Results 91 to 100 of about 694,106 (294)

Transcriptome-wide identification of A > I RNA editing sites by inosine specific cleavage [PDF]

open access: yes, 2013
Adenosine to inosine (A > I) RNA editing, which is catalyzed by the ADAR family of proteins, is one of the fundamental mechanisms by which transcriptomic diversity is generated.
Cattenoz, Pierre B.   +3 more
core   +2 more sources

Cis‐regulatory and long noncoding RNA alterations in breast cancer – current insights, biomarker utility, and the critical need for functional validation

open access: yesMolecular Oncology, EarlyView.
The noncoding region of the genome plays a key role in regulating gene expression, and mutations within these regions are capable of altering it. Researchers have identified multiple functional noncoding mutations associated with increased cancer risk in the genome of breast cancer patients.
Arnau Cuy Saqués   +3 more
wiley   +1 more source

CDK13 RNA Over-Editing Mediated by ADAR1 Associates with Poor Prognosis of Hepatocellular Carcinoma Patients

open access: yesCellular Physiology and Biochemistry, 2018
Background/Aims: Aberrant RNA editing, mediated by adenosine deaminases acting on RNA (ADAR), serves as a post-transcriptional event participating in tumorigenesis and prognosis. However, the RNA editing profiles during HCC progression and their clinical
Xiuqing Dong   +8 more
doaj   +1 more source

Large-scale analysis of structural, sequence and thermodynamic characteristics of A-to-I RNA editing sites in human Alu repeats [PDF]

open access: yes, 2010
Background Alu repeats in the human transcriptome undergo massive adenosine to inosine RNA editing. This process is selective, as editing efficiency varies greatly among different adenosines.
Yoav Kleinberger, Eli Eisenberg
core   +2 more sources

Monitoring of circulating tumor DNA allows early detection of disease relapse in patients with operable breast cancer

open access: yesMolecular Oncology, EarlyView.
Monitoring circulating tumor DNA (ctDNA) in patients with operable breast cancer can reveal disease relapse earlier than radiology in a subset of patients. The failure to detect ctDNA in some patients with recurrent disease suggests that ctDNA could serve as a supplement to other monitoring approaches.
Kristin Løge Aanestad   +35 more
wiley   +1 more source

CAS9 is a genome mutator by directly disrupting DNA-PK dependent DNA repair pathway. [PDF]

open access: yes, 2020
With its high efficiency for site-specific genome editing and easy manipulation, the clustered regularly interspaced short palindromic repeats (CRISPR)/ CRISPR associated protein 9 (CAS9) system has become the most widely used gene editing technology in ...
Chen, Qu   +6 more
core  

Cell surface interactome analysis identifies TSPAN4 as a negative regulator of PD‐L1 in melanoma

open access: yesMolecular Oncology, EarlyView.
Using cell surface proximity biotinylation, we identified tetraspanin TSPAN4 within the PD‐L1 interactome of melanoma cells. TSPAN4 negatively regulates PD‐L1 expression and lateral mobility by limiting its interaction with CMTM6 and promoting PD‐L1 degradation.
Guus A. Franken   +7 more
wiley   +1 more source

Plecstatin inhibits hepatocellular carcinoma tumorigenesis and invasion through cytolinker plectin

open access: yesMolecular Oncology, EarlyView.
The ruthenium‐based metallodrug plecstatin exerts its anticancer effect in hepatocellular carcinoma (HCC) primarily through selective targeting of plectin. By disrupting plectin‐mediated cytoskeletal organization, plecstatin inhibits anchorage‐dependent growth, cell polarization, and tumor cell dissemination.
Zuzana Outla   +10 more
wiley   +1 more source

RNA editing regulates insect gamma-aminobutyric acid receptor function and insecticide sensitivity [PDF]

open access: yes, 2008
A-to-I pre-mRNA editing by adenosine deaminase enzymes has been reported to enhance protein diversity in the nervous system. In Drosophila, the resistance to dieldrin (RDL) gamma-aminobutyric acid (GABA) receptor subunit displays an editing site (R122 ...
A. Hamon   +3 more
core   +3 more sources

Recurrent cancer‐associated ERBB4 mutations are transforming and confer resistance to targeted therapies

open access: yesMolecular Oncology, EarlyView.
We show that the majority of the 18 analyzed recurrent cancer‐associated ERBB4 mutations are transforming. The most potent mutations are activating, co‐operate with other ERBB receptors, and are sensitive to pan‐ERBB inhibitors. Activating ERBB4 mutations also promote therapy resistance in EGFR‐mutant lung cancer.
Veera K. Ojala   +15 more
wiley   +1 more source

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