Results 101 to 110 of about 1,861,609 (310)

G-quadruplex structural motifs modulate protein–RNA interactions within the transcriptome

open access: yesGenome Biology
Background RNA secondary structures, including G-quadruplexes (G4s), have emerged as vital players in protein–RNA interactions. The RNA-binding protein Fused in Sarcoma (FUS), which is strongly implicated in both neurodegenerative disease and cancer, is ...
Uditi Bhatt   +6 more
doaj   +1 more source

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

Expression of RNA-binding motif 10 is associated with advanced tumor stage and malignant behaviors of lung adenocarcinoma cancer cells

open access: yesTumor Biology, 2017
This study assessed RNA-binding motif 10 expression in lung adenocarcinoma tissues and examined the role and mechanism of RNA-binding motif 10 in the regulation of lung adenocarcinoma malignancy.
Guofang Guan   +8 more
doaj   +1 more source

Single nucleotide polymorphisms affect RNA-protein interactions at a distance through modulation of RNA secondary structures.

open access: yesPLoS Computational Biology, 2020
Single nucleotide polymorphisms are widely associated with disease, but the ways in which they cause altered phenotypes are often unclear, especially when they appear in non-coding regions. One way in which non-coding polymorphisms could cause disease is
Elan Shatoff, Ralf Bundschuh
doaj   +1 more source

A global function for transcription factors in assisting RNA polymerase II termination. [PDF]

open access: yes, 2017
The role of transcription factors (TFs) on nucleosome positioning, RNA polymerase recruitment, and transcription initiation has been extensively characterized.
Chanfreau, Guillaume F, Roy, Kevin
core   +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-binding proteins in Mendelian disease

open access: yesTrends in Genetics, 2013
RNA-binding proteins (RBPs) control all aspects of RNA fate, and defects in their function underlie a broad spectrum of human pathologies. We focus here on two recent studies that uncovered the in vivo mRNA interactomes of human cells, jointly implicating over 1100 proteins in RNA binding.
Castello, Alfredo   +3 more
openaire   +3 more sources

Therapeutic strategies for MMAE‐resistant bladder cancer through DPP4 inhibition

open access: yesMolecular Oncology, EarlyView.
We established monomethyl auristatin E (MMAE)‐resistant bladder cancer (BC) cell lines by exposure to progressively increasing concentrations of MMAE in vitro. RNA sequencing showed DPP4 expression was increased in MMAE‐resistant BC cells. Both si‐DPP4 and the DPP4 inhibitor sitagliptin suppressed the viability of MMAE‐resistant BC cells.
Gang Li   +10 more
wiley   +1 more source

To translate, or not to translate: viral and host mRNA regulation by interferon-stimulated genes. [PDF]

open access: yes, 2015
Type I interferon (IFN) is one of the first lines of cellular defense against viral pathogens. As a result of IFN signaling, a wide array of IFN-stimulated gene (ISG) products is upregulated to target different stages of the viral life cycle.
Li, Melody MH   +2 more
core   +1 more source

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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