Results 81 to 90 of about 11,560 (303)

Heterozygous loss‐of‐function alleles associate the conserved 3′‐5′ exoribonuclease EXOSC10 with hypersensitivity to the anticancer drug 5‐fluorouracil

open access: yesMolecular Oncology, EarlyView.
EXOSC10, an essential nuclear RNA exosome‐associated 3′‐5′ exoribonuclease, is inhibited by the anticancer drug 5‐fluorouracil (5‐FU), and EXOSC10 depletion increases 5‐FU sensitivity. The colon‐cancer variant EXOSC10S402T, located in a proteolysis motif, is stable and nuclear but nonfunctional in vivo.
Radhika Sain   +10 more
wiley   +1 more source

A PRELIMINARY STUDY ON ISOLATION AND ENUMERATION OF MYCOPLASMAS IN DENTAL PLAQUES: THE EFFECT OF SONICATION ON VIABILITY OF ORAL MYCOPLASMAS [PDF]

open access: yes, 1981
The effect of sonication on the viability of Mycoplasma salivarium and Mycoplasma orale was examined as a preliminary investigation on the quantitative studies on mycoplasmas in the dental plaques.
Masaroh, MATSUURA   +3 more
core   +2 more sources

Adaptor protein CIN85 potentiates the motility of osteosarcoma cells via the Akt/mTOR and MMP2‐COL3A1 axis

open access: yesMolecular Oncology, EarlyView.
CIN85 is highly expressed in osteosarcoma, particularly in metastatic lesions. Its overexpression increases cell migration and Matrigel invasion, while silencing CIN85 suppresses these behaviors. Transcriptome analysis shows that CIN85 regulates MMP2, COL3A1, and Akt/mTOR signaling. Targeting these pathways reverses CIN85‐induced motility, highlighting
Iryna Horak   +10 more
wiley   +1 more source

Mycoplasmas: Sophisticated, Reemerging, and Burdened by Their Notoriety [PDF]

open access: yes, 1997
Mycoplasmas are most unusual self-replicating bacteria, possessing very small genomes, lacking cell wall components, requiring cholesterol for membrane function and growth, using UGA codon for tryptophan, passing through "bacterial-retaining" filters ...
Joel B. Baseman, Joseph G. Tully
core   +1 more source

Interaction of HS1BP3 with cortactin modulates TKS5 localisation, cell secretion and cancer malignancy

open access: yesMolecular Oncology, EarlyView.
Here, we demonstrate that HS1BP3 interacts with Cortactin through a proline‐rich region (PRR3.1) and show that this interaction, and HS1BP3 itself, promote cancer cell proliferation and invasion. Inhibition of this interaction leads to build‐up of TKS5 in multivesicular endosomes and altered secretion of CD63 and CD9, providing an explanation for the ...
Arja Arnesen Løchen   +9 more
wiley   +1 more source

Ribonucleolytic activity of mycoplasmas [PDF]

open access: yes, 2014
Mycoplasmas are incapable of de novo synthesis of nucleotides and must therefore secrete nucleases in order to replenish the pool of nucleic acid precursors. The nucleolytic activity of mycoplasmas is an important factor in their pathogenicity. Bacterial
Ul'yanova V.   +11 more
core  

Preterm Premature Rupture of the Membranes and Genital Mycoplasmas [PDF]

open access: yes, 2009
Objective: The purpose of this study was to evaluate the prevalence of cervical colonization by genital mycoplasmas in patients with preterm premature rupture of the membranes (PPROM).
Jindřich Tošner   +2 more
core   +1 more source

Proteasome inhibitor, ixazomib prevents topoisomerase‐I degradation and reverses irinotecan resistance in colorectal cancer

open access: yesMolecular Oncology, EarlyView.
Ixazomib inhibits proteasome‐mediated degradation of topoisomerase I induced by irinotecan, thereby restoring drug sensitivity and promoting tumor cell death in colorectal cancer. Irinotecan, a topoisomerase I (topoI) inhibitor, is widely used for colorectal cancer, but resistance remains a major clinical challenge.
Yuho Ebata   +10 more
wiley   +1 more source

A Search For Mycoplasmas And Chlamydiae In Acne Lesions [PDF]

open access: yes, 1976
No mycoplasmas and no chlamydiae were found in cultures of 75 uninflamed comedones, 72 papulopustular lesions, and 7 cystic lesions from 14 subjects with acne.
Kenny, G E   +3 more
core   +1 more source

Developmental programmes drive cellular plasticity, disease progression and therapy resistance in lung adenocarcinoma

open access: yesMolecular Oncology, EarlyView.
This study shows that lung adenocarcinomas exploit developmental branching morphogenesis to acquire a therapy resistant basal‐like tumour cell state. This process was found to be regulated by combined TP53 loss‐of‐function and type‐I interferon signalling, identifying a novel axis for biomarker and therapeutic target discovery.
Kamila J Bienkowska   +13 more
wiley   +1 more source

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