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| 1 | Effect of phosphorylation of MAPK and Stat3 and expression of c-fos and c-jun proteins on hepatocarcinogenesis and their clinical significance显示文摘AIM To study the effect of phosphorylation ofMAPK and Stat3 and the expression of c-fos andc-jun proteins on hepatocellular carcinogenesisand their clinical significance.METHODS SP immunohistochemistry was usedto detect the expression of p42/44MAPK, p-Stat3,c-fos and c-jun proteins in 55 hepatocellularcarcinomas (HCC) and their surrounding livertissues.RESULTS The positive rates and expressionlevels of p42/44MAPK, p-Stat3, c-fos and c-junproteins in HCCs were significantly higher thanthose in pericarcinomatous liver tissues (PCLT).A positive correlation was observed between theexpression of p42/44MAPK and c-fos proteins, andbetween p-Stat3 and c-jun, but there was nosignificant correlation between p42/44MAPK and p-Stat3 in HCCs and their surrounding livertissues.CONCLUSION The abnormalities of Ras/Rat/MAPK and JAKs/ Stat3 cascade reaction maycontribute to malignant transformation ofhepatocytes. Hepatocytes which are positive forp42/ 44MAPK, c-fos or c-jun proteins may bepotential malignant pre-cancerous cells.Activation of MAPK and Stat3 proteins may be anearly event in hepatocellular carcinogenesis. | De Yun Feng Hui Zheng Yi Tan Rui Xue Cheng Department of Pathology, Hunan Medical University, Changsha 410078, Hunan Province, China New England Biolab, MA, USA | 2001 | World Journal of Gastroenterology2001，7，1： | 75 |
| 2 | Regulatory role of DREB transcription factors in plant drought, salt and cold tolerance显示文摘rd29A gene of Arabidopsis encodes a LEA-like hydrophilic protein, its expression is induced by drought, high-salt and cold stress. In the promoter region of rd29A gene, there are 2 ORE cis-acting elements involved in responses to these environmental stresses. 5 cDNAs (DREB1A-C and DREB2A-B) encoding DREB transcription factors, which specifically bind to ORE element and control the expression of reporter gene under drought, high-salt and stress, have been isolated by One-Hybrid screening method and with ORE element of rd29A promoter. DREB transcription factors and ORE element function in signal transduction of drought, high-salt and cold stress. One DREB transcription factor can control the expression of several target functional genes involved in plant tolerance to drought, high-salt and cold stress. Thus, it may be an effective strategy to achieve ideal, multiple and fundamental effect for improving plant stress-resistance by DREB gene transfer. | K.Yamaguch-Shinozaki K.Shinozaki | 2000 | Chinese Science Bulletin2000，45，11： | 34 |
| 3 | Suppression of P-gp induced multiple drug resistance in a drug resistant gastric cancer cell line by overexpression of Fas显示文摘AIM To observe the drug sensitizing effect andrelated mechanisms of fas gene transduction onhuman drug-resistant gastric cancer cellSGC7901/VCR(resistant to Vincristine).METHODS The cell cycle alteration wasobserved by FACS.The sensitivity of gastriccancer cells to apoptosis was determined by invitro apoptosis assay.The drug sensitization ofcells to several anti-tumor drugs was observedby MTT assay.Immunochemical method wasused to show expression of P-gp and Topo Ⅱ ingastric cancer cells.RESULTS Comparing to SGC7901 and pBK-SGC7901/VCR,fas-SGC7901/VCR showeddecreasing G2 cells and increasing S cells,theG2 phase fraction of pBK-SGC7901/VCR wasabout 3.0 times that of fas-SGC7901/VCR,but Sphase fraction of fas-SGC7901/VCR was about1.9 times that of pBK-SGC7901/VCR,indicatingS phase arrest of fas-SGC7901/VCR.FACS alsosuggested apoptosis of fas-SGC7901/VCR,fas-SGC7901/VCR was more sensitive to apoptosisinducing agent VM-26 than pBK-SGC7901/VCR.MTT assay showed increased sensitization offas-SGC7901/VCR to DDP,MMC and 5-FU,butsame sensitization to VCR according to pBK-SGC7901/VCR.SGC7901,pBK-SGC7901/ VCRand fas-SGC7901/VCR had positively stainedTopo Ⅱ equally.P-gp staining in pBK- SGC7901/VCR was stronger than in SG07901,but there was little staining of P-gp in fas.SGC7901/VCR.CONCLUSION fas gene transduction couldreverse the MDR of human drug-resistant gastriccancer cell SGC7901/VCR to a degree,possiblybecause of higher sensitization to apoptosis anddecreased expression of P-gp. | Yin F Shi YQ Zhao WP Xiao B Miao JY Fan DM | 2000 | World Journal of Gastroenterology2000，6，5： | 24 |
| 4 | Transduction of Fas gene or Bcl-2 antisense RNA sensitizes cultured drug resistant gastric cancer cells to chemotherapeutic drugs显示文摘INTRODUCTIONChemotherapyisoneofthemajormethodsintumortreatment,butitoftendoesnotworkduetomultidrugresistance(MDR).Recentstudi... | XIAO Bing, SHI Yong Quan, ZHAO Yan Qiu, YOU Han, WANG Zuo You, LIU Xian Ling, YIN Fang, QIAO Tai Dong and FAN Dai Ming | 1998 | World Journal of Gastroenterology1998，4，5： | 24 |
| 5 | Effect of vitamin E succinate on expression of TGF-β_1, c-Jun and JNK1 in human gastric cancer SGC-7901 cells显示文摘INTRODUCTIONVitamin E succinate (RRR-α-Tocopheryl Succinate,VES), a derivative of natural vitamin E, is acompound esterified by succinic acid and 6-hydroxyl-α-tocopheryl. | Kun Wu Bai He Liu Dan Yang Zhao Yan Zhao Department of Nutrition and Food Hygiene, School of Public Health, Harbin Medical University, Harbin 150001, Heilongjiang Province, China | 2001 | World Journal of Gastroenterology2001，7，1： | 17 |
| 6 | Plant protein kinase genes induced by drought, high salt and cold stresses显示文摘Drought, high salt and cold are three different kinds of environment stresses that severely influence the growth, development and productivity of crops. They all decrease the water state of plant cells, and consequently result in the harm of plant from water deficit. Several genes encoding protein kinases and induced by drought, high salt and low temperature have been isolated from Arabidopsis. These protein kinases include receptor protein kinase (RPK), MAP kinases, ribosomal-protein kinases and transcription-regulation protein kinase. The expression features of these genes and the regulatory roles of these protein kinases in stress response and signal transduction are discussed. | LIU Qiang , ZHANG Yong & Chen Shouyi1. Deparlmenl of Biological Science and Biotechnology, Tsinghua University, Beijing 100084, China 2. Department of Biological Science and Biotechnology, Slate Key Laboratory of Biomembrane and Membrane Biotechnology, Tsinghua University, Beijing 100084, China 3. Institute of Genetics, Chinese Academy of Sciences, Beijing 100101, China | 2000 | Chinese Science Bulletin2000，45，13： | 16 |
| 7 | TGF-β1 signal pathway in the regulation of inflammation in patients with atrial fibrillation显示文摘Objective:To observe the expression changes of inflammatory markers TGF-β1,Smad3 and IL-6 in patients with atrial fibrillation(AF),and to explore the significance of TGF-β1 signaling pathway in the structural remodeling of AF.Methods:The expression of TGF-β1,Smad3 and IL-6 in 50 cases with AF and 30 normal cases were detected by RT-PCR and ELISA.Results:The TGF-β1,Smad3 and IL-6 mRNA and protein expression levels in patients with AF were significantly higher than that in the control group(P<0.05),but there was no significantly different between the paroxysmal AF group and the persistent AF group(P>0.05).The TGF-β1mRNA expression in the≥50 years subgroup was significantly higher than that in the<50years subgroups,and it was higher in the NYHAⅢsubgroup than in theⅠ/Ⅱgrade subgroup.It was also higher in the left ventricular ejection fraction(LVEF)<50%subgroup than in LVEF≥50%group,and it was significantly higher in the AF time≥36 months subgroup than that in<36months subgroup(P<0.05).The Smad3 and IL-6 expressions in the in the LVEF<50%subgroup were both high that than that in LVEF≥50%group,and higher in the AF time≥36 months subgroup than that in<36 months subgroup(P<0.05).There were a positive correlation between TGF-β1,Smad3 and IL-6(r=0.687,r=0.547).There were also a positive correlation between Smad3 and IL-6 mRNA(r=0.823).Conclusions:AF is associated with inflammation,and the inflammation is also involved in the fibrillation and sustain of AF.The TGF-β1 signal pathway may be involved in the process of atrial structural remodeling in patients with AF,and iss related with the occurrence and maintenance of AF. | Ye Erbo lati.Ali Mira Muhuyati Wu-Hong Lu Peng-Yi He Zhi-Qiang Liu Yu-Chun Yang | 2013 | Asian Pacific Journal of Tropical Medicine2013，6，12： | 14 |
| 8 | The endocrine regulation network of growth hormone synthesis and secretion in fish: Emphasis on the signal integration in somatotropes显示文摘In teleosts, growth hormone (GH) production is governed by multiple neuroendocrine factors from the hypothalamus and other regulators from the pituitary and peripheral organs. Exploring the principles followed by pituitary somatotropes when differentiating and integrating the signals from these regulators at the cellular and intracellular level is essential for understanding the endocrine regulation network of growth hormone synthesis and secretion in fish. This paper discusses recent advances in the action mechanisms of GH regulation factors, including the neuroendocrine regulators, pituitary level factors and peripheral factors, primarily involved in their receptor systems as well as in post-receptor signal transduction pathways. | LI WenSheng & LIN HaoRan State Key Laboratory of Biocontrol, Institute of Aquatic Economic Animals and the Guangdong Provincial Key Laboratory for Aquatic Economic Animals, School of Life Sciences, Sun Yat-sen University, Guangzhou 510275, China | 2010 | Science China(Life Sciences)2010，53，4： | 11 |
| 9 | Modulation of the matrix redox signaling by mitochondrial Ca^(2+)显示文摘Mitochondria sense,shape and integrate signals,and thus function as central players in cellular signal transduction. Ca2+ waves and redox reactions are two such intracellular signals modulated by mitochondria. Mitochondrial Ca2+ transport is of utmost physio-pathological relevance with a strong impact on metabolism and cell fate. Despite its importance,the molecular nature of the proteins involvedin mitochondrial Ca2+ transport has been revealed only recently. Mitochondrial Ca2+ promotes energy metabolism through the activation of matrix dehydrogenases and downstream stimulation of the respiratory chain. These changes also alter the mitochondrial NAD(P)H/NAD(P)+ ratio,but at the same time will increase reactive oxygen species(ROS) production. Reducing equivalents and ROS are having opposite effects on the mitochondrial redox state,which are hard to dissect. With the recent development of genetically encoded mitochondrial-targeted redoxsensitive sensors,real-time monitoring of matrix thiol redox dynamics has become possible. The discoveries of the molecular nature of mitochondrial transporters of Ca2+ combined with the utilization of the novel redox sensors is shedding light on the complex relation between mitochondrial Ca2+ and redox signals and their impact on cell function. In this review,we describe mitochondrial Ca2+ handling,focusing on a number of newly identified proteins involved in mitochondrial Ca2+ uptake and release. We further discuss our recent findings,revealing how mitochondrial Ca2+ influences the matrix redox state. As a result,mitochondrial Ca2+ is able to modulate the many mitochondrial redox-regulated processes linked to normal physiology and disease. | Jaime Santo-Domingo Andreas Wiederkehr Umberto De Marchi | 2015 | World Journal of Biological Chemistry2015，6，4： | 11 |
| 10 | Identification of Conserved Cotton MicroRNAs and Their Targets显示文摘No study has been performed on identifying microRNAs(miRNAs) and their targets in cotton although cotton is one of the most important fiber and economic crops around the world.In this study, | ZHANG Bao-hong1,WANG Qing-lian2(1.Department of Biology,East Carolina University,Greenville,NC 27858,USA 2.Henan Institute of Science and Technology,Xinxiang,Henan 453003,China) | 2008 | 棉花学报2008，20，S1： | 10 |
| 11 | Upregulation of drug sensitivity of multidrug resistant SGC7901/VCR human gastric cancer cells by bax gene transduction显示文摘To investigate the role of bax in a vincristine (VCR) induced multidrug resistant (MDR) human gastric cancer cell line, SGC7901/VCR, in which the Bax protein expression level was significantly lower compared with that in parent cells Methods A bax eukaryotic expression vector was constructed and transfected into SGC7901/VCR cells by lipofectamine, and resistant clones were selected by G418 Western blotting detected Bax expression in transfectants Tetrazolium blue (MTT) assay evaluated the differences in drug sensitivity and cell cycle changes of transfectants were analyzed using flowcytometry (FCM) Results The bax eukaryotic expression vector was constructed and transfected into SGC7901/VCR cells Through G418 selection, resistant clones were obtained Western blotting demonstrated that the expression of Bax protein was markedly increased in bax transduced cells These cells were more sensitive to adriamycin (ADR) and VCR than mock vector transducted cells Moreover, bax transfection enhanced ADR induced apoptosis and VCR induced G 2/M phase arrest of SGC7901/VCR cells Conclusion Bax was involved in the MDR of SGC7901/VCR | 赵燕秋 肖冰 陈宝军 乔泰东 樊代明 | 2000 | Chinese Medical Journal2000，，11： | 10 |
| 12 | Knockout mouse models of insulin signaling: Relevance past and future显示文摘Insulin resistance is a hallmark of type 2 diabetes. In an effort to understand and treat this condition, re searchers have used genetic manipulation of mice to uncover insulin signaling pathways and determine the effects of their perturbation. After decades of research much has been learned, but the pathophysiology o insulin resistance in human diabetes remains contro versial, and treating insulin resistance remains a chal lenge. This review will discuss limitations of mouse models lacking select insulin signaling molecule genes In the most influential mouse models, glucose metabo lism differs from that of humans at the cellular, organ and whole-organism levels, and these differences limi the relevance and benefit of the mouse models both in terms of mechanistic investigations and therapeutic development. These differences are due partly to im mutable differences in mouse and human biology, and partly to the failure of genetic modifications to produce an accurate model of human diabetes. Several fac tors often limit the mechanistic insights gained from experimental mice to the particular species and strain including: developmental effects, unexpected meta bolic adjustments, genetic background effects, and technical issues. We conclude that the limitations and weaknesses of genetically modified mouse models of insulin resistance underscore the need for redirection of research efforts toward methods that are more directly relevant to human physiology. | Anne E Bunner P Charukeshi Chandrasekera Neal D Barnard | 2014 | World Journal of Diabetes2014，5，2： | 9 |
| 13 | Effects of estrogen on diverse stem cells and relevant intracellular mechanisms显示文摘Sexual dimorphism definitely exists in the pathogenesis of a variety of cardiovascular,neurodegenerative and bone metabolism disorders.Estrogen affects the healing of ischemic myocardium partially through paracrine growth hormone production by bone marrow mesenchymal stem cells(MSCs) and facilitation on mobilization of endothelial progenitors cells(EPCs) to the ischemic myocardium.Estrogen can also inhibit the proliferation of the cardiac fibroblasts.Therefore,estrogen effectively enhances the neovascularization at the ischemic border zone and limits pathological myocardial remodeling.Moreover,estrogen increases proliferation of embryonic neural stem cells and accelerates differentiation of neurons during neurogenesis,suggesting a possible role of estrogen in transplantation of neural stem cells as a therapeutic approach for neurodegenerative diseases.Finally,estrogen can modulate osteogenic progenitors and osteoclasts,preventing the osteoporosis.In general,estrogen offers significant benefits on diverse stem/progenitor cell populations.A great understanding of estrogens on these cells and relevant intracellular mechanisms will allow modulation of the potent stem cells directly for the ultimate clinical applications. | SUN HaiYing1,WANG HaiFeng2 & HU ShiYu1 1School of Pharmacy,Shanghai Jiao Tong University,Shanghai 200240,China 2First Affiliated Hospital,Henan University of Science and Technology,Luoyang 471003,China | 2010 | Science China(Life Sciences)2010，53，5： | 8 |
| 14 | Expression and function of leptin and its receptor in mouse mammary gland显示文摘Leptin is an autocrine and paracrine factor which affects the development of duct, formation of gland alveolus, expression of milk protein gene and onset involution of mammary gland. In order to know the function and mechanism of leptin in mammary gland, the protein expression and localization of leptin and its long form receptor (OB-Rb) were detected by a confocal laser scanning microscope. To study the impacts of leptin on mammary gland and leptin signal transduction pathway in pregnancy-, lacta-tion-and involution-stage mammary gland, explants were cultured and Western blotting was used. The results showed that in the whole development cycle of mammary gland, the expression of leptin and OB-Rb was in positive correlation. In virgin the leptin expression was the highest and then decreased in pregnancy. In lactation the expression of leptin was low and upgraded in involution, and recovered to the original level about virgin on involution 13 d. The localization of leptin and OB-Rb revealed that leptin induced the expression of OB-Rb specifically and controlled the development and physiological function of the mammary gland by binding to OB-Rb. In pregnancy stage, leptin stimulated proliferation and differentiation of ductal epithelial cells by JAK-MAPK signal pathway. In lactation, leptin induced gene expression of β-casein by JAK-STAT5 signal pathway, and in involution leptin induced mammary epithelial cell apoptosis and mammary gland restitution by JAK-STAT3 signal pathway. | LIN Ye LI QingZhang | 2007 | Science China(Life Sciences)2007，50，5： | 7 |
| 15 | Atorvastatin induces autophagy of mesenchymal stem cells underhypoxia and serum deprivation conditions by activating the mitogen-activated protein kinase/extracellular signal-regulatedkinase pathway显示文摘Background The survival ratio of implanted mesenchymal stem cells (MSCs) in the infarcted myocardium is low.Autophagy is a complex self-eating process and can be utilized for cell survival. We have found that atorvastatin (ATV)can effectively activate autophagy to enhance MSCs survival during hypoxia and serum deprivation (H/SD). The mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK/ERK) pathway is a non-canonical autophagy pathway.We hypothesized that the MEK/ERK pathway mediated ATV-induced autophagy of MSCs under H/SD. | | 2014 | Chinese Medical Journal2014，，6： | 7 |
| 16 | Regulation of mammalian pre-mRNA splicing显示文摘In eukaryotes,most protein-coding genes contain introns which are removed by precursor messenger RNA(pre-mRNA) splicing.Alternative splicing is a process by which multiple messenger RNAs(mRNAs) are generated from a single pre-mRNA,resulting in functionally distinct proteins.Recent genome-wide analyses of alternative splicing indicated that in higher eukaryotes alternative splicing is an important mechanism that generates proteomic complexity and regulates gene expression.Mis-regulation of splicing causes a wide range of human diseases.This review describes the current understanding of pre-mRNA splicing and the mechanisms that regulate mammalian pre-mRNA splicing.It also discusses emerging directions in the field of alternative splicing. | HUI JingYi State Key Laboratory of Molecular Biology,Institute of Biochemistry and Cell Biology,Shanghai Institutes for Biological Sciences,Chinese Academy of Sciences,Shanghai 200031,China | 2009 | Science China(Life Sciences)2009，52，3： | 6 |
| 17 | Emerging role of protein kinase C in energy homeostasis: A brief overview显示文摘Protein kinase C-β(PKCβ), a member of the lipidactivated serine/threonine PKC family, has been implicated in a wide range of important cellular processes. Very recently, the novel role of PKCβ in the regulation of triglyceride homeostasis via regulating mitochondrial function has been explored. In this review, I aim to provide an overview of PKCβ regarding regulation by lipids and recently gained knowledge on its role in energy homeostasis. Alterations in adipose PKCβ expression have been shown to be crucial for diet-induced obesity and related metabolic abnormalities. High-fat diet is shown to induce PKCβ expression in white adipose tissue in an isoform- and tissue-specific manner. Genetically manipulated mice devoid of PKCβ are lean with increased oxygen consumption and are resistant to high-fat diet-induced obesity and hepatic steatosis with improved insulin sensitivity. Available data support the model in which PKCβ functions as a 'diet-sensitive' metabolic sensor whose induction in adipose tissue by high-fat diet is among the initiating event disrupting mitochondrial homeostasis via intersecting with p66Shc signaling to amplify adipose dysfunction and have systemic consequences. Alterations in PKCβ expression and/orfunction may have important implications in health and disease and warrants a detailed investigation into the downstream target genes and the underlying mechanisms involved. Development of drugs that target the PKCβ pathway and identification of miRs specifically controlling PKCβ expression may lead to novel therapeutic options for treating age-related metabolic disease including fatty liver, obesity and type 2 diabetes. | Kamal D Mehta | 2014 | World Journal of Diabetes2014，5，3： | 6 |
| 18 | Immunomodulated signaling in macrophages: Studies on activation of Raf-1, MAPK, cPLA_2 and secretion of IL-12显示文摘Little is known about the mechanism and signal transduction by LPS-mediated immunomodulation of murine peritoneal macrophages. It is found that the signal molecules of the down-stream of Ras, Raf-1, MAPK p44, and MAPK p42 are phosphorylated, and cPLA2 is activated with a significant increase of the release of [ H3 ] AA by macrophages in response to LPS and PMA. Compared with the very recent finding that LPS and PMA trigger the activation and translocation of PKC-α and PKC-ε, these findings suggest that there is a connection between PKC signaling pathway and the Raf-1/MAPK pathway and that the activation of these main signaling events may be closely related to the secretion of IL-12 during LPS-induced modulation of macrophages. | 张宗梁 宋秋宝 林明群 丁跃梅 康小伟 姚錱 | 1997 | Science China(Life Sciences)1997，40，6： | 5 |
| 19 | Effect of emodin on mobility signal transduction system of gallbladder smooth muscle in Guinea pig with cholelithiasis显示文摘Objective: To study the effect of emodin on protein and gene expressions of the massagers in mobility signal transduction system of cholecyst smooth muscle cells in guinea pig with cholesterol calculus. Methods: The guinea pigs were randomly divided into 4 groups, such as control group, gall-stone(GS) group, emodin group and ursodesoxycholic acid(UA) group. Cholesterol calculus models were induced in guinea pigs of GS, emodin and UA groups of induced models by lithogenic diet, while emodin or UA were given to the corresponding group for 7 weeks. The histomorphological and ultrastructure change of gallbladder were detected by microscope and electron microscope, the content of plasma cholecystokinin(CCK) and [Ca^(2+)]i were analyzed successively by radioimmunoassay and flow cytometry. The protein and mR NA of Gsα, Giα and Cap in cholecyst cells were determined by western blotting and real time polymerase chain reaction(RT-PCR). Results: Emodin or UA can relieve pathogenic changes in epithelial cells and muscle cells in gallbladder of guinea pig with cholesterol calculus by microscope and transmission electron microscope. In the cholecyst cells of GS group, CCK levels in plasma and [Ca^(2+)]i decreased, the protein and m RNA of GS group were downregulated,the protein and m RNA of Gi and Cap were up-regulated. Emodin significantly decreased the formative rate of gallstone, improved the pathogenic change in epithelial cells and muscle cells, increased CCK levels in plasma and [Ca^(2+)]i in cholecyst cells, enhanced the protein and mR NA of Gs in cholecyst cells, reduced the protein and mR NA of Gi and Cap in cholecyst cells in guinea pig with cholesterol calculus. Conclusion: The dysfunction of gallbladder contraction gives rise to the disorders of mobility signal transduction system in cholecyst smooth muscle cells, including low content of plasma CCK and [Ca^(2+)]i in cholecyst cells, abnormal protein and mRNA of Gs, Gi and Cap. Emodin can enhance the contractibility of gallbladder and alleviate cholestasis by regulating plasma CCK levels, [Ca2+]i in cholecyst cells and the protein and mR NA of Gs, Gi and Cap. | Bang-Jiang Fang Jun-Yi Shen Hua Zhang Chuan-Zhu Lyu Yi-Qiang Xie Shuang Zhou | 2016 | Asian Pacific Journal of Tropical Medicine2016，9，10： | 5 |
| 20 | Protein kinase small molecule inhibitors for rheumatoid arthritis: Medicinal chemistry/clinical perspectives显示文摘Medicinal chemistry strategies have contributed to the development, experimental study of and clinical trials assessment of the first type of protein kinase small molecule inhibitor to target the Janus kinase/Signal Transducers and Activators of Transcription(JAK/STAT) signaling pathway. The orally administered small molecule inhibitor, tofacitinib, is the first drug to target the JAK/STAT pathway for entry into the armamentarium of the medical therapy of rheumatoid arthritis. The introduction of tofacitinib into general rheumatologic practice coupled with increasing understanding that additional cellular signal transduction pathways including the mitogen-activated protein kinase and phosphatidylinositide-3-kinase/Akt/mammalian target of rapa-mycin pathways as well as spleen tyrosine kinase also contribute to immune-mediated inflammatory in rheumatoid arthritis makes it likely that further development of orally administered protein kinase small molecule inhibitors for rheumatoid arthritis will occur in the near future. | Charles J Malemud David E Blumenthal | 2014 | World Journal of Orthopedics2014，5，4： | 5 |
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