The novel atypical retinoid ST1926 is active in ATRA resistant neuroblastoma cells acting by a different mechanism

2007 ◽  
Vol 73 (5) ◽  
pp. 643-655 ◽  
Author(s):  
Angela Maria Di Francesco ◽  
Daniela Meco ◽  
Anna Rita Torella ◽  
Giuseppe Barone ◽  
Maurizio D’Incalci ◽  
...  
Nanomaterials ◽  
2019 ◽  
Vol 9 (9) ◽  
pp. 1282 ◽  
Author(s):  
Neha Karekar ◽  
Anik Karan ◽  
Elnaz Khezerlou ◽  
Neela Prajapati ◽  
Chelsea D. Pernici ◽  
...  

The novel synthesis of metal-containing biohybrids using self-assembly methods at physiological temperatures (37 °C) was compared for copper and silver using the amino acid dimer cystine. Once assembled, the copper containing biohybrid is a stable, high-aspect ratio structure, which we call CuHARS. Using the same synthesis conditions, but replacing copper with silver, we have synthesized cystine-capped silver nanoparticles (AgCysNPs), which are shown here to form stable colloid solutions in contrast to the CuHARS, which settle out from a 1 mg/mL solution in 90 min. Both the copper and silver biohybrids, as synthesized, demonstrate very low agglomeration which we have applied for the purpose of applications with cell culture methods, namely, for testing as anti-cancer compounds. AgCysNPs (1000 ng/mL) demonstrated significant toxicity (only 6.8% viability) to glioma and neuroblastoma cells in vitro, with concentrations as low as 20 ng/mL causing some toxicity. In contrast, CuHARS required at least 5 μg/mL. For comparative purposes, silver sulfate at 100 ng/mL decreased viability by 52% and copper sulfate at 100 ng/mL only by 19.5% on glioma cells. Using these methods, the novel materials were tested here as metal–organic biohybrids (MOBs), and it is anticipated that the functionalization and dynamics of MOBs may result in building a foundation of new materials for cellular applications, including cell engineering of both normal and diseased cells and tissue constructs.


2013 ◽  
Vol 172-173 ◽  
pp. 14-19 ◽  
Author(s):  
Elsie A. Orellano ◽  
Michelle M. Cartagena ◽  
Karolyna Rosado ◽  
Néstor M. Carballeira

1994 ◽  
Vol 37 (6) ◽  
pp. 868-872 ◽  
Author(s):  
Alan P. Kozikowski ◽  
Abdul H. Fauq ◽  
Robert A. Wilcox ◽  
R. A. John Challiss ◽  
Stefan R. Nahorski

2011 ◽  
Vol 10 (12) ◽  
pp. 2373-2383 ◽  
Author(s):  
Tetyana Klymenko ◽  
Martin Brandenburg ◽  
Christopher Morrow ◽  
Caroline Dive ◽  
Guy Makin

2022 ◽  
Vol 23 (1) ◽  
pp. 554
Author(s):  
Tracey E. Swingler ◽  
Lingzi Niu ◽  
Matthew G. Pontifex ◽  
David Vauzour ◽  
Ian M. Clark

The complete molecular mechanisms underlying the pathophysiology of Alzheimer’s disease (AD) remain to be elucidated. Recently, microRNA-455-3p has been identified as a circulating biomarker of early AD, with increased expression in post-mortem brain tissue of AD patients. MicroRNA-455-3p also directly targets and down-regulates APP, with the overexpression of miR-455-3p suppressing its toxic effects. Here, we show that miR-455-3p expression decreases with age in the brains of wild-type mice. We generated a miR-455 null mouse utilising CRISPR-Cas9 to explore its function further. Loss of miR-455 resulted in increased weight gain, potentially indicative of metabolic disturbances. Furthermore, performance on the novel object recognition task diminished significantly in miR-455 null mice (p = 0.004), indicating deficits in recognition memory. A slight increase in anxiety was also captured on the open field test. BACE1 and TAU were identified as new direct targets for miR-455-3p, with overexpression of miR-455-3p leading to a reduction in the expression of APP, BACE1 and TAU in neuroblastoma cells. In the hippocampus of miR-455 null mice at 14 months of age, the levels of protein for APP, BACE1 and TAU were all increased. Such findings reinforce the involvement of miR-455 in AD progression and demonstrate its action on cognitive performance.


2014 ◽  
Vol 87 (4) ◽  
pp. 611-624 ◽  
Author(s):  
Jennifer C. Lennon ◽  
Sandra A. Bright ◽  
Eilis Carroll ◽  
Stefania Butini ◽  
Giuseppe Campiani ◽  
...  

2004 ◽  
Vol 68 (7) ◽  
pp. 1279-1288 ◽  
Author(s):  
Annemieke J.M. de Ruijter ◽  
Stephan Kemp ◽  
Gertjan Kramer ◽  
Rutger J. Meinsma ◽  
Judith O. Kaufmann ◽  
...  

2019 ◽  
Author(s):  
Emily C. Freund ◽  
Anne L. Sapiro ◽  
Qin Li ◽  
Sandra Linder ◽  
James J. Moresco ◽  
...  

AbstractAdenosine-to-Inosine RNA editing is catalyzed by ADAR enzymes that deaminate adenosine to inosine. While many RNA editing sites are known, few trans regulators have been identified. We perform BioID followed by mass-spectrometry to identify trans regulators of ADAR1 and ADAR2 in HeLa and M17 neuroblastoma cells. We identify known and novel ADAR-interacting proteins. Using ENCODE data we validate and characterize a subset of the novel interactors as global or site-specific RNA editing regulators. Our set of novel trans regulators includes all four members of the DZF-domain-containing family of proteins: ILF3, ILF2, STRBP, and ZFR. We show that these proteins interact with each ADAR and modulate RNA editing levels. We find ILF3 is a global negative regulator of editing. This work demonstrates the broad roles RNA binding proteins play in regulating editing levels and establishes DZF-domain containing proteins as a group of highly influential RNA editing regulators.


2010 ◽  
Vol 34 (8) ◽  
pp. S33-S33
Author(s):  
Wenchao Ou ◽  
Haifeng Chen ◽  
Yun Zhong ◽  
Benrong Liu ◽  
Keji Chen

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