three-fold higher in Dasan than in Sobi and Palawan. In all genotypes the APase activity increased in P-deficient plants, but the increase was higher in Sobi and Palawan. After 21 days of P deprivation, secreted APase activity increased more than eight-fold in Dasan and two-fold in Sobi and Palawan. Isoform profiles of shoot and root APases were most diverse in Dasan. The activities of the major isoforms in P-deficient shoots decreased in all three genotypes. Depending on the genotypes, further increases in constitutive isoforms and new induction of one to four isoforms occurred in P-deficient roots. The results indicate that tissue and genotype differences in the response of APase to P deficiency are primarily facilitated by the different responses of the isoforms.

Functional Analysis of MCNA, a Gene Encoding a Catalytic Subunit of Calcineurin, in the Rice Blast Fungus Magnaporthe oryzae

  • Choi, Jin-Hee;Kim, Yang-Seon;Lee, Yong-Hwan
    • Journal of Microbiology and Biotechnology
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    • v.19 no.1
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    • pp.11-16
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    • 2009
  • Magnaporthe oryzae, the causal agent of rice blast, forms a specialized infection structure, called an appressorium, which is crucial for penetration and infection of the host plant. Pharmacological data suggest that calcium/calmodulindependent signaling is involved in appressorium formation in this fungus. To understand the role of the calcium/calmodulin-activated protein phosphatase on appressorium formation at the molecular level, MCNA, a gene encoding the catalytic subunit of calcineurin, was functionally characterized in M. oryzae. Transformants expressing sense/antisense RNA of MCNA exhibited significant reductions in mycelial growth, conidiation, appressorium formation, and pathogenicity. cDNA of MCNA functionally complemented a calcineurin disruptant strain (cmp1::LEU2 cmp2::HIS3) of Saccharomyces cerevisiae. These data suggest that calcineurin A plays important roles in signal transduction pathways involved in the infection-related morphogenesis and pathogenicity of M. oryzae.

Development of protein tyrosine phosphatase 1B (PTPIB) Inhibitors from marine sources and other natural products-Future of Antidiabetic Therapy : A Systematic Review

  • KAUR, Kulvinder Kochar;ALLAHBADIA, Gautam;SINGH, Mandeep
    • The Korean Journal of Food & Health Convergence
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    • v.5 no.3
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    • pp.21-33
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    • 2019
  • The incidence of both obesity and Type 2 Diabetes Mellitus( DM) is increasing proportionately so that causes of deaths from these has overtaken from that of malnourishment. Hence it has been recommended to treat the 2 in parallel considering the role of diabesity on health. Important causes of T2DM are insulin resistance (IR) and /or inadequate insulin secretion. Protein tyrosine phosphatase 1B(PTPIB) has a negative impact in insulin signaling pathways and hence plays crucial role inT2DM,since its overexpression might induce IR. Thus PTPIB is considered a therapeutic target for both obesity and T2DM, there has been a search for novel ,promising natural inhibitors. We conducted a pubmed search for articles related to PTPIB inhibitors from natural causes be it marine sources or other natural sources. Out of 988 articles we selected 100 articles for review. Thus various bioactive molecules isolated from marine organisms that can acts as PTPIB Inhibitors and thus possess antidiabetic activity both in vitro/ in vivo studies ,besides products from fruits like Chinese raspberry or curcumin used as routine spices are described with their chemical classes, structure-activity relationships and potency as assessed by IC 50 values are discussed. More work is required to make this a reality.

Hsa_circ_0129047 sponges miR-665 to attenuate lung adenocarcinoma progression by upregulating protein tyrosine phosphatase receptor type B

  • Xiaofan Xia;Jinxiu Fan;Zhongjie Fan
    • The Korean Journal of Physiology and Pharmacology
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    • v.27 no.2
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    • pp.131-141
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    • 2023
  • Compelling evidence has demonstrated the critical role of circular RNAs (circRNAs) during lung adenocarcinoma (LUAD) progression. Herein, we explored a novel circRNA, circ_0129047, and detailed its mechanism of action. The expression of circ 0129047, microRNA-665 (miR-665), and protein tyrosine phosphatase receptor type B (PTPRB) in LUAD tissues and cells was determined using reverse transcription quantitative polymerase chain reaction and Western blotting. Cell Counting Kit8 and colony formation assays were conducted to detect LUAD cell proliferation, and western blotting was performed to quantify apoptosis-related proteins (Bcl2 and Bax). Luciferase reporter and RNA immunoprecipitation assays were used to validate the predicted interaction between miR-665 and circ_0129047 or PTPRB. A xenograft assay was used for the in vivo experiments. Circ_0129047 and PTPRB were downregulated in LUAD tissues and cells, whereas miR-665 expression was upregulated. Overexpression of circ_0129047 suppresses LUAD growth in vivo and in vitro. Circ_0129047 is the target of miR-665, and the miR-665 mimic ablated the antiproliferative and pro-apoptotic phenotypes of LUAD cells by circ_0129047 augmentation. MiR-665 targets the 3'UTR of PTPRB and downregulates PTPRB expression. PTPRB overexpression offsets the pro-proliferative potential of miR-665 in LUAD cells. Circ_0129047 sequestered miR-665 and upregulated PTPRB expression, thereby reducing LUAD progression, suggesting a promising approach for preventing LUAD.

Roles of Prostatic Acid Phosphatase in Prostate Cancer (Prostatic acid phosphatase의 전립선 암에서의 역할)

  • Kong, Hoon-Young;Lee, Hak-Jong;Byun, Jong-Hoe
    • Journal of Life Science
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    • v.21 no.6
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    • pp.893-900
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    • 2011
  • Prostatic acid phosphatase (PAP) is one of the widely used biomarkers in the diagnosis of prostate cancer. It was initially identified in 1935 and is the most abundant phosphatase in the human prostate. PAP is a prostate-specific enzyme that is synthesized in prostate epithelial cells. It belongs to the acid phosphatase group that shows enzymatic activity in acidic conditions. PAP is abundant in prostatic fluid and is thought to have a role in fertilization and oligospermia. It also has a potential role in reducing chronic pain. But one of the most apparent functions of PAP is the dephosphorylation of macromolecules such as HER-2 and PI3P that are involved in the ERK1/2 and MAPK pathways, which in turn leads to inhibition of cell growth and tumorigenesis. Currently, clinical trials using PAP DNA vaccine are underway and FDA-approved immunotherapy using PAP is commercially available. Despite these clinically important aspects, molecular mechanisms underlying PAP regulation are not fully understood. The promoter region of PAP was reported to be regulated by NF-${\kappa}B$, TNF-${\alpha}$, IL-1, androgen and androgen receptors. Here, the features of PAP gene and protein structures together with the function, regulation and roles of PAP in prostate cancer are discussed.

Identification of Differentially Expressed Genes in Human Small Cell Lung Carcinoma Using Subtractive Hybridization

  • Ahn Seung-Ju;Choi Jae-Kyoung;Joo Young Mi;Lee Min-A;Choi Pyung-Rak;Lee Yeong-Mi;Kim Myong-Shin;Kim So-Young;Jeon Eun-Hee;Min Byung-In;Kim Chong-Rak
    • Biomedical Science Letters
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    • v.10 no.3
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    • pp.195-202
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    • 2004
  • Lung cancer is a leading cause of cancer death worldwide; however, despite major advances in cancer treatment during the past two decades, the prognostic outcome of lung cancer patients has improved only minimally. This is largely due to the inadequacy of the traditional screening approach of diagnosis in lung cancer, which detects only well­established overt cancers and fails to identify precursor lesions in premalignant conditions of the bronchial tree. In recent years this situation has fundamentally changed with the identification of molecular abnormalities characteristic of premalignant changes; these concern tumour suppressor genes, loss of heterozygosity at crucial sites and activation of oncogenes. Basic knowledge at the molecular level has extremely important clinical implications with regard to early diagnosis, risk assessment and prevention, and therapeutic targets. In this study we used a 'cap-finder' subtractive hybridization method, 'long distance' polymerase chain reaction (PCR), streptavidin magnetic beads mediated subtraction, and spin column chromatography to detect differential expression genes of human small cell lung carcinoma. We have now isolated ninety two genes that expressed differentially in the human small cell lung carcinoma cells and analyzed of 12 clones with sequencing, nine cDNAs include tapasin (NGS-17) mRNA, BC200 alpha scRNA, chromosome 12q24 PAC RPCI3-462E2, protein phosphatase 1 (PPPICA), translocation protein 1 (TLOC1), ribosomal protein S24 (RPS24) mRNA, protein phosphatase (PPEF2), cathepsin Z, MDM2 gene and three novel genes. They may be oncogenesis­related proteins.

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Antihepatotoxic effect of Artemisia Iwayomogi methanol extract on acute hepatic injury by carbon tetrachloride in rat (사염화탄소에 의한 랫드의 간손상에 대한 인진호메타놀추출물의 억제효과)

  • Kim, Kil-soo;Park, Joon-hyoung
    • Korean Journal of Veterinary Research
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    • v.34 no.3
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    • pp.619-626
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    • 1994
  • The purpose of present study was to examine pharmacological effect of Artemisia Iwayomogi methanol extract(AIME) on biochemical parameters(activities of AST, ALT, LDH, and ALP, contents of total bilirubin, total protein, albumin and A/G ratio in serum and levels of hepatic microsomal lipid peroxide and glucose-6-phosphatase activities) against hepatic injury by carbon tetrachloride($CCl_4$) in rats. Increased AST, ALT and LDH activities by $CCl_4$ were decreased in AIMS treatment group at 48 or 72 hours. Together, increased ALP activity by $CCl_4$ almost returned toward normal value in AIME treatment group at 72 hours. Serum total bilirubin contents increased to 87, 79 and 31% compared with normal group by $CCl_4$ which were decreased to 64, 42 and 26% in AIME treatment group at 24, 48 and 72 hours, respectively. Decreased contents of total protein and albumin, and A/G ratio by $CCl_4$ were recovered in AIME treatment group. Hepatic microsomal lipid peroxide levels(nmol malonic dialdehyde/100mg protein) increased to 140, 95 and 78% compared with normal group by $CCl_4$ which were decreased to 107, 74 and 65% in AIME treatment group at 24, 48 and 72 hours, separately. Hepatic microsomal glucose-6-phosphatase activities decreased to 60, 50 and 53% compared with normal group by $CCl_4$ at 24, 48 and 72 hours, respectively, which were increased at 72 hours in AIME treatment group. In conclusion, AIME enhanced the amelioration process from $CCl_4$-induced lipid peroxidation, degeneration of liver cell, and impairment of protein and bilirubin metabolisms.

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Aspirin inhibits lipopolysaccharide-induced COX-2 expression and PGE2 production in porcine alveolar macrophages by modulating protein kinase C and protein tyrosine phosphatase activity

  • Duan, Yuzhong;Chen, Fanglin;Zhang, Anmei;Zhu, Bo;Sun, Jianguo;Xie, Qichao;Chen, Zhengtang
    • BMB Reports
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    • v.47 no.1
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    • pp.45-50
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    • 2014
  • Aspirin has been demonstrated to be effective in inhibiting COX-2 and $PGE_2$ in Alveolar macrophages (AMs). However, the mechanisms have not been fully understood. In the present study, we found that pretreatment with aspirin inhibited LPS-induced COX-2 and$PGE_2$ upregulation, $I{\kappa}B{\alpha}$ degradation, NF-${\kappa}B$ activation and the increase of PKC activity, but elevated LPS-induced the decrease of PTP activity. The PKC inhibitor calphostin C dramatically reduced the COX-2 mRNA and $PGE_2$ levels, but the PTP inhibitor peroxovanadium (POV) significantly increased the COX-2 mRNA and$PGE_2$ levels. Furthermore, the PTP inhibitor mitigated the inhibitory effect of aspirin on COX-2 and$PGE_2$ upregulation and NF-${\kappa}B$ activation, whereas the PKC inhibitor enhanced the inhibitory effects of aspirin on the production of COX-2 and$PGE_2$. Our data indicate a novel mechanism by which aspirin acts as a potent anti-inflammatory agent in alveolus macrophages and ALI.