Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Publication Date: 2018-04-06
    Description: Monocytes and macrophages play a key role in defending pathogens, removing the dead cells or cell debris, and wound healing. The mammalian target of rapamycin (mTOR) inhibitor rapamycin (RPM) is widely used in clinics to treat patients with organ transplantation or tumors. The role of mTOR in monocyte/macrophage development remains to be clarified. Here we found that mTOR intrinsically controls monocyte/macrophage development, as evidenced by the decreased percentages and cell numbers of CD11b + F4/80 + cells resulting from mTOR inhibition in SCID mice, mTOR-deficient mice, and mixed chimera mice, and the in vitro colony formation and monocyte/macrophage induction assays. However, Lyzs-mTOR knockout mice displayed normal levels of monocytes/macrophages, indicating that mTOR is not essential for the survival and maturation of monocytes/macrophages. Further studies showed that mTOR deficiency significantly reduced macrophage colony-stimulating factor receptor CD115 expression at the transcriptional and translational levels. The molecular mechanism studies indicate that the impaired monocyte/macrophage development caused by mTOR deficiency is mainly a result of the overactivated STAT5 and subsequent downregulation of IRF8, but not the altered cell metabolism and autophagy. Therefore, our work identifies that mTOR is an intrinsic master for monocyte/macrophage development at the early stages through regulating STAT5-IRF8-dependent CD115-expressing pathway. Long-term usage of RPM may cause a defect of myeloid progenitors in bone marrow.
    Keywords: Myeloid Neoplasia, Phagocytes, Granulocytes, and Myelopoiesis
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Signatur Availability
    BibTip Others were also interested in ...
  • 2
    Publication Date: 2016-03-29
    Description: The chirality, or 'handedness', of a biologically active molecule can alter its physiological properties. Thus it is routine procedure in the drug discovery and development process to prepare and fully characterize all possible stereoisomers of a drug candidate for biological evaluation. Despite many advances in asymmetric synthesis, developing general and practical strategies for obtaining all possible stereoisomers of an organic compound that has multiple contiguous stereocentres remains a challenge. Here, we report a stereodivergent copper-based approach for the expeditious construction of amino alcohols with high levels of chemo-, regio-, diastereo- and enantioselectivity. Specifically, we synthesized these amino-alcohol products using sequential, copper-hydride-catalysed hydrosilylation and hydroamination of readily available enals and enones. This strategy provides a route to all possible stereoisomers of the amino-alcohol products, which contain up to three contiguous stereocentres. We leveraged catalyst control and stereospecificity simultaneously to attain exceptional control of the product stereochemistry. Beyond the immediate utility of this protocol, our strategy could inspire the development of methods that provide complete sets of stereoisomers for other valuable synthetic targets.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4844805/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4844805/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shi, Shi-Liang -- Wong, Zackary L -- Buchwald, Stephen L -- GM-58160/GM/NIGMS NIH HHS/ -- R01 GM058160/GM/NIGMS NIH HHS/ -- England -- Nature. 2016 Apr 21;532(7599):353-6. doi: 10.1038/nature17191. Epub 2016 Mar 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27018656" target="_blank"〉PubMed〈/a〉
    Keywords: Amination ; Amino Alcohols/*chemical synthesis/*chemistry ; Catalysis ; *Chemistry Techniques, Synthetic ; Copper/*chemistry ; Molecular Structure ; Stereoisomerism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Signatur Availability
    BibTip Others were also interested in ...
  • 3
    Publication Date: 2011-09-06
    Description: Sperm and eggs carry distinctive epigenetic modifications that are adjusted by reprogramming after fertilization. The paternal genome in a zygote undergoes active DNA demethylation before the first mitosis. The biological significance and mechanisms of this paternal epigenome remodelling have remained unclear. Here we report that, within mouse zygotes, oxidation of 5-methylcytosine (5mC) occurs on the paternal genome, changing 5mC into 5-hydroxymethylcytosine (5hmC). Furthermore, we demonstrate that the dioxygenase Tet3 (ref. 5) is enriched specifically in the male pronucleus. In Tet3-deficient zygotes from conditional knockout mice, paternal-genome conversion of 5mC into 5hmC fails to occur and the level of 5mC remains constant. Deficiency of Tet3 also impedes the demethylation process of the paternal Oct4 and Nanog genes and delays the subsequent activation of a paternally derived Oct4 transgene in early embryos. Female mice depleted of Tet3 in the germ line show severely reduced fecundity and their heterozygous mutant offspring lacking maternal Tet3 suffer an increased incidence of developmental failure. Oocytes lacking Tet3 also seem to have a reduced ability to reprogram the injected nuclei from somatic cells. Therefore, Tet3-mediated DNA hydroxylation is involved in epigenetic reprogramming of the zygotic paternal DNA following natural fertilization and may also contribute to somatic cell nuclear reprogramming during animal cloning.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gu, Tian-Peng -- Guo, Fan -- Yang, Hui -- Wu, Hai-Ping -- Xu, Gui-Fang -- Liu, Wei -- Xie, Zhi-Guo -- Shi, Linyu -- He, Xinyi -- Jin, Seung-gi -- Iqbal, Khursheed -- Shi, Yujiang Geno -- Deng, Zixin -- Szabo, Piroska E -- Pfeifer, Gerd P -- Li, Jinsong -- Xu, Guo-Liang -- GM078458/GM/NIGMS NIH HHS/ -- England -- Nature. 2011 Sep 4;477(7366):606-10. doi: 10.1038/nature10443.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Group of DNA Metabolism, The State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21892189" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine/metabolism ; Alleles ; Animals ; *Cellular Reprogramming ; Cytosine/analogs & derivatives/metabolism ; DNA/chemistry/genetics/metabolism ; DNA Methylation/genetics ; DNA-Binding Proteins/deficiency/genetics/*metabolism ; Dioxygenases/genetics/*metabolism ; Embryo, Mammalian/embryology/metabolism ; Embryonic Development ; *Epigenesis, Genetic ; Female ; Fertility/genetics ; Gene Expression Regulation, Developmental ; Germ Cells/metabolism ; Male ; Mice ; Octamer Transcription Factor-3/genetics ; Oocytes/cytology/*enzymology/*metabolism ; Oxidation-Reduction ; Proto-Oncogene Proteins/deficiency/genetics/*metabolism ; Zygote/cytology/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Signatur Availability
    BibTip Others were also interested in ...
  • 4
    Publication Date: 2013-11-01
    Description: The 2002-3 pandemic caused by severe acute respiratory syndrome coronavirus (SARS-CoV) was one of the most significant public health events in recent history. An ongoing outbreak of Middle East respiratory syndrome coronavirus suggests that this group of viruses remains a key threat and that their distribution is wider than previously recognized. Although bats have been suggested to be the natural reservoirs of both viruses, attempts to isolate the progenitor virus of SARS-CoV from bats have been unsuccessful. Diverse SARS-like coronaviruses (SL-CoVs) have now been reported from bats in China, Europe and Africa, but none is considered a direct progenitor of SARS-CoV because of their phylogenetic disparity from this virus and the inability of their spike proteins to use the SARS-CoV cellular receptor molecule, the human angiotensin converting enzyme II (ACE2). Here we report whole-genome sequences of two novel bat coronaviruses from Chinese horseshoe bats (family: Rhinolophidae) in Yunnan, China: RsSHC014 and Rs3367. These viruses are far more closely related to SARS-CoV than any previously identified bat coronaviruses, particularly in the receptor binding domain of the spike protein. Most importantly, we report the first recorded isolation of a live SL-CoV (bat SL-CoV-WIV1) from bat faecal samples in Vero E6 cells, which has typical coronavirus morphology, 99.9% sequence identity to Rs3367 and uses ACE2 from humans, civets and Chinese horseshoe bats for cell entry. Preliminary in vitro testing indicates that WIV1 also has a broad species tropism. Our results provide the strongest evidence to date that Chinese horseshoe bats are natural reservoirs of SARS-CoV, and that intermediate hosts may not be necessary for direct human infection by some bat SL-CoVs. They also highlight the importance of pathogen-discovery programs targeting high-risk wildlife groups in emerging disease hotspots as a strategy for pandemic preparedness.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ge, Xing-Yi -- Li, Jia-Lu -- Yang, Xing-Lou -- Chmura, Aleksei A -- Zhu, Guangjian -- Epstein, Jonathan H -- Mazet, Jonna K -- Hu, Ben -- Zhang, Wei -- Peng, Cheng -- Zhang, Yu-Ji -- Luo, Chu-Ming -- Tan, Bing -- Wang, Ning -- Zhu, Yan -- Crameri, Gary -- Zhang, Shu-Yi -- Wang, Lin-Fa -- Daszak, Peter -- Shi, Zheng-Li -- R01AI079231/AI/NIAID NIH HHS/ -- R01TW005869/TW/FIC NIH HHS/ -- R56TW009502/TW/FIC NIH HHS/ -- England -- Nature. 2013 Nov 28;503(7477):535-8. doi: 10.1038/nature12711. Epub 2013 Oct 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Center for Emerging Infectious Diseases, State Key Laboratory of Virology, Wuhan Institute of Virology of the Chinese Academy of Sciences, Wuhan 430071, China [2].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24172901" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cercopithecus aethiops ; China ; Chiroptera/*virology ; Disease Reservoirs/virology ; Feces/virology ; Fluorescent Antibody Technique ; Genome, Viral/genetics ; Host Specificity ; Humans ; Molecular Sequence Data ; Pandemics/prevention & control/veterinary ; Peptidyl-Dipeptidase A/genetics/*metabolism ; Real-Time Polymerase Chain Reaction ; Receptors, Virus/genetics/metabolism ; SARS Virus/genetics/*isolation & purification/*metabolism/ultrastructure ; Severe Acute Respiratory Syndrome/prevention & ; control/transmission/veterinary/virology ; Species Specificity ; Spike Glycoprotein, Coronavirus/chemistry/metabolism ; Vero Cells ; Virion/isolation & purification/ultrastructure ; Virus Internalization ; Viverridae/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Signatur Availability
    BibTip Others were also interested in ...
  • 5
    Publication Date: 2018-09-07
    Description: Plant immunity often penalizes growth and yield. The transcription factor Ideal Plant Architecture 1 (IPA1) reduces unproductive tillers and increases grains per panicle, which results in improved rice yield. Here we report that higher IPA1 levels enhance immunity. Mechanistically, phosphorylation of IPA1 at amino acid Ser 163 within its DNA binding domain occurs in response to infection by the fungus Magnaporthe oryzae and alters the DNA binding specificity of IPA1. Phosphorylated IPA1 binds to the promoter of the pathogen defense gene WRKY45 and activates its expression, leading to enhanced disease resistance. IPA1 returns to a nonphosphorylated state within 48 hours after infection, resuming support of the growth needed for high yield. Thus, IPA1 promotes both yield and disease resistance by sustaining a balance between growth and immunity.
    Keywords: Botany
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
    Signatur Availability
    BibTip Others were also interested in ...
  • 6
    Publication Date: 2011-04-26
    Description: Neurotransmitter/Na(+) symporters (NSSs) terminate neuronal signalling by recapturing neurotransmitter released into the synapse in a co-transport (symport) mechanism driven by the Na(+) electrochemical gradient. NSSs for dopamine, noradrenaline and serotonin are targeted by the psychostimulants cocaine and amphetamine, as well as by antidepressants. The crystal structure of LeuT, a prokaryotic NSS homologue, revealed an occluded conformation in which a leucine (Leu) and two Na(+) are bound deep within the protein. This structure has been the basis for extensive structural and computational exploration of the functional mechanisms of proteins with a LeuT-like fold. Subsequently, an 'outward-open' conformation was determined in the presence of the inhibitor tryptophan, and the Na(+)-dependent formation of a dynamic outward-facing intermediate was identified using electron paramagnetic resonance spectroscopy. In addition, single-molecule fluorescence resonance energy transfer imaging has been used to reveal reversible transitions to an inward-open LeuT conformation, which involve the movement of transmembrane helix TM1a away from the transmembrane helical bundle. We investigated how substrate binding is coupled to structural transitions in LeuT during Na(+)-coupled transport. Here we report a process whereby substrate binding from the extracellular side of LeuT facilitates intracellular gate opening and substrate release at the intracellular face of the protein. In the presence of alanine, a substrate that is transported approximately 10-fold faster than leucine, we observed alanine-induced dynamics in the intracellular gate region of LeuT that directly correlate with transport efficiency. Collectively, our data reveal functionally relevant and previously hidden aspects of the NSS transport mechanism that emphasize the functional importance of a second substrate (S2) binding site within the extracellular vestibule. Substrate binding in this S2 site appears to act cooperatively with the primary substrate (S1) binding site to control intracellular gating more than 30 A away, in a manner that allows the Na(+) gradient to power the transport mechanism.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3178346/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3178346/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhao, Yongfang -- Terry, Daniel S -- Shi, Lei -- Quick, Matthias -- Weinstein, Harel -- Blanchard, Scott C -- Javitch, Jonathan A -- DA022413/DA/NIDA NIH HHS/ -- DA023694/DA/NIDA NIH HHS/ -- DA12408/DA/NIDA NIH HHS/ -- DA17293/DA/NIDA NIH HHS/ -- K05 DA022413/DA/NIDA NIH HHS/ -- R00 DA023694/DA/NIDA NIH HHS/ -- R00 DA023694-03/DA/NIDA NIH HHS/ -- R01 DA017293/DA/NIDA NIH HHS/ -- England -- Nature. 2011 Jun 2;474(7349):109-13. doi: 10.1038/nature09971. Epub 2011 Apr 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Molecular Recognition, Columbia University College of Physicians and Surgeons, 630 West 168th Street, New York, New York 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21516104" target="_blank"〉PubMed〈/a〉
    Keywords: Humans ; Ion Channel Gating/*drug effects ; Leucine/metabolism ; Lithium/metabolism ; *Models, Molecular ; Mutation ; Plasma Membrane Neurotransmitter Transport ; Proteins/chemistry/genetics/*metabolism ; Protein Binding/genetics ; Protein Structure, Secondary ; Sodium/metabolism/pharmacology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Signatur Availability
    BibTip Others were also interested in ...
  • 7
    Publication Date: 2018-04-28
    Description: Middle East respiratory syndrome coronavirus (MERS-CoV) causes a highly lethal pulmonary infection with ~35% mortality. The potential for a future pandemic originating from animal reservoirs or health care-associated events is a major public health concern. There are no vaccines or therapeutic agents currently available for MERS-CoV. Using a probe-based single B cell cloning strategy, we have identified and characterized multiple neutralizing monoclonal antibodies (MAbs) specifically binding to the receptor-binding domain (RBD) or S1 (non-RBD) regions from a convalescent MERS-CoV-infected patient and from immunized rhesus macaques. RBD-specific MAbs tended to have greater neutralizing potency than non-RBD S1-specific MAbs. Six RBD-specific and five S1-specific MAbs could be sorted into four RBD and three non-RBD distinct binding patterns, based on competition assays, mapping neutralization escape variants, and structural analysis. We determined cocrystal structures for two MAbs targeting the RBD from different angles and show they can bind the RBD only in the "out" position. We then showed that selected RBD-specific, non-RBD S1-specific, and S2-specific MAbs given prophylactically prevented MERS-CoV replication in lungs and protected mice from lethal challenge. Importantly, combining RBD- and non-RBD MAbs delayed the emergence of escape mutations in a cell-based virus escape assay. These studies identify MAbs targeting different antigenic sites on S that will be useful for defining mechanisms of MERS-CoV neutralization and for developing more effective interventions to prevent or treat MERS-CoV infections. IMPORTANCE MERS-CoV causes a highly lethal respiratory infection for which no vaccines or antiviral therapeutic options are currently available. Based on continuing exposure from established reservoirs in dromedary camels and bats, transmission of MERS-CoV into humans and future outbreaks are expected. Using structurally defined probes for the MERS-CoV spike glycoprotein (S), the target for neutralizing antibodies, single B cells were sorted from a convalescent human and immunized nonhuman primates (NHPs). MAbs produced from paired immunoglobulin gene sequences were mapped to multiple epitopes within and outside the receptor-binding domain (RBD) and protected against lethal MERS infection in a murine model following passive immunization. Importantly, combining MAbs targeting distinct epitopes prevented viral neutralization escape from RBD-directed MAbs. These data suggest that antibody responses to multiple domains on CoV spike protein may improve immunity and will guide future vaccine and therapeutic development efforts.
    Print ISSN: 0022-538X
    Electronic ISSN: 1098-5514
    Topics: Medicine
    Signatur Availability
    BibTip Others were also interested in ...
  • 8
    Publication Date: 2018-02-07
    Description: BACKGROUND Anaplastic thyroid cancer (ATC) is the rarest type of thyroid cancer and has the lowest overall survival. To the authors' knowledge, the impact of socioeconomic status and race/ethnicity has not yet been described. METHODS Data regarding 719 patients diagnosed with their first primary malignant ATC from January 1, 1998 to December 31, 2011 in the Surveillance, Epidemiology, and End Results program registries were examined. Differences in receipt of thyroidectomy, radiotherapy, and lymph node examination were examined by race/ethnicity. Survival also was examined by race/ethnicity. RESULTS Nearly 70% of patients were non-Hispanic white, and 55.4% of patients received treatment. Tumor size ( P  = .13), lymph node involvement ( P  = .60), and residence in high poverty neighborhoods ( P  = .08) did not vary by race/ethnicity. Nonwhite patients were more likely to receive no treatment (adjusted odds ratio, 0.29; 95% confidence interval [95% CI], 0.16-0.54). When receipt of radiotherapy was adjusted for, nonwhite patients had a higher risk of overall death (adjusted hazards ratio [aHR], 1.24; 95% CI, 1.01-1.54), although not disease-specific death (aHR, 1.14; 95% CI, 0.92-1.42). Patients living in areas of high poverty had lower overall survival (aHR, 1.54; 95% CI, 1.09-2.18) and disease-specific survival (aHR, 1.68; 95% CI, 1.19-2.36). CONCLUSIONS In this population-based study of patients with ATC, nonwhite patients were found to be less likely to receive treatment. Furthermore, nonwhite patients had poorer overall survival, and patients living in areas of high poverty had both worse overall and disease-specific survival. Racial/ethnic and socioeconomic disparities appear to exist in the treatment and survival of patients with ATC. Cancer 2018 . © 2018 American Cancer Society .
    Print ISSN: 0008-543X
    Electronic ISSN: 1097-0142
    Topics: Biology , Medicine
    Published by Wiley-Blackwell on behalf of The American Cancer Society.
    Signatur Availability
    BibTip Others were also interested in ...
  • 9
    Publication Date: 2015-10-16
    Description: Neuroblastoma is a malignant paediatric tumour of the sympathetic nervous system. Roughly half of these tumours regress spontaneously or are cured by limited therapy. By contrast, high-risk neuroblastomas have an unfavourable clinical course despite intensive multimodal treatment, and their molecular basis has remained largely elusive. Here we have performed whole-genome sequencing of 56 neuroblastomas (high-risk, n = 39; low-risk, n = 17) and discovered recurrent genomic rearrangements affecting a chromosomal region at 5p15.33 proximal of the telomerase reverse transcriptase gene (TERT). These rearrangements occurred only in high-risk neuroblastomas (12/39, 31%) in a mutually exclusive fashion with MYCN amplifications and ATRX mutations, which are known genetic events in this tumour type. In an extended case series (n = 217), TERT rearrangements defined a subgroup of high-risk tumours with particularly poor outcome. Despite a large structural diversity of these rearrangements, they all induced massive transcriptional upregulation of TERT. In the remaining high-risk tumours, TERT expression was also elevated in MYCN-amplified tumours, whereas alternative lengthening of telomeres was present in neuroblastomas without TERT or MYCN alterations, suggesting that telomere lengthening represents a central mechanism defining this subtype. The 5p15.33 rearrangements juxtapose the TERT coding sequence to strong enhancer elements, resulting in massive chromatin remodelling and DNA methylation of the affected region. Supporting a functional role of TERT, neuroblastoma cell lines bearing rearrangements or amplified MYCN exhibited both upregulated TERT expression and enzymatic telomerase activity. In summary, our findings show that remodelling of the genomic context abrogates transcriptional silencing of TERT in high-risk neuroblastoma and places telomerase activation in the centre of transformation in a large fraction of these tumours.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peifer, Martin -- Hertwig, Falk -- Roels, Frederik -- Dreidax, Daniel -- Gartlgruber, Moritz -- Menon, Roopika -- Kramer, Andrea -- Roncaioli, Justin L -- Sand, Frederik -- Heuckmann, Johannes M -- Ikram, Fakhera -- Schmidt, Rene -- Ackermann, Sandra -- Engesser, Anne -- Kahlert, Yvonne -- Vogel, Wenzel -- Altmuller, Janine -- Nurnberg, Peter -- Thierry-Mieg, Jean -- Thierry-Mieg, Danielle -- Mariappan, Aruljothi -- Heynck, Stefanie -- Mariotti, Erika -- Henrich, Kai-Oliver -- Gloeckner, Christian -- Bosco, Graziella -- Leuschner, Ivo -- Schweiger, Michal R -- Savelyeva, Larissa -- Watkins, Simon C -- Shao, Chunxuan -- Bell, Emma -- Hofer, Thomas -- Achter, Viktor -- Lang, Ulrich -- Theissen, Jessica -- Volland, Ruth -- Saadati, Maral -- Eggert, Angelika -- de Wilde, Bram -- Berthold, Frank -- Peng, Zhiyu -- Zhao, Chen -- Shi, Leming -- Ortmann, Monika -- Buttner, Reinhard -- Perner, Sven -- Hero, Barbara -- Schramm, Alexander -- Schulte, Johannes H -- Herrmann, Carl -- O'Sullivan, Roderick J -- Westermann, Frank -- Thomas, Roman K -- Fischer, Matthias -- England -- Nature. 2015 Oct 29;526(7575):700-4. doi: 10.1038/nature14980. Epub 2015 Oct 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Translational Genomics, Center of Integrated Oncology Cologne-Bonn, Medical Faculty, University of Cologne, 50931 Cologne, Germany. ; Center for Molecular Medicine Cologne (CMMC), University of Cologne, 50931 Cologne, Germany. ; Department of Pediatric Oncology and Hematology, University Children's Hospital of Cologne, Medical Faculty, University of Cologne, 50937 Cologne, Germany. ; Division Neuroblastoma Genomics (B087), German Cancer Research Center, 69120 Heidelberg, Germany. ; Department of Prostate Cancer Research, Institute of Pathology, Center for Integrated Oncology Cologne-Bonn, University Hospital of Bonn, 53127 Bonn, Germany. ; NEO New Oncology AG, 51105 Cologne, Germany. ; Department of Pharmacology and Chemical Biology, University of Pittsburgh Cancer Institute (UPCI), Hillman Cancer Center, Pittsburgh, Pennsylvania 15213, USA. ; Cologne Center for Genomics, University of Cologne, 50931 Cologne, Germany. ; Institute of Biostatistics and Clinical Research, University of Munster, 48149 Munster, Germany. ; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, 50931 Cologne, Germany. ; National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, Maryland 20894, USA. ; Department of Pathology, University of Kiel, 24118 Kiel, Germany. ; Functional Epigenomics, University of Cologne, 50931 Cologne, Germany. ; Department of Cell Biology, Center for Biologic Imaging, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA. ; Division of Theoretical Systems Biology, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany. ; Computing Center, University of Cologne, 50931 Cologne, Germany. ; Department of Informatics, University of Cologne, 50931 Cologne, Germany. ; Division of Biostatistics, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany. ; Department of Pediatric Oncology and Hematology, Charite University Medical Center Berlin, 10117 Berlin, Germany. ; Center for Medical Genetics, Ghent University, 9000 Ghent, Belgium. ; BGI-Shenzhen, Bei Shan Industrial Zone, Yantian District, Shenzhen, Guangdong, 518083 China. ; Center for Pharmacogenomics and Fudan-Zhangjiang Center for Clinical Genomics, State Key Laboratory of Genetic Engineering and MOE Key Laboratory of Contemporary Anthropology School of Pharmacy and School of Life Sciences, Fudan University, Shanghai 201203, China. ; Department of Pathology, University of Cologne, 50937 Cologne, Germany. ; Department of Pediatric Oncology and Hematology, University Children's Hospital, 45147 Essen, Germany. ; German Cancer Consortium (DKTK), 10117 Berlin, Germany. ; German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany. ; Institute of Pharmacy and Molecular Biotechnology, University of Heidelberg, 69120 Heidelberg, Germany. ; Bioquant Center, University of Heidelberg, 69120 Heidelberg, Germany. ; Division of Theoretical Bioinformatics, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany. ; Max Planck Institute for Metabolism Research, 50931 Cologne, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26466568" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Signatur Availability
    BibTip Others were also interested in ...
  • 10
    Publication Date: 2015-07-04
    Description: Catalytic assembly of enantiopure aliphatic amines from abundant and readily available precursors has long been recognized as a paramount challenge in synthetic chemistry. Here, we describe a mild and general copper-catalyzed hydroamination that effectively converts unactivated internal olefins-an important yet unexploited class of abundant feedstock chemicals-into highly enantioenriched alpha-branched amines (〉/=96% enantiomeric excess) featuring two minimally differentiated aliphatic substituents. This method provides a powerful means to access a broad range of advanced, highly functionalized enantioenriched amines of interest in pharmaceutical research and other areas.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4532314/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4532314/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Yang -- Shi, Shi-Liang -- Niu, Dawen -- Liu, Peng -- Buchwald, Stephen L -- GM 58160/GM/NIGMS NIH HHS/ -- R01 GM058160/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2015 Jul 3;349(6243):62-6. doi: 10.1126/science.aab3753.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. ; Department of Chemistry, University of Pittsburgh, Pittsburgh, PA 15260, USA. ; Department of Chemistry, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. sbuchwal@mit.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26138973" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Signatur Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...