scholarly journals Role of Order in the Mechanism of Charge Transport across Single-Stranded and Double-Stranded DNA Monolayers in Tunnel Junctions

2021 ◽  
Author(s):  
Nipun Kumar Gupta ◽  
Edward A. Wilkinson ◽  
Senthil Kumar Karuppannan ◽  
Lily Bailey ◽  
Ayelet Vilan ◽  
...  
Keyword(s):  
Charge Transport ◽  
Tunnel Junctions ◽  
Dna Monolayers ◽  
Double Stranded Dna

scholarly journals Cytosolic Ribosomal Mutations That Abolish Accumulation of Circular Intron in the Mitochondria Without Preventing Senescence of Podospora anserina

Genetics ◽  
1997 ◽  
Vol 145 (3) ◽  
pp. 697-705 ◽  
Author(s):  
Philippe Silar ◽  
France Koll ◽  
Michèle Rossignol
Keyword(s):  
Mitochondrial Dna ◽  
Ribosomal Proteins ◽  
Podospora Anserina ◽  
Cox1 Gene ◽  
Accuracy Control ◽  
Additional Function ◽  
Mutant Proteins ◽  
Double Stranded Dna ◽  
Dna Modifications

The filamentous fungus Podospora anserina presents a degeneration syndrome called Senescence associated with mitochondrial DNA modifications. We show that mutations affecting the two different and interacting cytosolic ribosomal proteins (S7 and S19) systematically and specifically prevent the accumulation of senDNAα (a circular double-stranded DNA plasmid derived from the first intron of the mitochondrial cox1 gene or intron α) without abolishing Senescence nor affecting the accumulation of other usually observed mitochondrial DNA rearrangements. One of the mutant proteins is homologous to the Escherichia coli S4 and Saccharomyces cerevisiae S13 ribosomal proteins, known to be involved in accuracy control of cytosolic translation. The lack of accumulation of senDNAα seems to result from a nontrivial ribosomal alteration unrelated to accuracy control, indicating that S7 and S19 proteins have an additional function. The results strongly suggest that modified expression of nucleus-encoded proteins contributes to Senescence in P. anserina. These data do not fit well with some current models, which propose that intron α plays the role of the cytoplasmic and infectious Determinant of Senescence that was defined in early studies.

scholarly journals Mechanical and Charge Transport Properties of Alkanethiol Self-Assembled Monolayers on a Au(111) Surface:  The Role of Molecular Tilt

Langmuir ◽  
2008 ◽  
Vol 24 (5) ◽  
pp. 2219-2223 ◽  
Author(s):  
Yabing Qi ◽  
Imma Ratera ◽  
Jeong Y. Park ◽  
Paul D. Ashby ◽  
Su Ying Quek ◽  
...  
Keyword(s):  
Charge Transport ◽  
Transport Properties ◽  
Self Assembled Monolayers ◽  
Assembled Monolayers ◽  
Self Assembled

scholarly journals Structural studies on M. tuberculosis O6-methylguanine methyltransferase

2014 ◽  
Vol 70 (a1) ◽  
pp. C832-C832
Author(s):  
Menico Rizzi ◽  
Riccardo Miggiano ◽  
Samarpita Lahiri ◽  
Giuseppe Perugino ◽  
Maria Ciaramella ◽  
...  
Keyword(s):  
Excision Repair ◽  
Single Step ◽  
Double Stranded Dna ◽  
Nucleotide Excision ◽  
Enzymatic Systems ◽  
Methylguanine Methyltransferase ◽  
Mutagenic Effects ◽  
Wild Type Form

Mycobacterium tuberculosis (MTB) is an extremely well adapted human pathogen capable to survive for decades inside the hostile environment represented by the host's infected macrophages despite exposure to multiple potential DNA-damaging stresses. In order to maintain a remarkable low level of genetic diversity, MTB deploys different strategies of DNA repair, including multi-enzymatic systems, such as Nucleotide Excision Repair, and single-step repair. In particular, to counteract the mutagenic effects of DNA alkylation, MTB performs the direct alkylated-base reversal by sacrificing one molecule of a DNA-protein alkyltransferase, such as O6-methylguanine methyltransferase (OGT; orf: Rv1316c). We present here the biochemical and structural characterization of recombinant mycobacterial OGT (MtOGT) in its wild-type form along with its mutated variants mimicking the ones occurring in relevant clinical strains (i.e. MtOGT-T15S and MtOGT-R37L). Our studies reveal that MtOGT-R37L is severely impaired in its activity as consequence of its ten-fold lower affinity for modified double-stranded DNA (dsDNA) (1). Further investigations on a new structure-based panel of OGT versions, designed to explore different molecular environment at position 37, allowed us a better understanding of the functional role of the MtOGT Arg37-bearing loop during catalysis. Moreover, we solved the crystal structure of MtOGT in covalent complex with modified dsDNA that reveals an unprecedented MtOGT::DNA architecture, suggesting that the MtOGT monomer performing the catalysis needs assisting unreacted subunits during cooperative DNA binding. This work is supported by European Community FP7 program SYSTEMTB (Health-F4-2010-241587)

The Maxwell-Wagner model for charge transport in ambipolar organic field-effect transistors: The role of zero-potential position

2012 ◽  
Vol 101 (24) ◽  
pp. 243302 ◽  
Author(s):  
Yasuhiro Mashiko ◽  
Dai Taguchi ◽  
Martin Weis ◽  
Takaaki Manaka ◽  
Mitsumasa Iwamoto
Keyword(s):  
Charge Transport ◽  
Field Effect ◽  
Field Effect Transistors ◽  
Organic Field Effect Transistors ◽  
Wagner Model ◽  
Zero Potential

YBCO/Pb tunnel junctions: reproducibility, cyclability and role of the oxygen content at the YBCO surface

1991 ◽  
Vol 27 (2) ◽  
pp. 1349-1352 ◽  
Author(s):  
A.M. Cucolo ◽  
R. Di Leo ◽  
P. Romano ◽  
L.F. Schneemeyer ◽  
J.V. Waszczak
Keyword(s):  
Oxygen Content ◽  
Tunnel Junctions

scholarly journals CRISPR enriches for cells with mutations in a p53-related interactome, and this can be inhibited

2021 ◽  
Author(s):  
Long Jiang ◽  
Katrine Ingelshed ◽  
Yunbing Shen ◽  
Sanjaykumar V. Boddul ◽  
Vaishnavi Srinivasan Iyer ◽  
...  
Keyword(s):  
Cellular Response ◽  
Human Cancer ◽  
Genetic Alterations ◽  
Dna Breaks ◽  
Data Set ◽  
Human Cancer Cell Lines ◽  
Cycle Arrest ◽  
Double Stranded Dna ◽  
A Cell

CRISPR/Cas9 can be used to inactivate or modify genes by inducing double-stranded DNA breaks1–3. As a protective cellular response, DNA breaks result in p53-mediated cell cycle arrest and activation of cell death programs4,5. Inactivating p53 mutations are the most commonly found genetic alterations in cancer, highlighting the important role of the gene6–8. Here, we show that cells deficient in p53, as well as in genes of a core CRISPR-p53 tumor suppressor interactome, are enriched in a cell population when CRISPR is applied. Such enrichment could pose a challenge for clinical CRISPR use. Importantly, we identify that transient p53 inhibition suppresses the enrichment of cells with these mutations. Furthermore, in a data set of >800 human cancer cell lines, we identify parameters influencing the enrichment of p53 mutated cells, including strong baseline CDKN1A expression as a predictor for an active CRISPR-p53 axis. Taken together, our data identify strategies enabling safe CRISPR use.

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