Molecular Membrane Biology最新文献

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Comparison between MassARRAY and pyrosequencing for CYP2C19 and ABCB1 gene variants of clopidogrel efficiency genotyping. 氯吡格雷效率基因分型CYP2C19和ABCB1基因变异的MassARRAY和焦磷酸测序比较
Molecular Membrane Biology Pub Date : 2019-12-01 DOI: 10.1080/09687688.2019.1597194
Juan Liu, Zesheng Xu, Ya Li, Shipeng Dai, Junying Liu, Junjun Pan, Yang Jiang
{"title":"Comparison between MassARRAY and pyrosequencing for CYP2C19 and ABCB1 gene variants of clopidogrel efficiency genotyping.","authors":"Juan Liu,&nbsp;Zesheng Xu,&nbsp;Ya Li,&nbsp;Shipeng Dai,&nbsp;Junying Liu,&nbsp;Junjun Pan,&nbsp;Yang Jiang","doi":"10.1080/09687688.2019.1597194","DOIUrl":"https://doi.org/10.1080/09687688.2019.1597194","url":null,"abstract":"<p><p>Clopidogrel is one of the most frequently used drugs in patients to reduce cardiovascular events. Since patients with different genetic variations respond quite differently to clopidogrel therapy, the related genetic testing plays a vital role in its dosage and genetic testing related to clopidogrel therapy is currently considered as routine test worldwide. In this study, we aim to use two different methods MALDI-TOF mass spectrometry and pyrosequencing to detect gene variant of CYP2C19 and ABCB1. Six single nucleotides polymorphisms (SNP) within CYP2C19 (*2, *3, *4, *5, *17) and ABCB1 C3435T in 458 Chinese Han patients were determined using both MassARRAY and Pyrosequencing. Sanger sequencing was used for verification. Results of both methods were analyzed and compared. Allele frequencies of each SNP and distribution of different genotypes were calculated based on the MassARRAY and Sanger sequencing results. Both methods provided 100% call rates for gene variants, while results of six samples were different with two methods. With Sanger sequencing as the reference results, MassARRAY generated all the same results. The minor allele frequencies of the above six SNPs were 27.1% (CYP2C19*), 5.9% (CYP2C19*3), 0% (CYP2C19*4), 0% (CYP2C19*5), 1.1% (CYP2C19*17), 40.9% (ABCB1), respectively. MassARRAY provides accurate clopidogrel related genotyping with relatively high cost-efficiency, throughput and short time when compared with pyrosequencing.</p>","PeriodicalId":18858,"journal":{"name":"Molecular Membrane Biology","volume":"35 1","pages":"1-8"},"PeriodicalIF":0.0,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/09687688.2019.1597194","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37270186","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 10
Zinc uptake in the Basidiomycota: Characterization of zinc transporters in Ustilago maydis. 担子菌门对锌的吸收:玉米黑鱼体内锌转运蛋白的特性。
Molecular Membrane Biology Pub Date : 2019-12-01 DOI: 10.1080/09687688.2019.1667034
Adriana M Martha-Paz, David Eide, David Mendoza-Cózatl, Norma A Castro-Guerrero, Elva T Aréchiga-Carvajal
{"title":"Zinc uptake in the Basidiomycota: Characterization of zinc transporters in <i>Ustilago maydis</i>.","authors":"Adriana M Martha-Paz,&nbsp;David Eide,&nbsp;David Mendoza-Cózatl,&nbsp;Norma A Castro-Guerrero,&nbsp;Elva T Aréchiga-Carvajal","doi":"10.1080/09687688.2019.1667034","DOIUrl":"https://doi.org/10.1080/09687688.2019.1667034","url":null,"abstract":"Abstract At present, the planet faces a change in the composition and bioavailability of nutrients. Zinc deficiency is a widespread problem throughout the world. It is imperative to understand the mechanisms that organisms use to adapt to the deficiency of this micronutrient. In the Ascomycetes fungi, the ZIP family of proteins is one of the most important for zinc transport and includes high affinity Zrt1p and low zinc affinity Zrt2p transporters. After identification and characterization of ZRT1/ZRT2-like genes in Ustilago maydis we conclude that they encode for high and low zinc affinity transporters, with no apparent iron transport activity. These conclusions were supported by the gene deletion in Ustilago and the functional characterization of ZRT1/ZRT2-like genes by measuring the intracellular zinc content over a range of zinc availability. The functional complementation of the S. cerevisiae ZRT1Δ ZRT2Δ mutant with U. maydis genes supports this as well. U. maydis ZRT2 gene, was found to be regulated by pH through Rim101 pathway, thus providing novel insights into how this Basidiomycota fungus can adapt to different levels of Zn availability.","PeriodicalId":18858,"journal":{"name":"Molecular Membrane Biology","volume":"35 1","pages":"39-50"},"PeriodicalIF":0.0,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/09687688.2019.1667034","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41205518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 11
The KdpFABC complex - K+ transport against all odds. KdpFABC复合物- K+输运克服了重重困难。
Molecular Membrane Biology Pub Date : 2019-12-01 DOI: 10.1080/09687688.2019.1638977
Bjørn P Pedersen, David L Stokes, Hans-Jürgen Apell
{"title":"The KdpFABC complex - K<sup>+</sup> transport against all odds.","authors":"Bjørn P Pedersen,&nbsp;David L Stokes,&nbsp;Hans-Jürgen Apell","doi":"10.1080/09687688.2019.1638977","DOIUrl":"https://doi.org/10.1080/09687688.2019.1638977","url":null,"abstract":"<p><p>In bacteria, K<sup>+</sup> is used to maintain cell volume and osmotic potential. Homeostasis normally involves a network of constitutively expressed transport systems, but in K<sup>+</sup> deficient environments, the KdpFABC complex uses ATP to pump K<sup>+</sup> into the cell. This complex appears to be a hybrid of two types of transporters, with KdpA descending from the superfamily of K<sup>+</sup> transporters and KdpB belonging to the superfamily of P-type ATPases. Studies of enzymatic activity documented a catalytic cycle with hallmarks of classical P-type ATPases and studies of ion transport indicated that K<sup>+</sup> import into the cytosol occurred in the second half of this cycle in conjunction with hydrolysis of an aspartyl phosphate intermediate. Atomic structures of the KdpFABC complex from X-ray crystallography and cryo-EM have recently revealed conformations before and after formation of this aspartyl phosphate that appear to contradict the functional studies. Specifically, structural comparisons with the archetypal P-type ATPase, SERCA, suggest that K<sup>+</sup> transport occurs in the first half of the cycle, accompanying formation of the aspartyl phosphate. Further controversy has arisen regarding the path by which K<sup>+</sup> crosses the membrane. The X-ray structure supports the conventional view that KdpA provides the conduit, whereas cryo-EM structures suggest that K<sup>+</sup> moves from KdpA through a long, intramembrane tunnel to reach canonical ion binding sites in KdpB from which they are released to the cytosol. This review discusses evidence supporting these contradictory models and identifies key experiments needed to resolve discrepancies and produce a unified model for this fascinating mechanistic hybrid.</p>","PeriodicalId":18858,"journal":{"name":"Molecular Membrane Biology","volume":"35 1","pages":"21-38"},"PeriodicalIF":0.0,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/09687688.2019.1638977","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37379409","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 17
BKCa channel is a molecular target of vitamin C to protect against ischemic brain stroke. BKCa通道是维生素C预防缺血性脑卒中的分子靶点。
Molecular Membrane Biology Pub Date : 2019-12-01 DOI: 10.1080/09687688.2019.1608378
Luyao Li, Shan Li, Chuanbing Hu, Li Zhou, Yujiao Zhang, Mingyan Wang, Zhi Qi
{"title":"BK<sub>Ca</sub> channel is a molecular target of vitamin C to protect against ischemic brain stroke.","authors":"Luyao Li,&nbsp;Shan Li,&nbsp;Chuanbing Hu,&nbsp;Li Zhou,&nbsp;Yujiao Zhang,&nbsp;Mingyan Wang,&nbsp;Zhi Qi","doi":"10.1080/09687688.2019.1608378","DOIUrl":"https://doi.org/10.1080/09687688.2019.1608378","url":null,"abstract":"<p><p>Epidemiological studies have demonstrated that vitamin C decreases the risk of stroke, which has generally been ascribed to its function as antioxidant and free radical scavenger. However, whether there is a defined molecular target for vitamin C on stroke is unknown. Utilizing middle cerebral artery occlusion (MCAO) in rats as a model for ischemic stroke, we demonstrated that long-term, low-dose administration of vitamin C prior to MCAO could exert significant neuroprotective effect on the brain damage. The long-term, low-dose vitamin C pretreated rats had decreased brain infarct size and decreased neurological deficit score compared with the vehicle or single high dose pretreated MCAO rats. Furthermore, electrophysiological experiments using patch clamp technique showed that vitamin C increased the whole-cell current of the large-conductance Ca<sup>2+</sup>-activated K<sup>+</sup> (BK<sub>Ca</sub>) channel. Moreover, vitamin C increased the open probability of the channel without change its amplitude. Importantly, blockade of the BK<sub>Ca</sub> channels abolished the neuroprotective effect of vitamin C on MCAO. Therefore, this study shows that long-term, low-dose pretreatment with vitamin C could reduce MCAO-induced brain damage through activation of the BK<sub>Ca</sub> channels, suggesting that the BK<sub>Ca</sub> channel is a molecular target of vitamin C on stroke.</p>","PeriodicalId":18858,"journal":{"name":"Molecular Membrane Biology","volume":"35 1","pages":"9-20"},"PeriodicalIF":0.0,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/09687688.2019.1608378","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37320888","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 9
Correction. 修正。
Molecular Membrane Biology Pub Date : 2019-12-01 DOI: 10.1080/09687688.2020.1829809
{"title":"Correction.","authors":"","doi":"10.1080/09687688.2020.1829809","DOIUrl":"https://doi.org/10.1080/09687688.2020.1829809","url":null,"abstract":"","PeriodicalId":18858,"journal":{"name":"Molecular Membrane Biology","volume":"35 1","pages":"86"},"PeriodicalIF":0.0,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/09687688.2020.1829809","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38464685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Potassium channels and their role in glioma: A mini review. 钾离子通道及其在胶质瘤中的作用:综述。
Molecular Membrane Biology Pub Date : 2019-12-01 DOI: 10.1080/09687688.2020.1729428
Jia Liu, Chao Qu, Chao Han, Meng-Meng Chen, Li-Jia An, Wei Zou
{"title":"Potassium channels and their role in glioma: A mini review.","authors":"Jia Liu,&nbsp;Chao Qu,&nbsp;Chao Han,&nbsp;Meng-Meng Chen,&nbsp;Li-Jia An,&nbsp;Wei Zou","doi":"10.1080/09687688.2020.1729428","DOIUrl":"https://doi.org/10.1080/09687688.2020.1729428","url":null,"abstract":"<p><p>K<sup>+</sup> channels regulate a multitude of biological processes and play important roles in a variety of diseases by controlling potassium flow across cell membranes. They are widely expressed in the central and peripheral nervous system. As a malignant tumor derived from nerve epithelium, glioma has the characteristics of high incidence, high recurrence rate, high mortality rate, and low cure rate. Since glioma cells show invasive growth, current surgical methods cannot completely remove tumors. Adjuvant chemotherapy is still needed after surgery. Because the blood-brain barrier and other factors lead to a lower effective concentration of chemotherapeutic drugs in the tumor, the recurrence rate of residual lesions is extremely high. Therefore, new therapeutic methods are needed. Numerous studies have shown that different K<sup>+</sup> channel subtypes are differentially expressed in glioma cells and are involved in the regulation of the cell cycle of glioma cells to arrest them at different stages of the cell cycle. Increasing evidence suggests that K<sup>+</sup> channels express in glioma cells and regulate glioma cell behaviors such as cell cycle, proliferation and apoptosis. This review article aims to summarize the current knowledge on the function of K<sup>+</sup> channels in glioma, suggests K<sup>+</sup> channels participating in the development of glioma.</p>","PeriodicalId":18858,"journal":{"name":"Molecular Membrane Biology","volume":"35 1","pages":"76-85"},"PeriodicalIF":0.0,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/09687688.2020.1729428","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37651874","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 16
Spatial organization of palmitoyl acyl transferases governs substrate localization and function. 棕榈酰转移酶的空间组织决定了底物定位和功能。
Molecular Membrane Biology Pub Date : 2019-12-01 DOI: 10.1080/09687688.2019.1710274
Julie M Philippe, Paul M Jenkins
{"title":"Spatial organization of palmitoyl acyl transferases governs substrate localization and function.","authors":"Julie M Philippe,&nbsp;Paul M Jenkins","doi":"10.1080/09687688.2019.1710274","DOIUrl":"https://doi.org/10.1080/09687688.2019.1710274","url":null,"abstract":"<p><p>Protein palmitoylation is a critical posttranslational modification that regulates protein trafficking, localization, stability, sorting and function. In mammals, addition of this lipid modification onto proteins is mediated by a family of 23 palmitoyl acyl transferases (PATs). PATs often palmitoylate substrates in a promiscuous manner, precluding our understanding of how these enzymes achieve specificity for their substrates. Despite generous efforts to identify consensus motifs defining PAT-substrate specificity, it remains to be determined whether additional factors beyond interaction motifs, such as local palmitoylation, participate in PAT-substrate selection. In this review, we emphasize the role of local palmitoylation, in which substrates are palmitoylated and trapped in the same subcellular compartments as their PATs, as a mechanism of enzyme-substrate specificity. We focus here on non-Golgi-localized PATs, as physical proximity to their substrates enables them to engage in local palmitoylation, compared to Golgi PATs, which often direct trafficking of their substrates elsewhere. PAT subcellular localization may be an under-recognized, yet important determinant of PAT-substrate specificity that may work in conjunction or completely independently of interaction motifs. We also discuss some current hypotheses about protein motifs that contribute to localization of non-Golgi-localized PATs, important for the downstream targeting of their substrates.</p>","PeriodicalId":18858,"journal":{"name":"Molecular Membrane Biology","volume":"35 1","pages":"60-75"},"PeriodicalIF":0.0,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/09687688.2019.1710274","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37567596","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 17
Uncoupling protein 2 prevents ischaemia reperfusion injury through the regulation ROS/NF-κB signalling in mice 解偶联蛋白2通过调节小鼠ROS/NF-κB信号传导预防缺血再灌注损伤
Molecular Membrane Biology Pub Date : 2019-01-01 DOI: 10.1080/09687688.2019.1701720
Yaolei Zhang, Xin Guo, Ting Li, Yaxing Feng, Wei Li, Xiaoyan Zhu, Rui Gu, Longfu Zhou
{"title":"Uncoupling protein 2 prevents ischaemia reperfusion injury through the regulation ROS/NF-κB signalling in mice","authors":"Yaolei Zhang, Xin Guo, Ting Li, Yaxing Feng, Wei Li, Xiaoyan Zhu, Rui Gu, Longfu Zhou","doi":"10.1080/09687688.2019.1701720","DOIUrl":"https://doi.org/10.1080/09687688.2019.1701720","url":null,"abstract":"Abstract Background and objective: Renal ischaemia reperfusion injury (IRI), characterized by excessive cell apoptosis and inflammation, remains a clinical challenge. Mitochondrial membrane potential is related to apoptosis and inflammation of IRI. Previous studies have indicated that uncoupling protein 2 (UCP2) and its receptors play an important role in inflammation, apoptosis and injuries, especially in oxidative stress injury. However, the underlying mechanisms of UCP2 in IRI are still not fully understood. Methods and results: In the present study, male C57 mice were randomly divided into three groups:sham, IR, and UCP2-/-+IR. The IRI model was established by removing the right kidney and clamping the left kidney for 45 min followed by reperfusion. Blood urea nitrogen (BUN) and creatinine were higher in UCP2-/-+IR mouse serum than in IR mouse serum. In addition, relative to the IR group, UCP2-/-+IR mouse renal cells had increased reactive oxygen species (ROS) production, aggravating tissue damage. We examined changes in the NFκB pathway and found that after UCP2 knockdown, IκB and IKK phosphorylation increased, and nuclear NFκB increased, which stimulated inflammation. Moreover, there was an increase in apoptosis in the UCP2-/-+IR group. Conclusion: UCP2 can prevent IRI in C57 mice. Mechanistically, UCP2 may decrease ROS expression, NFκB activation and caspase-3 cleavage, rendering UCP2 a potential therapeutic target against IRI.","PeriodicalId":18858,"journal":{"name":"Molecular Membrane Biology","volume":"35 1","pages":"51 - 59"},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/09687688.2019.1701720","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46660116","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 3
Engineering stability in NADPH oxidases: A common strategy for enzyme production. NADPH氧化酶的工程稳定性:酶生产的常用策略。
Molecular Membrane Biology Pub Date : 2017-05-01 Epub Date: 2019-01-10 DOI: 10.1080/09687688.2018.1535141
Marta Ceccon, Elisa Millana Fananas, Marta Massari, Andrea Mattevi, Francesca Magnani
{"title":"Engineering stability in NADPH oxidases: A common strategy for enzyme production.","authors":"Marta Ceccon,&nbsp;Elisa Millana Fananas,&nbsp;Marta Massari,&nbsp;Andrea Mattevi,&nbsp;Francesca Magnani","doi":"10.1080/09687688.2018.1535141","DOIUrl":"https://doi.org/10.1080/09687688.2018.1535141","url":null,"abstract":"<p><p>NADPH oxidases (NOXs) are membrane enzymes whose sole function is the generation of reactive oxygen species. Humans have seven NOX isoenzymes that feature distinct functions in immune response and cell signaling but share the same catalytic core comprising a FAD-binding dehydrogenase domain and a heme-binding transmembrane domain. We previously described a mutation that stabilizes the dehydrogenase domain of a prokaryotic homolog of human NOX5. The thermostable mutant exhibited a large 19 °C increase in the apparent melting temperature (app T<sub>m</sub>) and a much tighter binding of the FAD cofactor, which allowed the crystallization and structure determination of the domain holo-form. Here, we analyze the transferability of this mutation onto prokaryotic and eukaryotic full-length NOX enzymes. We found that the mutation exerts a significative stabilizing effect on the full-length NOX5 from both Cylindrospermum stagnale (app T<sub>m</sub> increase of 8 °C) and Homo sapiens (app ΔT<sub>m</sub> of 2 °C). Enhanced thermal stability resulted in more homogeneous preparations of the bacterial NOX5 with less aggregation problems. Moreover, we also found that the mutation increases the overall expression of recombinant human NOX4 and NOX5 in mammalian cells. Such a 2-5-fold increase is mainly due to the lowered cell toxicity, which leads to higher biomasses. Because of the high sequence identity of the catalytic core within this family of enzymes, this strategy can be a general tool to boost the production of all NOXs.</p>","PeriodicalId":18858,"journal":{"name":"Molecular Membrane Biology","volume":"34 3-8","pages":"67-76"},"PeriodicalIF":0.0,"publicationDate":"2017-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/09687688.2018.1535141","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36574971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 6
Corrigendum. 勘误表。
Molecular Membrane Biology Pub Date : 2017-02-01 DOI: 10.1080/09687688.2018.1503851
{"title":"Corrigendum.","authors":"","doi":"10.1080/09687688.2018.1503851","DOIUrl":"https://doi.org/10.1080/09687688.2018.1503851","url":null,"abstract":"","PeriodicalId":18858,"journal":{"name":"Molecular Membrane Biology","volume":"34 1-2","pages":"65"},"PeriodicalIF":0.0,"publicationDate":"2017-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/09687688.2018.1503851","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36559114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
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