检索结果-内蒙古大学图书馆

Visna/maedi virus Env protein expressed by a vaccinia virus recombinant induces cell-to-cell fusion in cells of different origins in the apparent absence of Env cleavage:: role of glycosylation and of proteoglycans

引用

ARCHIVES OF VIROLOGY 2002年第12期147卷 2377-2392页

作者： Sánchez, AB Rodríguez, D Garzón, A Amorena, B Esteban, M Rodríguez, JR CSIC Ctr Nacl Biotecnol Dept Biol Celular & Mol E-28049 Madrid Spain SIA DGA Zaragoza Spain UPNA CSIC Inst Agrobiotecnol & Recursos Nat Pamplona Spain

The in vivo productive infection by the ovine Visna/maedi lentivirus (VISNA) is restricted to cells of the monocyte/macrophage lineage. The basis for this restriction is not understood. Although the VISNA envelope (Env) glycoprotein is the main target for virus neutralization, studies on the role of this protein in virus infection are limited. A vaccinia virus recombinant (VV-env-MV) containing the entire VISNA env sequence was generated and shown to produce in infected cells a protein of about 165 kDa (referred to as gp150). During VV-env-MV infection, expression of env caused extensive cell-to-cell fusion in cell lines of different origins. Pulse-chase and Western blot analyses revealed that gp150 is not cleaved in VV-env-MV infected cells. The glycoprotein gp150 formed oligomers held by disulfide bonding. Cell-to-cell fusion was prevented in the presence of the inhibitor of glycosilation, tunicamycin, but it was markedly enhanced by an inhibitor of proteoglycan synthesis, beta-D-xyloside. These findings showed that the receptor for VISNA Env is widely distributed within cells, that fusion-from-within of cells can occur in the apparent absence of proteolytic cleavage of gp150, and that fusion require a glycosylated Env but not the addition of proteoglycan chains at the cell surface. This recombinant virus could have utility as a potential vaccine against VISNA.

关键词： 3T3细胞抗病毒药/药理学巨细胞/病毒学糖苷类/药理学糖基化/药物作用 HeLa细胞 L细胞(细胞系) 分子量蛋白聚糖类/代谢再装配病毒/代谢重组蛋白质类/生物合成种特异性衣霉素/药理学痘苗病毒/代谢病毒包膜蛋白质类/生物合成病毒包膜蛋白质类/遗传学病毒包膜蛋白质类/代谢维士那-梅地病毒/化学维士那-梅地病毒/遗传学维士那-梅地病毒/代谢动物人类小鼠

来源：评论

学校读者我要写书评

暂无评论

The addition of bisecting N-acetylglucosamine residues to E-cadherin down-regulates the tyrosine phosphorylation of β-catenin

引用

JOURNAL OF BIOLOGICAL CHEMISTRY 2001年第1期276卷 475-480页

作者： Kitada, T Miyoshi, E Noda, K Higashiyama, S Ihara, H Matsuura, N Hayashi, N Kawata, S Matsuzawa, Y Taniguchi, N Osaka Univ Grad Sch Med Dept Biochem Suita Osaka 5650871 Japan Osaka Univ Grad Sch Med Dept Internal Med & Mol Sci Suita Osaka 5650871 Japan Osaka Univ Grad Sch Med Dept Mol Therapeut Suita Osaka 5650871 Japan Osaka Univ Fac Med Sch Allied Hlth Sci Dept Biochem Suita Osaka 5650871 Japan Osaka Univ Fac Med Sch Allied Hlth Sci Dept Pathol Suita Osaka 5650871 Japan

The enzyme GnT-III (beta1,4-N-acetylglucosaminyltransferase III) catalyzes the addition of a bisecting N-acetylglucosamine (GlcNAc) residue on glycoproteins. Our previous study described that the transfection of GnT-lll into mouse melanoma cells results in the enhanced expression of E-cadherin, which in turn leads to, the suppression of lung metastasis. It has recently been proposed that the phosphorylation of a tyrosine residue of beta -catenin is associated with cell migration. The present study reports on the importance of bisecting GlcNAc residues by GnT-III on tyrosine phosphorylation of beta -catenin using three types of cancer cell lines. An addition of bisecting GlcNAc residues to E-cadherin leads to an alteration in cell morphology and the localization of beta -catenin after epidermal growth factor stimulation. These changes are the result of a down-regulation in the tyrosine phosphorylation of beta -catenin, In addition, tyrosine phosphorylation of beta -catenin by transfection of constitutively active c-src was suppressed in GnT-III transfectants as well as in the case of epidermal growth factor stimulation. Treatment with tunicamycin abolished any differences in beta -catenin phosphorylation for the mock vis a vis the GnT-III transfectants. Thus, the addition of a specific N-glycan structure, the bisecting GlcNAc to E-cadherin-beta -catenin complex, down-regulates the intracellular signaling pathway, suggesting its implication in cell motility and the suppression of cancer metastasis.

关键词：乙酰葡萄糖胺/化学乙酰葡萄糖胺/遗传学乙酰葡萄糖胺/代谢印迹法蛋白质钙黏着糖蛋白类/化学钙黏着糖蛋白类/遗传学钙黏着糖蛋白类/代谢碳水化合物序列细胞大小/药物作用细胞支架蛋白质类/代谢酶激活表皮生长因子/药理学糖基化/药物作用显微镜检查荧光分子序列数据 N-乙酰氨基葡糖转移酶类/遗传学 N-乙酰氨基葡糖转移酶类/代谢磷酰化/药物作用磷酸酪氨酸/代谢 RNA 信使/代谢受体表皮生长因子/代谢重组融合蛋白质类/化学重组融合蛋白质类/代谢信号传导/药物作用反式激活因子类转染肿瘤细胞培养的衣霉素/药理学 β连环素 src族激酶类/遗传学动物小鼠

来源：评论

学校读者我要写书评

暂无评论

The phosphorylation state and expression of soybean BiP isoforms are differentially regulated following abiotic stresses

引用

JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第19期275卷 14494-14500页

作者： Cascardo, JCM Almeida, RS Buzeli, RAA Carolino, SMB Otoni, WC Fontes, EPB Univ Fed Vicosa Inst Biotecnol Aplicado Agropecuaria Dept Bioquim & Biol Mol BIOAGRODBB BR-36571000 Vicosa MG Brazil Univ Fed Vicosa Inst Biotecnol Aplicado Agropecuaria Dept Biol Vegetal BR-36571000 Vicosa MG Brazil

The mammalian BiP is regulated by phosphorylation, and it is generally accepted that its unmodified form constitutes the biologically active species. In fact, the glycosylation inhibitor tunicamycin induces dephosphorylation of mammalian BiP, The stress-induced phosphorylation state of plant BiP has not been examined, Here, we demonstrated that soybean BiP exists in interconvertible phosphorylated and nonphosphorylated forms, and the equilibrium can be shift to either direction in response to different stimuli. In contrast to tunicamycin treatment, water stress condition stimulated phosphorylation of BiP species in soybean cultured cells and stressed leaves. Despite their phosphorylation state, we demonstrated that BiP isoforms from water-stressed leaves exhibit protein binding activity, suggesting that plant BiP functional regulation may differ from other eukaryotic BiPs, We also compared the induction of the soybean BiP gene family, which consists of at least four members designated soyBiPA, soyBiPB, soyBiPC, and soyBiPD, by tunicamycin and osmotic stress. Although all soybean BiP genes were induced by tunicamycin, just the soyBiPA RNA was upregulated by osmotic stress. In addition, these stresses promoted BiP induction with different kinetics and acted synergistically to increase BiP accumulation. These results suggest that the soybean BiP gene family is differentially regulated by abiotic stresses through distinct signaling pathways.

关键词：拟南芥蛋白质类碱基序列载体蛋白质类/遗传学载体蛋白质类/代谢 DNA引物 DNA 互补基因表达调控植物磷酰化植物蛋白质类/遗传学植物蛋白质类/代谢蛋白质亚型/遗传学蛋白质亚型/代谢黄豆/药物作用黄豆/代谢衣霉素/药理学水

来源：评论

学校读者我要写书评

暂无评论

Caspase-12 mediates endoplasmic-reticulum-specific apoptosis and cytotoxicity by amyloid-β

引用

NATURE 2000年第6765期403卷 98-103页

作者： Nakagawa, T Zhu, H Morishima, N Li, E Xu, J Yankner, BA Yuan, JY Harvard Univ Sch Med Dept Cell Biol Boston MA 02115 USA RIKEN Inst Phys & Chem Res Biodesign Res Grp Wako Saitama 3510198 Japan Massachusetts Gen Hosp Cardiovasc Res Ctr Charlestown MA 02119 USA Harvard Univ Sch Med Dept Neurol Boston MA 02115 USA Childrens Hosp Boston MA 02115 USA

Apoptosis, or cellular suicide, is important for normal development and tissue homeostasis, but too much or too Little apoptosis can also cause disease(1,2). The family of cysteine proteases, the so-called caspases, are critical mediators of programmed cell death(3), and thus far 14 family members have been identified. Some of these, such as caspase-(8) (refs 4, 5), mediate signal transduction downstream of death receptors located on the plasma membrane. Others, such as caspase-9 (ref. 6), mediate apoptotic signals after mitochondrial damage. Stress in the endoplasmic reticulum (ER) can also result in apoptosis(7). Here we show that caspase-12 is localized to the ER and activated by ER stress, including disruption of ER calcium homeostasis and accumulation of excess proteins in ER, but not by membrane- or mitochondrial-targeted apoptotic signals. Mice that are deficient in caspase-12 are resistant to ER stress-induced apoptosis, but their cells undergo apoptosis in response to other death stimuli. Furthermore, we show that caspase-12-deficient cortical neurons are defective in apoptosis induced by amyloid-beta protein but not by staurosporine or trophic factor deprivation. Thus, caspase-12 mediates an ER-specific apoptosis pathway and may contribute to amyloid-beta neurotoxicity.

关键词：阿尔茨海默病/酶学阿尔茨海默病/病因学细胞凋亡半胱氨酸天冬氨酸蛋白酶12 半胱氨酸天冬氨酸蛋白酶/遗传学半胱氨酸天冬氨酸蛋白酶/代谢细胞培养的大脑皮质/细胞学大脑皮质/药物作用细胞毒素类/代谢细胞毒素类/毒性内质网/药物作用内质网/酶学酶激活 HeLa细胞肾/细胞学肾/药物作用小鼠基因敲除诱变神经元/生理学 PC12细胞胸腺/细胞学衣霉素/药理学动物人类小鼠大鼠

来源：评论

学校读者我要写书评

暂无评论

Maturation and pro-peptide cleavage of β-secretase

引用

JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第40期275卷 30849-30854页

作者： Capell, A Steiner, H Willem, M Kaiser, H Meyer, C Walter, J Lammich, S Multhaup, G Haass, C Univ Munich Adolf Butenandt Inst Dept Biochem Lab Alzheimers Dis Res D-80336 Munich Germany Univ Heidelberg Ctr Mol Biol ZMBH D-69120 Heidelberg Germany

Amyloid beta-peptide is generated by two sequential proteolytic cleavages mediated by beta-secretase (BACE) and gamma-secretase. PACE was recently identified as a membrane-associated aspartyl protease. We have now analyzed the maturation and pro-peptide cleavage of BACE. Pulse-chase experiments revealed that BACE is posttranslationally modified during transport to the cell surface, which can be monitored by a significant increase in the molecular mass. The increase in molecular mass is caused by complex N-glycosylation. Treatment with tunicamycin and N-glycosidase F led to a PACE derivative with a molecular weight corresponding to an unmodified version. In contrast, the mature form of BACE was resistant to endoglycosidase Il treatment. The cytoplasmic tail of PACE was required for efficient maturation and trafficking through the Golgi;a BACE variant lacking the cytoplasmic tail undergoes inefficient maturation. In contrast a soluble BACE variant that does not contain a membrane anchor matured more rapidly than full-length BACE. Pro-BACE was predominantly located within the endoplasmic reticulum, Propeptide cleavage occurred immediately before full maturation and trafficking through the Golgi.

关键词：酰胺基水解酶类/药理学淀粉样前体蛋白分泌酶类抗菌药/药理学天冬氨酸内肽酶类/化学天冬氨酸内肽酶类/代谢生物转运脑/代谢细胞系细胞膜/代谢克隆分子培养基条件性 DNA 互补/代谢内肽酶类内质网/代谢基因文库糖苷水解酶类/药理学糖基化高尔基体/代谢免疫组织化学显微镜检查荧光诱变定点肽-N4-(N-乙酰-β-葡糖胺)天冬酰胺酰胺酶肽类/代谢沉淀素试验蛋白质结构三级时间因素转染衣霉素/药理学人类

来源：评论

学校读者我要写书评

暂无评论

N-linked oligosaccharides on the meprin A metalloprotease are important for secretion and enzymatic activity, but not for apical targeting

引用

JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第33期275卷 25577-25584页

作者： Kadowaki, T Tsukuba, T Bertenshaw, GP Bond, JS Penn State Univ Coll Med Dept Biochem & Mol Biol Hershey PA 17033 USA

The alpha and beta subunits of meprins, mammalian zinc metalloendopeptidases, are extensively glycosylated;similar to 25% of the total molecular mass of the subunits is carbohydrate. The aim of this study was to investigate the roles of the N-linked oligosaccharides on the secreted form of mouse meprin A. Recombinant meprin cu and mutants in which one of the 10 potential Asn glycosylation sites was mutated to Can were all secreted and sorted exclusively into the apical medium of polarized Madin-Darby canine kidney cells, indicating that no specific N-linked oligosaccharide acts as a determinant for apical targeting of meprin rw. Several of the mutant proteins had decreased enzymatic activity using a bradykinin analog as substrate, and deglycosylation of the wildtype protein resulted in loss of 75-100% activity. Some of the mutants were also more sensitive to heat inactivation. In studies with agents that inhibit glycosylation processes in vivo, tunicamycin markedly decreased secretion of meprin, whereas castanospermine and swainsonine had little effect on secretion, sorting, or enzymatic properties of meprin, When all the potential glycosylation sites on a truncated form of meprin cy (alpha-(1-445)) were mutated, the protein was not secreted into the medium, but was retained within the cells even after 10 h. These results indicate that there is no one specific glycosylation site or type of oligosaccharide thigh mannose- or complex-type) that determines apical sorting, but that core N-linked carbohydrates are required for optimal enzymatic activity and for secretion of meprin alpha.

关键词：抗菌药/药理学天冬酰胺/化学缓激肽/类似物和衍生物布雷菲德菌素A/药理学细胞系秋水仙碱/药理学 DNA突变分析电泳聚丙烯酰氨凝胶酶抑制剂/药理学谷氨酰胺/化学糖苷水解酶类/代谢糖基化热免疫印迹法吲哚嗪类/药理学金属内肽酶类/化学金属内肽酶类/遗传学诱变定点寡糖类/拮抗剂和抑制剂寡糖类/化学质粒/代谢点突变蛋白质构象蛋白质合成抑制药/药理学重组蛋白质类/化学重组蛋白质类/代谢苦马豆素/药理学时间因素转染胰蛋白酶/代谢衣霉素/药理学动物狗人类小鼠

来源：评论

学校读者我要写书评

暂无评论

Herp, a new ubiquitin-like membrane protein induced by endoplasmic reticulum stress

引用

JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第42期275卷 32846-32853页

作者： Kokame, K Agarwala, KL Kato, H Miyata, T Natl Cardiovasc Ctr Res Inst Suita Osaka 5658565 Japan

Hyperhomocysteinemia, a risk factor for vascular disease, injures endothelial cells through undefined mechanisms. We previously identified several homocysteine-responsive genes in cultured human vascular endothelial cells, including the endoplasmic reticulum (ER)-resident molecular chaperone GRP78/BiP. Here, we demonstrate that homocysteine induces the ER stress response and leads to the expression of a novel protein, Herp, containing a ubiquitin-like domain at the N terminus. mRNA expression of Herp was strongly upregulated by inducers of ER stress, including mercaptoethanol, tunicamycin, A23187, and thapsigargin. The ER stress-dependent induction of Herp was also observed at the protein level. Immunochemical analyses using Herp-specific antibodies indicated that Herp is a 54-kDa, membrane-associated ER protein. Herp is the first integral membrane protein regulated by the ER stress response pathway. Both the N and C termini face the cytoplasmic side of the ER;this membrane topology makes it unlikely that Herp acts as a molecular chaperone for proteins in the ER, in contrast to GRP78 and other ER stress-responsive proteins. Herp may, therefore, play an unknown role in the cellular survival response to stress.

关键词：氨基酸序列碱基序列卡西霉素/药理学细胞培养的克隆分子内质网/药物作用内质网/生理学内皮血管/药物作用内皮血管/生理学基因表达调控/药物作用基因表达调控/生理学细胞内膜/生理学细胞内膜/超微结构膜蛋白质类/生物合成膜蛋白质类/化学膜蛋白质类/遗传学巯基乙醇/药理学分子序列数据蛋白质生物合成蛋白质构象 RNA 信使/遗传学重组蛋白质类/生物合成重组蛋白质类/化学序列比对序列同源性氨基酸毒胡萝卜内酯/药理学转录遗传/药物作用衣霉素/药理学泛素类/化学脐静脉动物人类小鼠

来源：评论

学校读者我要写书评

暂无评论

Sialomucin complex (rat Muc4) is regulated by transforming growth factor β in mammary gland by a novel post-translational mechanism

引用

JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第23期275卷 17800-17807页

作者： Price-Schiavi, SA Zhu, XY Aquinin, R Carraway, KL Univ Miami Sch Med Dept Cell Biol & Anat R124 Miami FL 33101 USA Univ Miami Sch Med Sylvester Comprehens Canc Ctr Miami FL 33101 USA

Sialomucin complex (SMC, rat Muc4) is a heterodimeric glycoprotein complex consisting of a mucin subunit ASGP-1 (for ascites sialoglycoprotein-1) and a transmembrane subunit ASGP-2, produced from a single gene and precursor. SMC expression is tightly regulated in mammary gland;the level in lactating mammary gland is about 100-fold that in virgin gland. In rat mammary epithelial cells, SMC is post-transcriptionally regulated by Matrigel by inhibition of SMC precursor synthesis. SMC is also posttranscriptionally regulated by transforming growth factor-beta (TGF beta), The repression of SMC expression by TGF beta is rapid, is independent of TGF beta-induced cell cycle arrest, and does not require new protein synthesis. Unlike Matrigel, TGF beta does not reduce SMC protein synthesis, as SMC precursor accumulation is equivalent in TGF beta-treated and untreated cells. Instead, SMC precursor in TGF beta-treated cells is more persistent and does not become processed as rapidly into mature ASGP-1 and ASGP-2, indicating that TGF beta disrupts processing of SMC precursor. These results indicate that SMC, a product of normal mammary gland and milk, is regulated by TGF beta by a novel post-translational mechanism. Thus, SMC is regulated by multiple posttranscriptional mechanisms, which serve to repress potential deleterious effects of overexpression.

关键词：细胞培养的共有序列放线菌酮/药理学上皮细胞/细胞学上皮细胞/代谢基因表达调控/生理学泌乳乳腺动物/细胞学乳腺动物/代谢乳房肿瘤实验性黏蛋白4 黏蛋白类/遗传学黏蛋白类/代谢蛋白质加工转译后/药物作用嘌呤霉素/药理学大鼠近交F344 唾液糖蛋白类/生物合成唾液糖蛋白类/遗传学转化生长因子β/药理学肿瘤细胞培养的衣霉素/药理学动物女(雌)性人类妊娠大鼠

来源：评论

学校读者我要写书评

暂无评论

Distinct domains within yeast Sec61p involved in post-translational translocation and protein dislocation

引用

JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第1期275卷 521-529页

作者： Wilkinson, BM Tyson, JR Reid, PJ Stirling, CJ Univ Manchester Sch Biol Sci Manchester M13 9PT Lancs England

The translocation of secretory polypeptides into and across the membrane of the endoplasmic reticulum (ER) occurs at the translocon, a pore-forming structure that orchestrates the transport and maturation of polypeptides at the ER membrane. Recent data also suggest that misfolded or unassembled polypeptides exit the ER via the translocon for degradation by the cytosolic ubiquitin/proteasome pathway. Sec61p is a highly conserved multispanning membrane protein that constitutes a core component of the translocon, We have found that the essential function of the Saccharomyces cerevisiae Sec61p is retained upon deletion of either of two internal regions that include transmembrane domains 2 and 3, respectively, However, a deletion mutation encompassing both of these domains was found to be nonfunctional, Characterization of yeast mutants expressing the viable deletion alleles of Sec61p has revealed defects in post-translational translocation. In addition, the transmembrane domain 3 deletion mutant is induced for the unfolded protein response and is defective in the dislocation of a misfolded ER protein. These data demonstrate that the various activities of Sec61p can be functionally dissected, In particular, the transmembrane domain 2 region plays a role in post-translational translocation that is required neither for cotranslational translocation nor for protein dislocation.

关键词：氨基酸序列生物转运二硫苏糖醇/药理学内质网真菌蛋白质类/代谢膜蛋白质类/遗传学膜蛋白质类/代谢膜转运蛋白质类分子序列数据突变表型蛋白质生物合成蛋白质变性蛋白质折叠蛋白质前体/代谢酿酒酵母菌酿酒酵母蛋白质类序列缺失衣霉素/药理学

来源：评论

学校读者我要写书评

暂无评论

Biosynthesis and post-translational processing of lectin-like oxidized low density lipoprotein receptor-1 (LOX-1) -: N-linked glycosylation affects cell-surface expression and ligand binding

引用

JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第9期275卷 6573-6579页

作者： Kataoka, H Kume, N Miyamoto, S Minami, M Murase, T Sawamura, T Masaki, T Hashimoto, N Kita, T Kyoto Univ Grad Sch Med Dept Geriatr Med Sakyo Ku Kyoto 6068507 Japan Kyoto Univ Grad Sch Med Dept Neurosurg Sakyo Ku Kyoto 6068507 Japan Natl Cardiovasc Ctr Res Inst Dept Biosci Osaka 5658565 Japan

LOX-1 (lectin-like oxidized low density lipoprotein receptor-1) is a type II membrane protein belonging to the C-type lectin family that can act as a cell-surface receptor for atherogenic oxidized low density lipoprotein (Ox-LDL) and may play crucial roles in atherogenesis. In this study, we show, by pulse-chase labeling and glycosidase digestion, that LOX-1 is synthesized as a 40-kDa precursor protein with N-linked high mannose carbohydrate chains (pre-LOX-1), which is subsequently further glycosylated and processed into the 48-kDa mature form within 40 min, Furthermore, when treated with an N-glycosylation inhibitor, tunicamycin, both tumor necrosis factor-alpha-activated bovine aortic endothelial cells and CHO-K1 cells stably expressing bovine LOX-1 (BLOX-1-CHO) exclusively produced a 32-kDa deglycosylated form of LOX-1, Cell enzyme-linked immunosorbent assay, flow cytometry, and immunofluorescence confocal microscopy demonstrated that the deglycosylated form of LOX-1 is not efficiently transported to the cell surface, but is retained in the endoplasmic reticulum or Golgi apparatus in tumor necrosis factor-alpha-activated bovine aortic endothelial cells, but not in BLOX-1-CHO cells. Radiolabeled Ox-LDL binding studies revealed that the deglycosylated form of LOX-1 expressed on the cell surface of BLOX-1-CHO cells has a reduced affinity for Ox-LDL binding, Taken together, N-linked glycosylation appears to play key roles in the cell-surface expression and ligand binding of LOX-1.

关键词：酰胺基水解酶类/代谢 CHO细胞细胞培养的仓鼠亚科内皮血管流式细胞术荧光抗体技术糖基化碘放射性同位素脂蛋白类 LDL/代谢肽-N4-(N-乙酰-β-葡糖胺)天冬酰胺酰胺酶蛋白质结合蛋白质前体/代谢蛋白质加工转译后受体 LDL/生物合成受体 LDL/代谢受体氧化LDL 清道夫受体 E类肿瘤坏死因子α/药理学衣霉素/药理学动物牛

来源：评论

学校读者我要写书评

暂无评论

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

请选择保存的检索档案：

请选择收藏分类：

通借通还

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：