scholarly journals An integrated multi-molecular sensor for simultaneous BRAFV600E protein and DNA single point mutation detection in circulating tumour cells

Lab on a Chip ◽  
2019 ◽  
Vol 19 (5) ◽  
pp. 738-748 ◽  
Author(s):  
Shuvashis Dey ◽  
Kevin M. Koo ◽  
Zhaoran Wang ◽  
Abu A. I. Sina ◽  
Alain Wuethrich ◽  
...  
Keyword(s):  
Point Mutation ◽  
Mutation Detection ◽  
Biological Fluids ◽  
Single Point ◽  
Single Point Mutation ◽  
Circulating Tumour Cells ◽  
Cell Capture ◽  
Entire Sample ◽  
Molecular Sensor ◽  
On Chip

We report an integrated multi-molecular sensor (IMMS) platform for an entire sample-to-answer protocol encompassing melanoma cell capture in biological fluids, on-chip cell lysis, and combined quantification of intracellular BRAFV600E DNA and protein amounts.

Protein Adsorption and Reorganization on Nanoparticles Probed by the Coffee-Ring Effect: Application to Single Point Mutation Detection

2016 ◽  
Vol 138 (36) ◽  
pp. 11623-11632 ◽  
Author(s):  
Stéphanie Devineau ◽  
Manos Anyfantakis ◽  
Laurent Marichal ◽  
Laurent Kiger ◽  
Mathieu Morel ◽  
...  
Keyword(s):  
Protein Adsorption ◽  
Point Mutation ◽  
Mutation Detection ◽  
Single Point ◽  
Single Point Mutation ◽  
Coffee Ring ◽  
Coffee Ring Effect ◽  
Ring Effect

Single point mutation detection in living cancer cells by far-red emitting PNA–FIT probes

2016 ◽  
Vol 52 (11) ◽  
pp. 2405-2407 ◽  
Author(s):  
N. Kolevzon ◽  
D. Hashoul ◽  
S. Naik ◽  
A. Rubinstein ◽  
E. Yavin
Keyword(s):  
Cancer Cells ◽  
Point Mutation ◽  
Mutation Detection ◽  
Single Point ◽  
Living Cells ◽  
Single Point Mutation ◽  
Snp Detection ◽  
First Time

SNP detection of the mutated kRAS oncogene in living cells is shown to be achieved for the first time by cell-permeable and far-red emitting PNA–FIT probes.

scholarly journals Single-point mutation detection in RNA extracts using gold nanoparticles modified with hydrophobic molecular beacon-like structures

2014 ◽  
Vol 50 (23) ◽  
pp. 3018-3020 ◽  
Author(s):  
Alfonso Latorre ◽  
Christian Posch ◽  
Yolanda Garcimartín ◽  
Susana Ortiz-Urda ◽  
Álvaro Somoza
Keyword(s):  
Gold Nanoparticles ◽  
Point Mutation ◽  
Mutation Detection ◽  
Molecular Beacon ◽  
Single Point ◽  
Point Mutations ◽  
Single Point Mutation ◽  
Target Sequence ◽  
Cholesterol Derivative ◽  
Single Point Mutations

The functionalization of gold nanoparticles with a cholesterol derivative affords a sensor that is able to detect single-point mutations. The solubility of the nanoparticles is modulated by the presence of the target sequence inducing its aggregation.

scholarly journals A single point mutation converts a proton-pumping rhodopsin into a red-shifted, turn-on fluorescent sensor for chloride

2021 ◽  
Author(s):  
Jasmine N. Tutol ◽  
Jessica Lee ◽  
Hsichuan Chi ◽  
Farah N. Faizuddin ◽  
Sameera S. Abeyrathna ◽  
...  
Keyword(s):  
Point Mutation ◽  
Fluorescent Sensor ◽  
Single Point ◽  
Proton Pumping ◽  
Single Point Mutation ◽  
Turn On ◽  
Gloeobacter Violaceus

By utilizing laboratory-guided evolution, we have converted the fluorescent proton-pumping rhodopsin GR from Gloeobacter violaceus into GR1, a red-shifted, turn-on fluorescent sensor for chloride.

scholarly journals Structural basis for a complex I mutation that blocks pathological ROS production

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Zhan Yin ◽  
Nils Burger ◽  
Duvaraka Kula-Alwar ◽  
Dunja Aksentijević ◽  
Hannah R. Bridges ◽  
...  
Keyword(s):  
Point Mutation ◽  
Complex I ◽  
Structural Changes ◽  
Ischemia Reperfusion ◽  
Single Point ◽  
Structural Basis ◽  
Single Point Mutation ◽  
Ros Production

AbstractMitochondrial complex I is central to the pathological reactive oxygen species (ROS) production that underlies cardiac ischemia–reperfusion (IR) injury. ND6-P25L mice are homoplasmic for a disease-causing mtDNA point mutation encoding the P25L substitution in the ND6 subunit of complex I. The cryo-EM structure of ND6-P25L complex I revealed subtle structural changes that facilitate rapid conversion to the “deactive” state, usually formed only after prolonged inactivity. Despite its tendency to adopt the “deactive” state, the mutant complex is fully active for NADH oxidation, but cannot generate ROS by reverse electron transfer (RET). ND6-P25L mitochondria function normally, except for their lack of RET ROS production, and ND6-P25L mice are protected against cardiac IR injury in vivo. Thus, this single point mutation in complex I, which does not affect oxidative phosphorylation but renders the complex unable to catalyse RET, demonstrates the pathological role of ROS production by RET during IR injury.

Sign in / Sign up

Export Citation Format

Share Document