Results 191 to 200 of about 24,946,429 (302)
Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer
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
HIV disease progression among heterosexually-infected individuals before the introduction of universal ART in China: A linear mixed-effects model. [PDF]
Tang L +8 more
europepmc +1 more source
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
Application of Linear Mixed-Effects Model, Principal Component Analysis, and Clustering to Direct Energy Deposition Fabricated Parts Using FEM Simulation Data. [PDF]
Pazireh S, Mirazimzadeh SE, Urbanic J.
europepmc +1 more source
Linear mixed-effects model of QTc prolongation for olmesartan medoxomil. [PDF]
Song S, Matsushima N, Lee J, Mendell J.
europepmc +1 more source
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
[Prediction of hearing change in children with enlarged vestibular aqueduct with different genotypes by linear mixed-effects model]. [PDF]
Deng L +7 more
europepmc +1 more source
Isocitrate dehydrogenase 1 (IDH1) mutations are highly recurrent in multiple human cancer types, including cholangiocarcinoma and glioma. IDH1 R132C is the most common IDH1 mutation in cholangiocarcinoma and likely arises from APOBEC3A‐ or APOBEC3B‐mediated deamination.
Kelly E. Butler +3 more
wiley +1 more source

