Results 91 to 100 of about 1,593,705 (264)

Partial FAK suppression promotes tumor growth, an effect reversed by macrophage p110δ PI3K inactivation

open access: yesMolecular Oncology, EarlyView.
Partial inhibition of focal adhesion kinase (FAK) can paradoxically promote tumor growth, rather than simply producing a weaker antitumor effect than that observed with strong FAK suppression. In breast cancer and melanoma models, targeting p110δ PI3K, particularly in macrophages, counteracted these tumor‐promoting effects, highlighting the importance ...
Lydia Xenou   +4 more
wiley   +1 more source

RNA and DNA nanoparticles for triggering RNA interference: DOI: 10.14800/rd.724

open access: yes, 2015
Control over the delivery of different functionalities and their synchronized activation in vivo is a challenging undertaking that requires careful design and implementation.
Ziad El Tannir, Kirill A Afonin, Bruce A Shapiro
core   +1 more source

Maf1-mediated repression of RNA polymerase III transcription inhibits tRNA degradation via RTD pathway [PDF]

open access: yes, 2012
tRNA precursors, which are transcribed by RNA polymerase III, undergo end-maturation, splicing and base modifications. Hypomodified tRNAs, such as tRNAVal(AAC), lacking 7-methylguanosine and 5-methylcytidine modifications, are subject to degradation by a
Boguta, Magdalena   +3 more
core   +1 more source

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

Genomewide Patterns of Substitution in Adaptively Evolving Populations of the RNA Bacteriophage MS2 [PDF]

open access: yes, 2009
Experimental evolution of bacteriophage provides a powerful means of studying the genetics of adaptation, as every substitution contributing to adaptation can be identified and characterized.
Charlesworth, Brian   +1 more
core   +1 more source

Overview of RNA interference therapeutics [PDF]

open access: yesSongklanakarin Journal of Science and Technology (SJST), 2012
Since the term RNA interference (RNAi) was coined in 1998, much knowledge about RNAi has accumulated. Presently,RNAi is known as a power tool for studying gene function as well as a potential therapeutic molecular technique for a widerange of disorders ...
Nattanan T-Thienprasert Panjaworayan
doaj  

The VHL tumor suppressor at the crossroad of protein folding, aggregation, and cancer

open access: yesMolecular Oncology, EarlyView.
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

Disease-Causing Allele-Specific Silencing by RNA Interference

open access: yesPharmaceuticals, 2013
Small double-stranded RNAs (dsRNAs) of approximately 21-nucleotides in size, referred to as small interfering RNA (siRNA) duplexes, can induce sequence-specific posttranscriptional gene silencing, or RNA interference (RNAi).
Hirohiko Hohjoh
doaj   +1 more source

A role for eIF5A in translational control of stress‐inducible proteins in multiple myeloma cell lines

open access: yesMolecular Oncology, EarlyView.
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

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

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