Institution
University of Marburg
Education•Marburg, Germany•
About: University of Marburg is a education organization based out in Marburg, Germany. It is known for research contribution in the topics: Population & Gene. The organization has 23195 authors who have published 42907 publications receiving 1506069 citations. The organization is also known as: Philipps University of Marburg & Philipps-Universität.
Topics: Population, Gene, Crystal structure, Laser, Catalysis
Papers published on a yearly basis
Papers
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TL;DR: The unreduced detergent delipidized protein moiety from Lp(a) lipoprotein shows a single band of M r ∼700000 in SDS—polyacrylamide gel electrophoresis and the immunoprecipitates formed against anti‐Lp( a) and anti‐apo B by the unreducing protein show a reaction of immunological identity.
240 citations
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TL;DR: The editing function may have played a central role in restricting the genetic code to 20 amino acids and disabling this editing function offers a powerful approach for diversifying the chemical composition of proteins and for emulating evolutionary stages of ambiguous translation.
Abstract: Aminoacyl transfer RNA (tRNA) synthetases establish the rules of the genetic code by catalyzing the aminoacylation of tRNAs. For some synthetases, accuracy depends critically on an editing function at a site distinct from the aminoacylation site. Mutants ofEscherichia coli that incorrectly charge tRNAValwith cysteine were selected after random mutagenesis of the whole chromosome. All mutations obtained were located in the editing site of valyl-tRNA synthetase. More than 20% of the valine in cellular proteins from such an editing mutant organism could be replaced with the noncanonical aminobutyrate, sterically similar to cysteine. Thus, the editing function may have played a central role in restricting the genetic code to 20 amino acids. Disabling this editing function offers a powerful approach for diversifying the chemical composition of proteins and for emulating evolutionary stages of ambiguous translation.
240 citations
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TL;DR: TAT-PEG-PEI represents a new approach to non-viral gene carriers for lung therapy, comprising protection for plasmid DNA, low toxicity and significantly enhanced transfection efficiency under in vivo conditions.
240 citations
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TL;DR: In this article, human apolipoprotein A-IV (apoA-IV) was expressed in the liver of C57BL/6 mice and mice deficient in apoE, both of which are prone to atherosclerosis.
Abstract: Apolipoproteins are protein constituents of plasma lipid transport particles. Human apolipoprotein A-IV (apoA-IV) was expressed in the liver of C57BL/6 mice and mice deficient in apoE, both of which are prone to atherosclerosis, to investigate whether apoA-IV protects against this disease. In transgenic C57BL/6 mice on an atherogenic diet, the serum concentration of high density lipoprotein (HDL) cholesterol increased by 35 percent, whereas the concentration of endogenous apoA-I decreased by 29 percent, relative to those in transgenic mice on a normal diet. Expression of human apoA-IV in apoE-deficient mice on a normal diet resulted in an even more severe atherogenic lipoprotein profile, without affecting the concentration of HDL cholesterol, than that in nontransgenic apoE-deficient mice. However, transgenic mice of both backgrounds showed a substantial reduction in the size of atherosclerotic lesions. Thus, apoA-IV appears to protect against atherosclerosis by a mechanism that does not involve an increase in HDL cholesterol concentration.
240 citations
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TL;DR: It is shown in human and murine cell lines that oncogenic levels of MYC establish a dependence on AMPK-related kinase 5 (ARK5; also known as NUAK1) for maintaining metabolic homeostasis and for cell survival, and that targeting cellular energyHomeostasis is a valid therapeutic strategy to eliminate tumour cells that express deregulated MYC.
Abstract: Deregulated expression of the MYC oncoprotein contributes to the genesis of many human tumours, yet strategies to exploit this for a rational tumour therapy are scarce. MYC promotes cell growth and proliferation, and alters cellular metabolism to enhance the provision of precursors for phospholipids and cellular macromolecules. Here we show in human and murine cell lines that oncogenic levels of MYC establish a dependence on AMPK-related kinase 5 (ARK5; also known as NUAK1) for maintaining metabolic homeostasis and for cell survival. ARK5 is an upstream regulator of AMPK and limits protein synthesis via inhibition of the mammalian target of rapamycin 1 (mTORC1) signalling pathway. ARK5 also maintains expression of mitochondrial respiratory chain complexes and respiratory capacity, which is required for efficient glutamine metabolism. Inhibition of ARK5 leads to a collapse of cellular ATP levels in cells expressing deregulated MYC, inducing multiple pro-apoptotic responses as a secondary consequence. Depletion of ARK5 prolongs survival in MYC-driven mouse models of hepatocellular carcinoma, demonstrating that targeting cellular energy homeostasis is a valid therapeutic strategy to eliminate tumour cells that express deregulated MYC.
240 citations
Authors
Showing all 23488 results
Name | H-index | Papers | Citations |
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John C. Morris | 183 | 1441 | 168413 |
Russel J. Reiter | 169 | 1646 | 121010 |
Martin J. Blaser | 147 | 820 | 104104 |
Christopher T. Walsh | 139 | 819 | 74314 |
Markus Cristinziani | 131 | 1140 | 84538 |
James C. Paulson | 126 | 443 | 52152 |
Markus F. Neurath | 124 | 934 | 62376 |
Nicholas W. Wood | 123 | 614 | 66270 |
Florian Lang | 116 | 1421 | 66496 |
Howard I. Maibach | 116 | 1821 | 60765 |
Thomas G. Ksiazek | 113 | 398 | 46108 |
Frank Glorius | 113 | 663 | 49305 |
Eberhard Ritz | 111 | 1109 | 61530 |
Manfred T. Reetz | 110 | 959 | 42941 |
Wolfgang H. Oertel | 110 | 653 | 51147 |