PCR free multiple ligase reactions and probe cleavages for the SNP detection of KRAS mutation with attomole sensitivity

The Analyst ◽  
2016 ◽  
Vol 141 (23) ◽  
pp. 6381-6386 ◽  
Author(s):  
Joong Hyun Kim
Keyword(s):  
Point Mutation ◽  
Kras Mutation ◽  
Single Point ◽  
Single Point Mutation ◽  
Snp Detection ◽  
Target Dna

A method to produce multiple ligated primers without PCR for a target DNA containing a single point mutation is presented.

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 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.

Scarcity of λ1 B cells in mice with a single point mutation in Cλ1 is due to a low BCR signal caused by misfolded lambda1 light chain

2007 ◽  
Vol 44 (6) ◽  
pp. 1417-1428 ◽  
Author(s):  
Veronica V. Volgina ◽  
Tianhe Sun ◽  
Grazyna Bozek ◽  
Terence E. Martin ◽  
Ursula Storb
Keyword(s):  
B Cells ◽  
Point Mutation ◽  
Light Chain ◽  
Single Point ◽  
Single Point Mutation

Shifting Substrate Specificity of Human Glutathione Transferase (from Class Pi to Class Alpha) by a Single Point Mutation

1998 ◽  
Vol 252 (1) ◽  
pp. 184-189 ◽  
Author(s):  
Marzia Nuccetelli ◽  
Anna P. Mazzetti ◽  
Jamie Rossjohn ◽  
Michael W. Parker ◽  
Philip Board ◽  
...  
Keyword(s):  
Substrate Specificity ◽  
Point Mutation ◽  
Glutathione Transferase ◽  
Single Point ◽  
Single Point Mutation
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