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Signaling mechanisms mediated by G-protein coupled receptors in human platelets

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Acta Pharmacologica Sinica 2004年第7期25卷 41-46页

作者： Sheikh Arshad SAEED,Huma RASHEED,Faisal A Wahed FECTO,Mohammad Ilyas ACHAKZAI,Rahmat ALI,John Dennis CONNOR,Anwar-ul-Hassan GILANI Department of Biological and Biomedical Sciences TheAga Khan University Karachi-74800 Pakistan Department of Biological and Biomedical Sciences TheAga Khan University Karachi-74800 Pakistan Department of Biological and Biomedical Sciences TheAga Khan University Karachi-74800 Pakistan Department of Biological and Biomedical Sciences TheAga Khan University Karachi-74800 Pakistan Department of Biological and Biomedical Sciences TheAga Khan University Karachi-74800 Pakistan Department of Biological and Biomedical Sciences TheAga Khan University Karachi-74800 Pakistan Department of Biological and Biomedical Sciences TheAga Khan University Karachi-74800 Pakistan

AIM: The present study deals with the investigation of mechanisms involved in the synergistic interaction between epinephrine and arachidonic acid (AA). METHODS: Venous blood was taken from healthy human volunteers reported to be free of medications for one week. Platelet aggregation was monitored at 37oC using Dual-channel Lumi-aggregometer. The resulting aggregation was recorded for 5 min by the measurement of light transmission as a function of time. RESULTS: The data show that a synergism in platelet aggregation mediated by subthreshold concentrations of epinephrine (1 μmol/L) and AA (0.2 μmol/L) was inhibited by the α2-receptor antagonist (yohimbine, IC50=0.6 μmol/L) and an inhibitor of AA-cyclooxygenase (COX), indomethacin (IC50=0.25 μmol/L). In examining receptor influence on intraplatelet signalling pathways, it was found that the synergistic effect was inhibited by calcium channel blockers, verapamil (IC50=0.4 μmol/L) and diltiazem (IC50=2.5 μmol/L), as well as by low concentrations of inhibitors of phospholipase C (PLC) (U73122; IC50=0.2 μmol/L) and mitogens activated protein kinase (mapK) (PD 98059; IC50=3.8 μmol/L). Herbimycin A, a specific inhibitor of tyrosine light chain kinase (TLCK), showed inhibition at IC50 value of 15 μmol/L, whereas chelerythrine, a protein kinase C (PKC) inhibitor, had no effect up to 20 μmol/L. CONCLUSION: These data suggest that synergism between epinephrine and AA in platelet aggregation is triggered through receptors coupled to G-protein, which in turn, activate PLC, COX, and map kinase-signaling pathways.

关键词： platelet aggregation epinephrine arachidonic acid cyclooxygenase phospholipase C calcium channel blockers nitric oxide map kinase

Reprogramming plant specialized metabolism by manipulating protein kinases

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aBIOTECH 2021年第3期2卷 226-239页

作者： Ruiqing Lyu Sanjay K.Singh Yongliang Liu Barunava Patra Yan Zhou Bingwu Wang Sitakanta Pattanaik Ling Yuan Department of Plant and Soil Sciences and the Kentucky Tobacco Research and Development Center University of Kentucky1401 University DriveLexingtonKY 40546USA South China Botanical Garden Chinese Academy of SciencesGuangzhou 510650China Tobacco Breeding Center Yunnan Academy of Tobacco Agricultural SciencesKunming 650021YunnanChina

Being sessile,plants have evolved sophisticated mechanisms to balance between growth and defense to survive in the harsh *** transition from growth to defense is commonly achieved by factors,such as protein kinases(PKs)and transcription factors,that initiate signal transduction and regulate specialized *** produce an array of lineage-specific specialized metabolites for chemical defense and stress *** of these molecules are also used by humans as ***,many of these defense-responsive metabolites are toxic to plant cells and inhibitory to growth and *** have,thus,evolved complex regulatory networks to balance the accumulation of the toxic *** of external stimuli is a vital part of the regulatory *** kinase-mediated signaling activates a series of defense responses by phosphorylating the target pro-teins and translating the stimulus into downstream cellular *** biosynthesis of specialized metabolites is triggered when plants perceive stimuli,a possible connection between PKs and spe-cial ized meta bolism is well ***,the roles of PKs in plant specialized metabolism have not received much attention until ***,we summarize the recent advances in understanding PKs in plant specialized *** aim to highlight how the stimulatory signals are transduced,leading to the biosynthesis of corresponding *** discuss the post-translational regulation of specialized metabolism and provide insights into the mechanisms by which plants respond to the external *** addition,we propose possible strategies to increase the production of plant spe-cial ized metabolites in biotechnological applications using PKs.

关键词： Medicinal plants Protein kinases map kinase Specialized metabolites Post-translational regulation Signal transd uction

mapKs and acetyl-CoA are associated with Curvularia lunata pathogenicity and toxin production in maize

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Journal of Integrative Agriculture 2018年第1期17卷 139-148页

作者： NI Xuan GAO Jin-xin YU Chuan-jin WANG Meng SUN Jia-nan LI Ya-qian CHEN Jie School of Agriculture and Biology Shanghai Jiao Tong University/State Key Laboratory of Microbial Metabolism Shanghai JiaoTong UniversityKey Laboratory of Urban Agriculture (South) Ministry of Agriculture Shanghai 200240 P.R.China

Mitogen-activated protein kinase （mapK） cascades play an important role in extracellular signal transduction and are involved in the pathogenicity of fungal pathogens to host plants. In Curvularia lunata, the roles of two mapK genes, Clkl and CIm 1, have already been studied. Clkl is involved in conidia formation and pathogenicity, and Clmf is closely related to pathogen cell wall formation and pathogenicity to maize leaves. In this study, a third C. lunata mapK gene, Clhl, which is homologous to hog1, was successfully cloned. We found that a Clhl deletion mutant had lower intracellular glycerol accumulation than the wild-type stain and was unable to grow normally under osmotic stress conditions. Furthermore, the deletion mutants of three C. lunata mapK genes （Clkl, Clml and Clhl） had lower levels of acetyI-CoA, which is an important intermediate product in the synthesis of melanin and furan toxin, and down-regulated expression of pathogenicity-associated genes. Furthermore, pathogenicity and the ability to produce toxin were restored after adding acetyI-CoA to the culture medium, suggesting that acetyI-CoA is closely involved in the pathogen mapK signaling pathway.

关键词： Curvularia lunata map kinase acetyI-CoA pathology

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Sam68 is a regulator of Toll-like receptor signaling

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Cellular & Molecular Immunology 2017年第1期14卷 107-117页

作者： Jeffrey A Tomalka Tristan J de Jesus Parameswaran Ramakrishnan Department of Pathology School of Medicine Case Western Reserve University and University Hospitals Case Medical Center Cleveland OH 44106 USA

Recognition of pathogens by Toll-like receptors （TLR） activate multiple signaling cascades and expression of genes tailored to mount a primary immune response, inflammation, cell survival and apoptosis. Although TLR-induced activation of pathways, such as nuclear factor kappaB （NF-κB） and mitogen-activated protein kinases （mapK）, has been well studied, molecular entities controlling quantitative regulation of these pathways during an immune response remain poorly defined. We identified Sam68 as a novel regulator of TLR-induced NF-κB and mapK activation. We found that TLR2 and TLR3 are totally dependent, whereas TLR4 is only partially dependent on Sam68 to induce the activation of NF-KB c-Rel. Absence of Sam68 greatly decreased TLR2- and TLR3-induced NF-κB p65 activation, whereas TLR4- induced p65 activation in a Sam68-independent manner. In contrast, Sam68 appeared to be a negative regulator of mapK pathways because absence of Sam68 enhanced TLR2-induced activation of extracellular signal-regulated kinases （ERK） and c-Jun N-terminal kinases （JNK）. Interestingly, TLR2- and TLR3-induced gene expression showed a differential requirement of Sam68. Absence of Sam68 impaired TLR2-induced gene expression, suggesting that Sam68 has a critical role in myeloid differentiation primary response gene 88-dependent TLR2 signaling. TLR3-induced gene expression that utilize Toll/Interleukin-1 receptor-domain-containing adapter-inducing beta interferon pathway, depend only partially on Sam68. Our findings suggest that Sam68 may function as an immune rheostat that balances the activation of NF-κB p65 and c-Rel, as well as mapK, revealing a potential novel target to manipulate TLR signaling.

关键词： innate immunity map kinase NF-kappaB Sam68 TLR

IL-1β activates p44/42 and p38 mitogen-activated protein kinases via different pathways in cat esophageal smooth muscle cells

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World Journal of Gastroenterology 2006年第5期12卷 716-722页

作者： Tai Sang Lee Hyun Ju Song Ji Hoon Jeong Young Sil Min Chang Yell Shin Uy Dong Sohn Department of Pharmacology College of PharmacyChung-Ang UniversitySeoul 156-756Republic of Korea Research Laboratory Dong-A Pharmaceuticals Co.LtdKyunggidoRepublic of Korea

AIM： To examine the pathway related to the IL-1β induced activation of mitogen-activated protein （map） kinases in cat esophageal smooth muscle cells. METHODS： Culture of the esophageal smooth muscle cells from cat was prepared. Specific inhibitors were treated before applying the IL-β3. Western blot analysis was performed to detect the expressions of COX, iNOS and map kinases. RESULTS： In the primary cultured cells, although IL-β3 failed to upregulate the COX and iNOS levels, the levels of the phosphorylated forms of 1344142 HAP kinase and p38 map kinase increased in both concentration- and time-dependent manner, of which the level of activation reached a maximum within 3 and 18 h, respectively. The pertussis toxin reduced the level of p44/42 map kinase phosphorylation. Tyrphostin 51 and genistein also inhibited this activation. Neomycin decreased the density of the p44/42 HAP kinase band to the basal level. Phosphokinase C （PKC） was found to play a mediating role in the IL-1β-induced p44/42 map kinase activity. In contrast, the activation of p38 map kinase was inhibited only by a pretreatment with forskolin, and was unaffected by the other compounds. CONCLUSION： Based on these results, IL-1β-induced p44/42 map kinase activation is mediated by the Gi protein, tyrosine kinase, phospholipase C （PLC） and PKC. The pathway for p38 map kinase phosphorylation is different from that of p44/42 map kinase, suggesting that it plays a different role in the cellular response to IL- 1β.

关键词： IL-1β map kinase Esophageal smoothmuscle cells

Signal transduction of bombesin-induced circular smooth muscle cell contraction in cat esophagus

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World Journal of Gastroenterology 2006年第14期12卷 2259-2263页

作者： Sung-Uk Park Chang-Yell Shin Jung-Su Ryu Hyen-O La Sun-Young Park Hyun-Ju Song Young-Sil Min Dong-Seok Kim Uy-Dong Sohn Department of Pharmacology College of Pharmacy Chung Ang UniversitySeoul 156-756Republic of Korea Department of Pharmacology College of Pharmacy Chung Ang UniversitySeoul 156-756Republic of Korea Research LaboratoryDong-A Pharm. Co. LtdYongin 449-905Kyunggi-DoRepublic of Korea Department of Pharmacology College of Medicine The Catholic University of KoreaSeoul 137-701Republic of Korea Research Division for Human Life Sciences Seoul National University 28 Yongon-DongChongno-GuSeoul 110-744Republic of Korea

AIM： To investigate the mechanism of bombesin-induced circular smooth muscle cell contraction in cat esophagus. METHODS： Specific G protein or phospholipase C involved in cat esophagus contraction was identified, muscle cells were permeabilized with saponin. After per- meabilization of muscle cells, the Gi3 antibody inhibited bombesin-induced smooth muscle cell contraction. RESULTS： Incubation of permeabilized circular muscle cells with PLC-β3 antibody could inhibit bombesin-induced contraction. H-7, chelerythrine （PKC inhibitor） and genistein （protein tyrosine kinase inhibitor） inhibited bombesin-induced contraction, but DAG kinase inhibitor, R59949, could not inhibit it. To examine which mitogen-activated protein kinase （mapK） was involved in bombesin-induced contTaction, the specific mapK inhibitors （MEK inhibitor, PD98059 and p38 mapK inhibitor, SB202190） were used. Preincubation of PD98059 blocked the contraction induced by bombesin in a concentration-dependent manner. However, SB202190 had no effects on contraction. CONCLUSION： Bombesin-induced circular muscle cell contraction in cat esophagus is mediated via a PKC or a PTK-dependent pathway or p44/p42 HAPK pathway.

关键词： Bombesin G protein Phospholipase C Protein kinase C Protein tyrosine kinase map kinase Cell contraction

Effects and mechanism of glucagon-like peptide-1 on injury of rats cardiomyocytes induced by hypoxia-reoxygenation

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Chinese Medical Journal 2008年第21期121卷 2134-2138页

作者： XIE Yun WANG Shao-xin SHA Wei-wei ZHOU Xue WANG Wei-tin HAN Li-pin LI Dai-qing YU De-min Department of Diabetic Neurology Metabolic Disease Hospital Tianjin Medical University Tianjin 300070 China Department Of Endocrinology Beijing Changping District Hosoital Beijing 102200 China Department of Endocrinology Chinese People's Liberation Army 252 Hospital Baoding Hebei 071000 China

Background Although the insulinotropic role of glucagon-like peptide-1 （GLP-1） in type 2 diabetes mellitus has been substantiated, its role in cardioprotection remains largely unknown. This study aimed to determine the effects of GLP-1 on injury of rats cardiac myocytes induced by hypoxia-reoxygenation （H/R） and the possible mechanisms. Methods The cultured neonatal rats cardiac myocytes were randomly divided into seven groups： the normal control group, the H/R group, the GLP-1＋H/R group, the GLP-1＋H/R＋UO126 （the p42/44 mitogen-activated protein kinase （mapK） inhibitor） group, the GLP-1＋H/R＋LY294002 （phosphatidylinositol 3-kinase （PI3K） inhibitor） group, the H/R＋UO126 group, and the H/R＋LY294002 group. The lactate dehydrogenase （LDH） activity, apoptosis rate of cardiac myocytes, and caspase-3 activity were detected after the injury of H/R. Results Compared with the normal control group, the activity of LDH, cardiac myocyte apoptosis rate, and caspase-3 activity all increased significantly in the H/R group （P 〈0.01）. Compared with the H/R group, these three indices all decreased in the H/R＋GLP-1 group （P 〈0.01）. However, the changes of LDH activity, apoptosis rate, and caspase-3 activity were inhibited by LY294002 and UO126 respectively. Conclusions GLP-1 can directly act on cardiac myocytes and protect them from H/R injury mainly by inhibiting their apoptosis. Its mechanism may be through the PI3K-Akt pathway and the mapK signaling pathway.

关键词： glucagon-like peptide-1 hypoxia-reoxygenation apoptosis caspase-3 map kinase PI3K/Akt

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Role of Tyrosine kinase Receptors in Growth Factor Mediated Signal Transduction, with Specific Reference to mapK/Rasand p13k-Akt Containing Pathways in Oncogenesis: A Qualitative Database Review

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American Journal of Molecular Biology 2022年第4期12卷 135-146页

作者： Chanjugaa Uthayakumar Rajavarthani Sanjeev Trincomalee Campus Eastern University Chenkaladi Sri Lanka Department of Human Biology Faculty of Health-Care Sciences Eastern University Chenkaladi Sri Lanka

Receptor Tyrosine kinases (RTKs) play a crucial role in the signal transduction pathways at cellular levels. RTK plays a vital role in cellular communication and transmission of signals to the adjacent cells and regulates different functions of the cell, such as cellular growth, differentiation, metabolism and motility. RTK s triggers growth factor receptors such as epidermal growth factor, insulin growth factor-1 receptor, platelet derived growth factor receptor, and fibro blast growth factor receptor and vascular endothelial growth factor receptor, thereby initiating and regulating cell growth and proliferation. mapK/RAS and PI3/AKT pathways are the major pathways of RTK’s function. Dysregulation of these RTK’s and pathways often leads to many diseases such as Noonan Syndrome, Logius Syndrome, CFC syndrome and different types of cancer. Point mutation and over expression of receptors and mutations in Ras leads to 30% of human cancers. Also over expression of different growth factor receptors by RTK too lead to several types of cancers as Glioblastoma, Thyroid cancer, Colon cancer and Non-small cell lung cancer. PTEN mutation in PI3/AKT pathway often leads to carcinoma relative to Thyroid, Skin, Large intestine, eye and Bone. Therefore, these RTK’s often used as targets for cancer therapies. The medical sector uses various types of small molecule tyrosine kinase inhibitors such as ATP competitive inhibitors, Allosteric inhibitors and covalent inhibitors which are known as Afatinib, Crizotinib, Eroltinib, Icotinib, Lepatinib and Lenvatinib in treatment and management of differential carcinomas.

关键词： Receptor Tyrosine kinase PI3/AKT map kinase PTEN Cancer Receptor Inhibitor

Function and interaction of maturation-promoting factor and mitogen-activated protein kinase during meiotic maturation and fertilization of oocyte

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Progress in Natural Science:Materials International 2004年第7期 10-15页

作者： HUO Lijun, FAN Hengyu, CHEN Dayuan and SUN Qingyuan*(State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100080, China)

Mitogen-activated protein kinase (map kinase) cascade and maturation-promoting factor (MPF) play very important roles during meiotic maturation and fertilization of oocyte. Interaction between map kinase and MPF influences meiotic maturation and fertilization of oocyte throughout the animal kingdom, including stimulation of germinal vesicle breakdown (GVBD), suppression of DNA replication, control of meiotic chromosome segregation, maintenance of metaphase II arrest, and resumption and completion of second meiosis. This review focuses on the function and interaction of map kinase and MPF during meiotic maturation and fertilization of oocyte.

关键词： oocyte meiosis fertilization map kinase MPF.