Results 141 to 150 of about 685,668 (343)
A Sequence-Specific RNA-Binding Protein Complements Apobec-1 To Edit Apolipoprotein B mRNA [PDF]
Anuradha Mehta, Donna M. Driscoll
openalex +1 more source
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
Systematic analysis reveals cis and trans determinants affecting C-to-U RNA editing in Arabidopsis thaliana [PDF]
Duan Chu, Lai Wei
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Cell surface interactome analysis identifies TSPAN4 as a negative regulator of PD‐L1 in melanoma
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
Targeted RNA base editing for therapeutic: mechanisms and advances
RNA base editing, which enables RNA base modification through effector proteins guided by targeting systems, is a powerful technology to correct disease-associated point mutations.
Weikai Yan, Xiaocheng Weng
doaj +1 more source
Plecstatin inhibits hepatocellular carcinoma tumorigenesis and invasion through cytolinker plectin
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
Heritable CRISPR-Cas9 editing of plant genomes using RNA virus vectors [PDF]
Mireia Uranga +3 more
openalex +1 more source
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

