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Identification of eight genes that are potentially involved in tamoxifen sensitivity in breast cancer cells

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cell Research 2005年第6期15卷 439-446页

作者： Tyler ZARUBIN department of Immunology The Scripps Research Institute 10550 north torrey pines road La Jolla CA 92037 USA

Although the antiestrogen agent tamoxifen has long been used to treat women with hormone receptor positive inva-sive breast carcinoma, the mechanisms of its action and acquired resistance to tamoxifen during treatment are largelyunknown. A number of studies have revealed that over-activation of some signaling pathways can cause tamoxifenresistance; however, very little information is available regarding the genes whose loss-of-function alternation contrib-ute to tamoxifen resistance. Here we used a forward genetic approach in vitro to generate tamoxifen resistant cells fromthe tamoxifen sensitive breast cancer cell line ZR-75-1, and further identified the disrupted gene in different tamoxifenresistant clones. Retinol binding protein 7, DNA polymerase-transactivated protein 3, γ-glutamyltransferase-like activity 1,slit-robo RhoGTPase-activating protein, tetraspan NET-4, HSPC194, amiloride-sensitive epithelial sodium channel gene,and Notch2, were the eight mutated genes identified in different tamoxifen resistant clones, suggesting their requirementfor tamoxifen sensitivity in ZR-75-1 cells. Since the functions of these genes are not related to each other, it suggeststhat multiple pathways can influence tamoxifen sensitivity in breast cancer cells.

关键词： tamoxifen breast cancer gene identification.

p38γ regulates UV-induced checkpoint signaling and repair of UV-induced DNA damage

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Protein & cell 2010年第6期1卷 573-583页

作者： Chia-Cheng Wu Xiaohua Wu Jiahuai Han Peiqing Sun department of Immunology and Microbial Science The Scripps Research Institute10550 N.Torrey Pines Road.La JollaCA 92037USA department of Molecular and Experimental Medicine The Scripps Research Institute10550 N.Torrey Pines Road.La JollaCA 92037USA Key Laboratory of Ministry of Education for cell biology and Tumor cell Engineering School of Life SciencesXiamen UniversityXiamen 361005China Dempartment of Molecular biology The Scripps Research Institute10550 N.Torrey Pines Road.La JollaCA 92037USA

In eukaryotic cells,DNA damage triggers activation of checkpoint signaling pathways that coordinate cell cycle arrest and repair of damaged *** DNA damage responses serve to maintain genome stability and prevent accumulation of genetic mutations and development of *** p38 MAPK was previously implicated in cellular responses to several types of DNA ***,the role of each of the four p38 isoforms and the mechanism for their involvement in DNA damage responses remained poorly *** this study,we demonstrate that p38γ,but not the other p38 isoforms,contributes to the survival of UV-treated *** of p38γsensitizes cells to UV exposure,accompanied by prolonged S phase cell cycle arrest and increased rate of *** investigation reveal that p38γis essential for the optimal activation of the checkpoint signaling caused by UV,and for the efficient repair of UVinduced DNA *** findings have established a novel role of p38γin UV-induced DNA damage responses,and suggested that p38γcontributes to the ability of cells to cope with UV exposure by regulating the checkpoint signaling pathways and the repair of damaged DNA.

关键词： p38γ DNA damage UV DNA repair checkpoint signaling

Activation and signaling of the p38 MAP kinase pathway

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cell Research 2005年第1期15卷 11-18页

作者： Tyler ZARUBIN La Jolla USA department of Immunology 10550 N. torrey pines road The Scripps Research Institute CA 92037

The family members of the mitogen-activated protein (MAP) kinases mediate a wide variety of cellular behaviors in response to extracellular stimuli. One of the four main sub-groups, the p38 group of MAP kinases, serve as a nexus for signal transduction and play a vital role in numerous biological processes. In this review, we highlight the known characteristics and components of the p38 pathway along with the mechanism and consequences of p38 activation. We focus on the role of p38 as a signal transduction mediator and examine the evidence linking p38 to inflammation, cell cycle, cell death, development, cell differentiation, senescence and tumorigenesis in specific cell types. Upstream and downstream components of p38 are described and questions remaining to be answered are posed. Finally, we propose several directions for future research on p38.

关键词： p38 MAP kinase signaling pathway nexus inflammation differentiation senescence tumorigenesis.

PD-L1 expression is regulated by ATP-binding of the ERBB3 pseudokinase domain

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Genes & Diseases 2023年第4期10卷 1702-1713页

作者： Yamu Li Zhonghua Liu Yiqing Zhao Jie Yang Tsan Sam Xiao Ronald A.Conlon Zhenghe Wang department of Genetics and Genome Sciences Case Western Reserve UniversityClevelandOH 44106USA Case Comprehensive Cancer Center Case Western Reserve UniversityClevelandOH 44106USA department of Pathology Case Western Reserve UniversityClevelandOH 44106USA department of Physiology and Biophysics Case Western Reserve UniversityClevelandOH 44106USA department of Integrative Structural and Computational biology The Scripps Research Institute10550 North Torrey Pines RdTRY-21La JollaCA 92037USA.

How PD-L1 expression is regulated in cancer is poorly ***,we report that the ATP-binding activity of ERBB3 pseudokinase regulates PD-L1 gene expression in colorectal cancers(CRCs).ERBB3 is one of the four members of the EGF receptor family,all with protein tyrosine kinase ***3 is a pseudokinase with a high binding affin-ity to *** showed that ERBB3 ATP-binding inactivation mutant reduces tumorigenicity in genetically engineered mouse models and impairs xenograft tumor growth of CRC cell *** ERBB3 ATP-binding mutant cells dramatically reduce IFN-g-induced PD-L1 ***,ERBB3 regulates IFN-g-induced PD-L1 expression through the IRS1-PI3K-PDK1-RSK-CREB signaling *** is the transcription factor that regulates PD-L1 gene expression in CRC *** of a tumor-derived ERBB3 mutation located in the ki-nase domain sensitizes mouse colon cancers to anti-PD1 antibody therapy,suggesting that ERBB3 mutations could be predictive biomarkers for tumors amenable to immune check-point therapy.

关键词： Colon cancer ERBB3 Immunotherapy PD-L1 Pseudokinase

Shape Selectivity of a Metallo Cavitand Host Allows Separation of n-Alkanes from Isooctane

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Chinese Journal of Chemistry 2021年第6期39卷 1498-1502页

作者： Yun-Hui Wan Faiz-Ur Rahman Julius Rebek Jr. Yang Yu Center for Supramolecular Chemistry&Catalysis and department of Chemistry College of ScienceShanghai University99 Shang-Da RoodShanghai 200444China Skaggs Institute for Chemical biology and department of Chemistry The Scripps Research Institute10550 North Torrey Pines Roadio JolloCA 92037USA

The use of a metallo cavitand for the selective sequestration of n-alkanes from their mixtures with isooctane is *** experiments and NMR spectroscopy are used to show the preference of a water-soluble cavitand host for guests that are hydro-phobic and have narrow or flat *** host showed selectivity for trans 1,4-dimethylcyclohexane over the *** sep-arations of n-alkanes from isooctane by gas/liquid adsorption and a liquid/liquid extraction are detailed.

关键词： Metallo cavitand Shape selectivity eceptor Alkane separation Host-guest system

The JCIMPT - Innovative New Technologies for Membrane Protein Structural biology

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The JCIMPT - Innovative New Technologies for Membrane Protei...

In vitro derivation of functional insulin-producing cells from human embryonic stem cells

The 4th ISGO International Conference on Structural Genomics

作者： Raymond C.Stevens Peter Kuhn Geoffrey Chang Kurt Wüthrich Mark Yeager M.G.Finn department of Molecular biology10550 north torrey pines road La JollaCA 92037USA Department of Chemistry The Scripps Research Institute 10550 North Torrey Pines RoadLa JollaCA 92037USA department of cell biology 10550 north torrey pines road La JollaCA 92037USA department of Molecular biology 10550 north torrey pines road La JollaCA 92037USA department of Molecular biology 10550 north torrey pines road La JollaCA 92037USA Department of Chemistry The Scripps Research Institute10550 North Torrey Pines RoadLa JollaCA 92037USA department of cell biology 10550 north torrey pines road La JollaCA 92037 USA department of Chemistry The Scripps Research Institute 10550 north torrey pines road La JollaCA 92037 USA

＜正＞The mission of the Joint Center for Innovative Membrane Protein Technologies （JCIMPT;http://***） is to develop and disseminate methods and technologies for structure-grade production and stabilization of integral membrane proteins. Miniaturization and automation are major components in the systematic investigation of membrane proteins and in the development of novel genetically engineered expression systems and sample preparation technologies.

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来源： cnki会议评论

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cell Research 2007年第4期17卷 333-344页

作者： Wei Jiang~(1,*) Yan Shi~(1,5,*) Dongxin Zhao~1 Song Chen~1 Jun Yong~1 Jing Zhang~2 Tingting Qing~1 Xiaoning Sun~(1,3) Peng Zhang~1 Mingxiao Ding~1 Dongsheng Li~4 Hongkui Deng~(1,2,3) ~1department of cell biology and Genetics,College of Life Sciences,Peking University,Beijing 100871,China ~2Beijing Laboratory Animals Research Center,Beijing 100012,China ~3Laboratory of Chemical Genomics,Shenzhen Graduate School of Peking Universit,the University Town,Shenzhen 518055,China ~4provincial Kev Laboratory of Embryonic Stem cell Research,Tai-He Hospital Yunyang Medical College,32 S.Renmin Rd.,Shiyan 442000,China department of cell biology and Genetics College of Life Sciences Peking University Beijing China 5Present address: The Scripps Research Institute Chemistry Department SP3130 10550 North Torrey Pines Road La Jolla CA USA. Beijing Laboratory Animals Research Center Beijing China Laboratory of Chemical Genomics Shenzhen Graduate School of Peking University the University Town Shenzhen China Provincial Key Laboratory of Embryonic Stem cell Research Tai-He Hospital Yunyang Medical College Shiyan China

The capacity for self-renewal and differentiation of human embryonic stem(ES)cells makes them a potential source forgeneration of pancreatic beta cells for treating type I diabetes ***,we report a newly developed and effectivemethod,carried out in a serum-free system,which induced human ES cells to differentiate into insulin-producing *** A was used in the initial stage to induce definitive endoderm differentiation from human ES cells,as detectedby the expression of the definitive endoderm markers Sox 17 and ***,all-trans retinoic acid(RA)wasused to promote pancreatic differentiation,as indicated by the expression of the early pancreatic transcription factorspdr1 and *** maturation in DMEM/F12 serum-free medium with bFGF and nicotinamide,the differentiatedcells expressed islet specific markers such as C-peptide,insulin,glucagon and *** percentage of C-peptide-posi-tive cells exceeded 15%.The secretion of insulin and C-peptide by these cells corresponded to the variations in *** transplanted into renal capsules of Streptozotocin(STZ)-treated nude mice,these differentiated human EScells survived and maintained the expression of beta cell marker genes,including C-peptide,pdx1,glucokinase,nkx6.1,IAPP,pax6 and *** percent of the transplanted nude mice exhibited apparent restoration of stable euglycemia;and the corrected phenotype was sustained for more than six *** new method provides a promising in vitro dif-ferentiation model for studying the mechanisms of human pancreas development and illustrates the potential of usinghuman ES cells for the treatment of type I diabetes mellitus.

关键词： human embryonic stem cell direct differentiation insulin-producing cell diabetes

铁硫蛋白活性中心铁硫簇的对称性破缺密度泛函计算

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化学学报 2000年第12期58卷 1529-1533页

作者：黎健 department of Chemistry and Biophysics Texas Biotechnology Corporation7000 Fannin StreetHoustonTexas 77030 USA and Department of Molecular Biology TPC-15The Scripps Research Institute10550 N.Torrey Pines RoadLa JollaCalifornia 92037U.S.A.

应用密度泛函方法(DFT)计算了铁硫金属蛋白中的铁硫簇[Fe_2S_2(SCH_3)_4]^()2-,[Fe_3S_4(SCH_3)_3]^(2-)以及[Fe_4S_4(SCH_3)_4]^(2-)的几何参数和磁偶合性质.采用对称性破缺态(BS)来描述Fe—Fe自旋偶合.计算结果表明:采用高自旋态(HS)计算的Fe—Fe间距与实验值有较大偏差,而由BS方法所计算的Fe—Fe间距与晶体结构测定数据相吻合.根据HS态和BS态的能量,计算了体系的海森堡偶合参数J,计算结果也较为接近实验估算值.

关键词：密度泛函理论铁硫簇自旋偶合铁硫蛋白金属酶

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AMPD3 is involved in anthrax LeTx-induced macrophage cell death

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Protein & cell 2011年第7期2卷 564-572页

作者： Sangun Lee Yanhai Wang Sung Ouk Kim Jiahuai Han department of Immunology and Microbial Science The Scripps Research Institute10550 North Torrey Pine RoadLa JollaCA 92037USA The State Key Laboratory of cellular Stress biology School of Life SciencesXiamen UniversityXiamen 361005China Current address department of Biomedical Sciences Tufts UniversityCummings School of Veterinary MedicineNorth GraftonMassachusetts 01536USA Current address department of Microbiology and Immunology Siebens-Drake Research InstituteUniversity of Western OntarioLondonOntarioCanada

The responses of macrophages to Bacillus anthracis infection are important for the survival of the host,since macrophages are required for the germination of *** spores in lymph nodes,and macrophage death exacerbates anthrax lethal toxin(LeTx)-induced organ *** elucidate the mechanism of macrophage cell death induced by LeTx,we performed a genetic screen to search for genes associated with LeTx-induced macrophage cell ***264.7 cells,a macrophage-like cell line sensitive to LeTx-induced death,were randomly mutated and LeTx-resistant mutant clones were *** deaminase 3(AMPD3),an enzyme that converts AMP to IMP,was identified to be mutated in one of the resistant *** requirement of AMPD3 in LeTxinduced cell death of RAW 264.7 cells was confirmed by the restoration of LeTx sensitivity with ectopic reconstitution of AMPD3 ***3 deficiency does not affect LeTx entering cells and the cleavage of mitogen-activated protein kinase kinase(MKK)by lethal factor inside cells,but does impair an unknown downstream event that is linked to cell *** data provides new information regarding LeTx-induced macrophage death and suggests that there is a key regulatory site downstream of or parallel to MKK cleavage that controls the cell death in LeTx-treated macrophages.

关键词： AMP deaminase 3 anthrax lethal toxin macrophage cell death