Results 91 to 100 of about 199,160 (290)
GbSER02 with a single base change (SNP517G) encodes normal serpin protein and interacts with transcription factor VOZ1 to alleviate the repression of VOZ1 on GA3ox1 and promote GA3 biosynthesis. Further, GA3 induces the expression of cell wall loosening‐related genes and decreases flavonoid content, ultimately facilitating fiber cell elongation in ...
Hao Jia+12 more
wiley +1 more source
Nonsense mutations constitute ~10% of TP53 mutations in cancer. They introduce a premature termination codon that gives rise to truncated p53 protein with impaired function.
Michael W Ferguson+9 more
doaj +1 more source
The termination of translation in Saccharomyces cerevisiae is controlled by two interacting polypeptide chain release factors, eRF1, and eRF3. Two regions in eRF1, at position 281-305 and 411-415, were proposed to be involved on the interaction to eRF3 ...
PRIMA ENDANG SUSILOWATI+3 more
doaj +1 more source
Precursor RNAs Harboring Nonsense Codons Accumulate Near the Site of Transcription [PDF]
Messenger RNAs containing premature termination codons (PTCs) are selectively eliminated by nonsense-mediated mRNA decay (NMD). Paradoxically, although cytoplasmic ribosomes are the only known species capable of PTC recognition, in mammals many PTC-containing mRNAs are apparently eliminated prior to release from the nucleus.
Oliver Mühlemann+7 more
openaire +3 more sources
Base editing enables precise nucleotide substitutions but limited by bystander editing. This study engineers plant base editors by fusing optimized TadA variants with PAM‐flexible SpRY nickase, enabling A‐to‐G, C‐to‐T, and dual‐base conversions in a highly condensed window (≤3 nucleotides). Additionally, TadDBE (TadA Dual‐Base Editor)‐mediated directed
Kangli Sun+14 more
wiley +1 more source
Targeting nonsense-mediated mRNA decay in colorectal cancers with microsatellite instability
Nonsense-mediated mRNA decay (NMD) is responsible for the degradation of mRNAs with a premature termination codon (PTC). The role of this system in cancer is still quite poorly understood. In the present study, we evaluated the functional consequences of
A'dem Bokhari+16 more
semanticscholar +1 more source
Therapeutic targeting of TP53 nonsense mutations in cancer
Mutations in the TP53 tumor suppressor gene occur with high prevalence in a wide range of human tumors. A significant fraction of these mutations (around 10%) are nonsense mutations, creating a premature termination codon (PTC) that leads to the ...
Charlotte Strandgren, Klas G. Wiman
doaj +1 more source
Mutations in the human ether-a-go-go-related gene (hERG) result in long QT syndrome type 2 (LQT2). The hERG gene encodes a K+ channel that contributes to the repolarization of the cardiac action potential.
Gong, Qiuming+3 more
core +1 more source
Unassigned Codons, Nonsense Suppression, and Anticodon Modifications in the Evolution of the Genetic Code [PDF]
The origin of the genetic code is a central open problem regarding the early evolution of life. Here, we consider two undeveloped but important aspects of possible scenarios for the evolutionary pathway of the translation machinery: the role of unassigned codons in early stages of the code and the incorporation of tRNA anticodon modifications.
Wouter D. Hoff+1 more
openaire +3 more sources
ABSTRACT Genitopatellar syndrome (GPS) and Say‐Barber‐Biesecker‐Young‐Simpson Syndrome (SBBYSS) are clinically distinct neurodevelopmental disorders caused by monoallelic pathogenic variants in KAT6B. In some cases, GPS and SBBYSS features can overlap, determining an intermediate phenotype.
Vittorio Maglione+12 more
wiley +1 more source