Search results for "N-3"
showing 10 items of 365 documents
CCDC 607533: Experimental Crystal Structure Determination
2007
Related Article: A.Hoffmann-Roder, E.Schweizer, J.Egger, P.Seiler, U.Obst-Sander, B.Wagner, M.Kansy, D.W.Banner, F.Diederich|2006|ChemMedChem|1|1205|doi:10.1002/cmdc.200600124
CCDC 1565154: Experimental Crystal Structure Determination
2018
Related Article: Mirella Wawryszyn, Paul F. Sauter, Martin Nieger, Martin R.Koos, Christine Koehler, Burkhard Luy, Edward A. Lemke, Stefan Bräse|2018|Eur.J.Org.Chem.|2018|4296|doi:10.1002/ejoc.201800602
CCDC 1428734: Experimental Crystal Structure Determination
2015
Related Article: Nora M. Kaluza, Dieter Schollmeyer, Udo Nubbemeyer|2016|Eur.J.Org.Chem.|2016|357|doi:10.1002/ejoc.201501341
High‐power ultrasound altered the polyphenolic content and antioxidant capacity in cloudy apple juice during storage
2019
The aim was to investigate the influence of high‐power ultrasound treatment (HPU) on polyphenolic stability and antioxidant capacity in cloudy apple juice during 7 days of storage at 4°C. HPU (100 W, 30 kHz frequency) was operated at: (i) amplitude 40 versus 80%, (ii) the probe diameter 7 versus 10 mm, and (iii) treatment time of 3, 6, and 9 min. Total phenols (TP), total flavan‐3‐ols (TFL), and in vitro antioxidant capacity (DPPH and FRAP) were determined spectrophotometrically. Findings revealed that HPU significantly decreased TP, TFL, and antioxidant capacity in the samples. However, results indicated that examined sonication parameters, represented as the probe diameter and treatment t…
Long Pentraxin 3-Mediated Fibroblast Growth Factor Trapping Impairs Fibrosarcoma Growth
2018
Fibrosarcomas are soft tissue mesenchymal tumors originating from transformed fibroblasts. Fibroblast growth factor-2 (FGF2) and its tyrosine-kinase receptors (FGFRs) play pivotal roles in fibrosarcoma onset and progression, FGF2 being actively produced by fibroblasts in all stages along their malignant transformation to the fibrosarcoma stage. The soluble pattern recognition receptor long pentraxin-3 (PTX3) is an extrinsic oncosuppressor whose expression is reduced in different tumor types, including soft tissue sarcomas, via hypermethylation of its gene promoter. PTX3 interacts with FGF2 and other FGF family members, thus acting as a multi-FGF antagonist able to inhibit FGF-dependent neov…
Effects of the MDM-2 inhibitor Nutlin-3a on PDAC cells containing and lacking WT-TP53 on sensitivity to chemotherapy, signal transduction inhibitors …
2019
Abstract Mutations at the TP53 gene are readily detected (approximately 50–75%) in pancreatic ductal adenocarcinoma (PDAC) patients. TP53 was previously thought to be a difficult target as it is often mutated, deleted or inactivated on both chromosomes in certain cancers. In the following study, the effects of restoration of wild-type (WT) TP53 activity on the sensitivities of MIA-PaCa-2 pancreatic cancer cells to the MDM2 inhibitor nutlin-3a in combination with chemotherapy, targeted therapy, as well as, nutraceuticals were examined. Upon introduction of the WT-TP53 gene into MIA-PaCa-2 cells, which contain a TP53 gain of function (GOF) mutation, the sensitivity to the MDM2 inhibitor incre…
Roles of TP53 in determining therapeutic sensitivity, growth, cellular senescence, invasion and metastasis.
2016
TP53 is a critical tumor suppressor gene that regulates cell cycle progression, apoptosis, cellular senescence and many other properties critical for control of normal cellular growth and death. Due to the pleiotropic effects that TP53 has on gene expression and cellular physiology, mutations at this tumor suppressor gene result in diverse physiological effects. T53 mutations are frequently detected in numerous cancers. The expression of TP53 can be induced by various agents used to treat cancer patients such as chemotherapeutic drugs and ionizing radiation. Radiation will induce Ataxia telangiectasia mutated (ATM) and other kinases that results in the phosphorylation and activation of TP53…
New insights into the mechanism of action of pyrazolo[1,2-a]benzo[1,2,3,4]tetrazin-3-one derivatives endowed with anticancer potential
2018
Due to the scarce biological profile, the pyrazolo[1,2-a]benzo[1,2,3,4]tetrazine-3-one scaffold (PBT) has been recently explored as promising core for potential anticancer candidates. Several suitably decorated derivatives (PBTs) exhibited antiproliferative activity in the low-micromolar range associated with apoptosis induction and cell cycle arrest on S phase. Herein, we selected the most active derivatives and submitted them to further biological explorations to deepen the mechanism of action. At first, a DNA targeting is approached by means of flow Linear Dichroism experiments so as to evaluate how small planar molecules might interact with DNA, including the interference with the catal…
IL-33/ST2 pathway drives regulatory T cell dependent suppression of liver damage upon cytomegalovirus infection.
2017
Regulatory T (Treg) cells dampen an exaggerated immune response to viral infections in order to avoid immunopathology. Cytomegaloviruses (CMVs) are herpesviruses usually causing asymptomatic infection in immunocompetent hosts and induce strong cellular immunity which provides protection against CMV disease. It remains unclear how these persistent viruses manage to avoid induction of immunopathology not only during the acute infection but also during life-long persistence and virus reactivation. This may be due to numerous viral immunoevasion strategies used to specifically modulate immune responses but also induction of Treg cells by CMV infection. Here we demonstrate that liver Treg cells …
Sema3a plays a role in the pathogenesis of CHARGE syndrome
2018
CHARGE syndrome is an autosomal dominant malformation disorder caused by heterozygous loss of function mutations in the chromatin remodeler CHD7. Chd7 regulates the expression of Sema3a, which also contributes to the pathogenesis of Kallmann syndrome, a heterogeneous condition with the typical features hypogonadotropic hypogonadism and an impaired sense of smell. Both features are common in CHARGE syndrome suggesting that SEMA3A may provide a genetic link between these syndromes. Indeed, we find evidence that SEMA3A plays a role in the pathogenesis of CHARGE syndrome. First, Chd7 is enriched at the Sema3a promotor in neural crest cells and loss of function of Chd7 inhibits Sema3a expression…