Results 121 to 130 of about 1,104,645 (398)

Targeting of PTP4A3 overexpression sensitises HGSOC cells towards chemotherapeutic drugs

open access: yesMolecular Oncology, EarlyView.
In HGSOC with normal KRAS expression, high PTP4A3 expression regulates autophagy activation. Conversely, in HGSOC with high KRAS expression, KRAS dictates autophagy control, and PTP4A3 is not required. When high PTP4A3 expression is inhibited, HGSOC cells are preferentially sensitised towards DNA‐damaging agents.
Ana López‐Garza   +3 more
wiley   +1 more source

RKIP overexpression reduces lung adenocarcinoma aggressiveness and sensitizes cells to EGFR‐targeted therapies

open access: yesMolecular Oncology, EarlyView.
RKIP, a metastasis suppressor protein, modulates key oncogenic pathways in lung adenocarcinoma. In silico analyses linked low RKIP expression to poor survival. Functional studies revealed RKIP overexpression reduces tumor aggressiveness and enhances sensitivity to EGFR‐targeted therapies, while its loss promotes resistance.
Ana Raquel‐Cunha   +10 more
wiley   +1 more source

Cryptic transcripts from a ubiquitous plasmid origin of replication confound tests for cis-regulatory function. [PDF]

open access: yes, 2012
A vast amount of research on the regulation of gene expression has relied on plasmid reporter assays. In this study, we show that plasmids widely used for this purpose constitutively produce substantial amounts of RNA from a TATA-containing cryptic ...
Hiraoka, Kei   +3 more
core   +2 more sources

YAP1::TFE3 mediates endothelial‐to‐mesenchymal plasticity in epithelioid hemangioendothelioma

open access: yesMolecular Oncology, EarlyView.
The YAP1::TFE3 fusion protein drives endothelial‐to‐mesenchymal transition (EndMT) plasticity, resulting in the loss of endothelial characteristics and gain of mesenchymal‐like properties, including resistance to anoikis, increased migratory capacity, and loss of contact growth inhibition in endothelial cells.
Ant Murphy   +9 more
wiley   +1 more source

Emerging role of ARHGAP29 in melanoma cell phenotype switching

open access: yesMolecular Oncology, EarlyView.
This study gives first insights into the role of ARHGAP29 in malignant melanoma. ARHGAP29 was revealed to be connected to tumor cell plasticity, promoting a mesenchymal‐like, invasive phenotype and driving tumor progression. Further, it modulates cell spreading by influencing RhoA/ROCK signaling and affects SMAD2 activity. Rho GTPase‐activating protein
Beatrice Charlotte Tröster   +3 more
wiley   +1 more source

A bacterial gene-drive system efficiently edits and inactivates a high copy number antibiotic resistance locus. [PDF]

open access: yes, 2019
Gene-drive systems in diploid organisms bias the inheritance of one allele over another. CRISPR-based gene-drive expresses a guide RNA (gRNA) into the genome at the site where the gRNA directs Cas9-mediated cleavage.
Bier, Ethan   +3 more
core   +1 more source

Deletion of parasite immune modulatory sequences combined with immune activating signals enhances vaccine mediated protection against filarial nematodes [PDF]

open access: yes, 2012
<p>Background: Filarial nematodes are tissue-dwelling parasites that can be killed by Th2-driven immune effectors, but that have evolved to withstand immune attack and establish chronic infections by suppressing host immunity. As a consequence, the
AB Fredriksen   +63 more
core   +3 more sources

Differentiation of IncL and IncM Plasmids Associated with the Spread of Clinically Relevant Antimicrobial Resistance

open access: yesPLoS ONE, 2015
Introduction bla OXA-48, bla NDM-1 and bla CTX-M-3 are clinically relevant resistance genes, frequently associated with the broad-host range plasmids of the IncL/M group.
A. Carattoli   +4 more
semanticscholar   +1 more source

Modeling hepatic fibrosis in TP53 knockout iPSC‐derived human liver organoids

open access: yesMolecular Oncology, EarlyView.
This study developed iPSC‐derived human liver organoids with TP53 gene knockout to model human liver fibrosis. These organoids showed elevated myofibroblast activation, early disease markers, and advanced fibrotic hallmarks. The use of profibrotic differentiation medium further amplified the fibrotic signature seen in the organoids.
Mustafa Karabicici   +8 more
wiley   +1 more source

Inhibition of CDK9 enhances AML cell death induced by combined venetoclax and azacitidine

open access: yesMolecular Oncology, EarlyView.
The CDK9 inhibitor AZD4573 downregulates c‐MYC and MCL‐1 to induce death of cytarabine (AraC)‐resistant AML cells. This enhances VEN + AZA‐induced cell death significantly more than any combination of two of the three drugs in AraC‐resistant AML cells.
Shuangshuang Wu   +18 more
wiley   +1 more source

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