Results 101 to 110 of about 2,617,421 (301)

Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer

open access: yesMolecular Oncology, EarlyView.
Cancer cells' high translational demand creates opportunities to therapeutically target ribosome function. Ribosome stalling and collisions activate ZAKα and the ribotoxic stress response (RSR), which can trigger rapid, p53‐independent apoptosis in cancer.
Anastassiya Kim   +7 more
wiley   +1 more source

Competitive binding of MOP to CquiOBP1.

open access: yes, 2013
Fluorescence emission spectra of CquiOBP1 alone (15 µg/ml; black), in the presence of NPN (2 µl, 3.2 mM; light red), and after titrating with increasing amounts of MOP (1–3 µl, 3.2 mM; green, blue, and dark red lines).
Rosângela M. R. Barbosa (376861)   +9 more
core   +1 more source

Hsa_circ_0000423 promotes colorectal cancer EMT and immune escape by competitive adsorption of miR-369-3p mediating CCND1 expression

open access: yesDiscover Oncology
Background This investigation evaluated the mechanism of hsa_circ_0000423 in colorectal cancer (CRC). Methods The hsa_circ_0000423 gene was identified by bioinformatics analyses of GEO circRNA microarrays, and its expression in CRC was investigated ...
TianFu Huang   +5 more
doaj   +1 more source

An overview of pharmacodynamic

open access: yesSaudi Pharmaceutical Journal, 2017
The study of the magnitude and variation of drug response is defined as pharmacodynamics (PDs). PD models examine plasma concentration and effect relationship. It can predict the archetypal effect (E) of a drug as a function of the drug concentration (C)
Mohammed Saji Salahudeen   +1 more
doaj   +1 more source

Regulation of the lncRNA NEAT1 by p53‐ΔNp63 crosstalk modulates the DNA damage response and therapeutic efficacy in HNSCC

open access: yesMolecular Oncology, EarlyView.
In head and neck squamous cell carcinoma (HNSCC) p53 and p63 exert opposite roles on the transcription regulation of the lncRNA NEAT1. Under basal conditions, p53 levels are low and p63 represses NEAT1 expression. Upon genotoxic stress, p53 is rapidly induced, displacing p63 from the NEAT1 promoter leading to NEAT1 transcriptional activation and ...
Sara De Domenico   +5 more
wiley   +1 more source

Binding Specificity of Two PBPs in the Yellow Peach Moth Conogethes punctiferalis (Guenée)

open access: yesFrontiers in Physiology, 2018
Pheromone binding proteins (PBPs) play an important role in olfaction of insects by transporting sex pheromones across the sensillum lymph to odorant receptors.
Xing Ge   +6 more
doaj   +1 more source

Paclitaxel induces NM2‐dependent cellular contraction through GEF‐H1 dissociation from microtubules and RhoA/ROCK activation in cancer cells

open access: yesMolecular Oncology, EarlyView.
Taxanes are widely used chemotherapeutics whose effects on cellular mechanics remain poorly understood. We show that paclitaxel induces rapid cellular contraction by promoting GEF‐H1 dissociation from microtubules and non‐muscle myosin II activation through RhoA/ROCK.
Gloria Asensio‐Juárez   +5 more
wiley   +1 more source

p190A/ARHGAP35 and p190B/ARHGAP5 proteins in endometrial cancer: a novel cancer‐relevant paralog interplay

open access: yesMolecular Oncology, EarlyView.
This study identifies ARHGAP5, in addition to the frequently mutated ARHGAP35, as significantly mutated in endometrial cancer. Mutations in both genes co‐occur and are associated with their correlated downregulation. Functional CRISPR studies show that both paralogs regulate similar pathways, including actin cytoskeleton organization.
Mathilde Pinault   +12 more
wiley   +1 more source

Competitive protein binding assay for methotrexate

open access: yes, 1975
A competitive protein binding assay has been developed for methotrexate based on the tight binding of this drug to Lactobacillus casei dihydrofolate reductase (= tetrahydrofolate dehydrogenase; 5,6,7,8-tetrahydrofolate: NADP+ oxidoreductase; EC 1.5.1.3).
Myers, C E   +3 more
core   +1 more source

SPHINX31 acts as a SRPK1 inhibitor targeting the ATR/DNA‐PKcs/CHK1 replicative checkpoint to inhibit cell growth in non‐small cell lung cancer

open access: yesMolecular Oncology, EarlyView.
The kinase SRPK1 directly interacts with the protein TOPBP1 and regulates the pre‐mRNA splicing of WIZ thereby contributing to the activation of the ATR/CHK1 replicative checkpoint in response to replicative stress. This allows cancer cells' genomic stability and survival.
Amani Shreim   +17 more
wiley   +1 more source

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