Results 181 to 190 of about 21,426,149 (319)
Harnessing Quantitative Medicine to Advance Oncology Drug Development. [PDF]
Wu B, Yoshida K, Chanu P, Li C.
europepmc +1 more source
Loss of eIF5A rewires thapsigargin‐mediated endoplasmic reticulum stress responses in multiple myeloma cells by selective translation of mRNA transcripts, consequently dampening thapsigargin‐induced unfolded protein response (UPR) activation and shifting the balance from induction of apoptosis toward cell survival and proliferation.
Demi Both +7 more
wiley +1 more source
Organoids as an emerging platform for osteoarthritis drug development. [PDF]
Lyu X, Wang J, Su J.
europepmc +1 more source
High‐risk bladder cancer is typically treated with Bacillus Calmette‐Guérin (BCG), but 30–40% of patients relapse. No FDA‐ or CE‐approved biomarkers currently predict or prognosticate BCG failure. We systematically reviewed the literature and identified 72 eligible studies, revealing several promising biomarkers associated with BCG treatment response ...
Rui Ribeiro‐Pereira +7 more
wiley +1 more source
Progress in Anti-Obesity Drug Development: A Pharmacodynamics Perspective. [PDF]
Ahmad I +9 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
Role of health digital twins in oncology drug development - a primer. [PDF]
Garcia Requesens M +10 more
europepmc +1 more source
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
Mutant p53R273H disrupts PDPK1 homodimerization and contributes to PDPK1 activation
How mutant p53R273H drives AKT signaling is unclear. We show that p53R273H, but not wild‐type, directly binds PDPK1 via a mutation‐dependent conformational change. This interaction disrupts inhibitory PDPK1 homodimerization and enhances AKT phosphorylation.
Mei Chee Lim +11 more
wiley +1 more source
Advancing Neonatal Drug Development Through Industry-Academic Collaboration. [PDF]
Ramanathan R +3 more
europepmc +1 more source

