Results 71 to 80 of about 598,360 (260)
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
The VHL tumor suppressor at the crossroad of protein folding, aggregation, and cancer
Mutations, environmental stress, and chaperone dysfunction can destabilize pVHL, promoting its conversion from the native folded state into amyloid‐like assemblies. This transition may contribute to protein storage, cell dormancy, survival, and drug resistance.
Lara Abad +2 more
wiley +1 more source
Effect of telephone follow-up on retention and balance in an alcohol intervention trial
Objectives: Telephone follow-up is not currently recommended as a strategy to improve retention in randomized trials. The aims of this study were to estimate the effect of telephone follow-up on retention, identify participant characteristics predictive ...
Natalie A. Johnson +10 more
doaj +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
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
Factors associated with retention in HIV care at Sediba Hope Medical Centre
Background: Lost to follow-up (LTFU) is a major challenge that hinders the success of antiretroviral treatment (ART). Objective: To identify factors conducted to a low LTFU rate. Methods: We conducted a two-part descriptive and quantitative study. Part
Nishana Ramdas +2 more
doaj +1 more source
Targeting the EpCAM‐AXL axis to overcome drug resistance in lung cancer
Lung cancer cells often evade therapy by hijacking signaling pathways. We reveal that cleaved EpCAM (sEpCAM) stabilizes the oncogenic protein AXL, driving NF‐κB and STAT3‐mediated chemoresistance. This EpCAM‐AXL axis identifies a high‐risk patient subset with poor prognosis.
Alexa Guerrero‐Alba +5 more
wiley +1 more source
LVRF (lymphatic and vascular resistance factor) is a VEGFA splice variant upregulated in response to anti‐angiogenic therapy that fosters tumor adaptation through enhanced vascularization, lymphangiogenesis, and metastatic dissemination. Targeting LVRF with fully human neutralizing antibodies disrupts these processes and limits resistant tumor growth ...
Marion David +12 more
wiley +1 more source
Drop out in a clinic of preterm development follow-up: rates and causes
Objective: To make a survey of the dropping out rate and investigate its possible causes in preterm infants follow-up program. Method: Descriptive study, using the quantitative and qualitative methodology, developed in a follow-up preterm born children ...
Mariana Lacerda Gontijo +3 more
doaj
USP7 inhibits FOXO1 activity in chronic lymphocytic leukaemia cells enhancing cell survival
CLL cells rely on BCR‐mediated signalling for survival and proliferation in part through suppression of FOXO1. FOXO1 activity is regulated by a plethora of post‐translational modifications including phosphorylation and ubiquitination. We demonstrated that dual inhibition of BCR signalling and the deubiquitinase USP7 activates FOXO1, modulating its ...
Hassan N.B. Almuhanna +8 more
wiley +1 more source

