Relevant bibliographies by topics / C26 cells

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Academic literature on the topic 'C26 cells'

Author: Grafiati
Published: 20 February 2024

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Journal articles on the topic "C26 cells"

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Kutkowska-Kaźmierczak, Anna, Małgorzata Rydzanicz, Aleksander Chlebowski, Kamila Kłosowska-Kosicka, Adriana Mika, Jakub Gruchota, Elżbieta Jurkiewicz, et al. "Dominant ELOVL1 mutation causes neurological disorder with ichthyotic keratoderma, spasticity, hypomyelination and dysmorphic features." Journal of Medical Genetics 55, no. 6 (March 1, 2018): 408–14. http://dx.doi.org/10.1136/jmedgenet-2017-105172.

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BackgroundIchthyosis and neurological involvement occur in relatively few known Mendelian disorders caused by mutations in genes relevant both for epidermis and neural function.ObjectivesTo identify the cause of a similar phenotype of ichthyotic keratoderma, spasticity, mild hypomyelination (on MRI) and dysmorphic features (IKSHD) observed in two unrelated paediatric probands without family history of disease.MethodsWhole exome sequencing was performed in both patients. The functional effect of prioritised variant in ELOVL1 (very-long-chain fatty acids (VLCFAs) elongase) was analysed by VLCFA profiling by gas chromatography–mass spectrometry in stably transfected HEK2932 cells and in cultured patient’s fibroblasts.ResultsProbands shared novel heterozygous ELOVL1 p.Ser165Phe mutation (de novo in one family, while in the other family, father could not be tested). In transfected cells p.Ser165Phe: (1) reduced levels of FAs C24:0-C28:0 and C26:1 with the most pronounced effect for C26:0 (P=7.8×10−6 vs HEK293 cells with wild type (wt) construct, no difference vs naïve HEK293) and (2) increased levels of C20:0 and C22:0 (P=6.3×10−7, P=1.2×10−5, for C20:0 and C22:0, respectively, comparison vs HEK293 cells with wt construct; P=2.2×10−7, P=1.9×10−4, respectively, comparison vs naïve HEK293). In skin fibroblasts, there was decrease of C26:1 (P=0.014), C28:0 (P=0.001) and increase of C20:0 (P=0.033) in the patient versus controls. There was a strong correlation (r=0.92, P=0.008) between the FAs profile of patient’s fibroblasts and that of p.Ser165Phe transfected HEK293 cells. Serum levels of C20:0–C26:0 FAs were normal, but the C24:0/C22:0 ratio was decreased.ConclusionThe ELOVL1 p.Ser165Phe mutation is a likely cause of IKSHD.
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Schutgens, R. B., I. W. Bouman, A. A. Nijenhuis, R. J. Wanders, and M. E. Frumau. "Profiles of very-long-chain fatty acids in plasma, fibroblasts, and blood cells in Zellweger syndrome, X-linked adrenoleukodystrophy, and rhizomelic chondrodysplasia punctata." Clinical Chemistry 39, no. 8 (August 1, 1993): 1632–37. http://dx.doi.org/10.1093/clinchem/39.8.1632.

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Abstract Profiles of saturated very-long-chain (> C22) fatty acids were studied in plasma, fibroblasts, erythrocytes, platelets, and leukocytes of patients affected by peroxisomal disorders such as Zellweger syndrome, X-linked adrenoleukodystrophy (X-ALD), and classic rhizomelic chondrodysplasia punctata (RCDP) and in controls. In Zellweger patients, the concentration of hexacosanoic acid (C26:0) and the C26:0/C22:0 ratio are greatly increased in plasma and fibroblasts. However, the plasma concentration of docosanoic acid (C22:0) is greatly decreased. Also in platelets, leukocytes, and to a lesser extent erythrocytes, the C26:0 concentrations and both the C26:0/C22:0 and C24:0/C22:0 ratios are greatly increased. The C24:0/C22:0 ratio is significantly increased in plasma, platelets, and leukocytes, but not in erythrocytes. In X-ALD, the C26:0 concentration and the C26:0/C22:0 and C24:0/C22:0 ratios are significantly increased in plasma, fibroblasts, platelets, and leukocytes, but the erythrocytes show substantial overlap in the 5-90% ranges between controls and patients. In RCDP, slightly increased C26:0 and C26:0/C22:0 ratios are found in erythrocytes, platelets, and leukocytes, but not in plasma and fibroblasts. We conclude that plasma and fibroblasts are the specimens of choice for biochemical diagnosis of Zellweger syndrome and X-ALD, respectively. The slight increase in C26:0 in blood cells of RCDP patients suggests a decreased flux of very-long-chain fatty acids through the peroxisomal beta-oxidation pathway in liver in this genetic disorder.
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Yamaguchi, A., T. Katagiri, T. Ikeda, J. M. Wozney, V. Rosen, E. A. Wang, A. J. Kahn, T. Suda, and S. Yoshiki. "Recombinant human bone morphogenetic protein-2 stimulates osteoblastic maturation and inhibits myogenic differentiation in vitro." Journal of Cell Biology 113, no. 3 (May 1, 1991): 681–87. http://dx.doi.org/10.1083/jcb.113.3.681.

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The in vitro effect of recombinant human bone morphogenetic protein-2 (rhBMP-2) on osteogenic and myogenic differentiation was examined in two clonal cell lines of rat osteoblast-like cells at different differentiation stages, ROB-C26 (C26) and ROB-C20 (C20). The C26 is a potential osteoblast precursor cell line that is also capable of differentiating into muscle cells and adipocytes; the C20 is a more differentiated osteoblastic cell line. Proliferation was stimulated by rhBMP-2 in C26 cells, but inhibited in C20 cells. rhBMP-2 greatly increased alkaline phosphate (ALP) activity in C26 cells, but not in C20 cells. The steady-state level of ALP mRNA was also increased by rhBMP-2 in C26 cells, but not in C20 cells. Production of 3',5'-cAMP in response to parathyroid hormone (PTH) was dose-dependently enhanced by adding rhBMP-2 in both C26 and C20 cells, though the stimulatory effect was much greater in the former. There was neither basal expression of osteocalcin mRNA nor its protein synthesis in C26 cells, but they were strikingly induced by rhBMP-2 in the presence of 1 alpha,25-dihydroxyvitamin D3. rhBMP-2 induced no appreciable changes in procollagen mRNA levels of type I and type III in the two cell lines. Differentiation of C26 cells into myotubes was greatly inhibited by adding rhBMP-2. The inhibitory effect of rhBMP-2 on myogenic differentiation was also observed in clonal rat skeletal myoblasts (L6). Like BMP-2, TGF-beta 1 inhibited myogenic differentiation. However, unlike BMP-2, TGF-beta 1 decreased ALP activity in both C26 and C20 cells. TGF-beta 1 induced neither PTH responsiveness nor osteocalcin production in C26 cells, but it increased PTH responsiveness in C20 cells. These results clearly indicate that rhBMP-2 is involved, at least in vitro, not only in inducing differentiation of osteoblast precursor cells into more mature osteoblast-like cells, but also in inhibiting myogenic differentiation.
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Zarrouk, Amira, Anne Vejux, Thomas Nury, Hammam I. El Hajj, Madouda Haddad, Mustapha Cherkaoui-Malki, Jean-Marc Riedinger, Mohamed Hammami, and Gérard Lizard. "Induction of Mitochondrial Changes Associated with Oxidative Stress on Very Long Chain Fatty Acids (C22:0, C24:0, or C26:0)-Treated Human Neuronal Cells (SK-NB-E)." Oxidative Medicine and Cellular Longevity 2012 (2012): 1–15. http://dx.doi.org/10.1155/2012/623257.

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In Alzheimer's disease, lipid alterations point towards peroxisomal dysfunctions. Indeed, a cortical accumulation of saturated very long chain fatty acids (VLCFAs: C22:0, C24:0, C26:0), substrates for peroxisomalβ-oxidation, has been found in Alzheimer patients. This study was realized to investigate the effects of VLCFAs at the mitochondrial level since mitochondrial dysfunctions play crucial roles in neurodegeneration. On human neuronal SK-NB-E cells treated with C22:0, C24:0, or C26:0 (0.1–20 μM; 48 h), an inhibition of cell growth and mitochondrial dysfunctions were observed by cell counting with trypan blue, MTT assay, and measurement of mitochondrial transmembrane potential (Δψm) with DiOC6(3). A stimulation of oxidative stress was observed with DHE and MitoSOX used to quantify superoxide anion production on whole cells and at the mitochondrial level, respectively. With C24:0 and C26:0, by Western blotting, lower levels of mitochondrial complexes III and IV were detected. After staining with MitoTracker and by transmission electron microscopy used to study mitochondrial topography, mass and morphology, major changes were detected in VLCFAs treated-cells: modification of the cytoplasmic distribution of mitochondria, presence of large mitochondria, enhancement of the mitochondrial mass. Thus, VLCFAs can be potential risk factors contributing to neurodegeneration by inducing neuronal damages via mitochondrial dysfunctions.
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Santalova, Elena A., Alexandra S. Kuzmich, Ekaterina A. Chingizova, Ekaterina S. Menchinskaya, Evgeny A. Pislyagin, and Pavel S. Dmitrenok. "Phytoceramides from the Marine Sponge Monanchora clathrata: Structural Analysis and Cytoprotective Effects." Biomolecules 13, no. 4 (April 14, 2023): 677. http://dx.doi.org/10.3390/biom13040677.

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In our research on sphingolipids from marine invertebrates, a mixture of phytoceramides was isolated from the sponge Monanchora clathrata (Western Australia). Total ceramide, ceramide molecular species (obtained by RP-HPLC, high-performance liquid chromatography on reversed-phase column) and their sphingoid/fatty acid components were analyzed by NMR (nuclear magnetic resonance) spectroscopy and mass spectrometry. Sixteen new (1b, 3a, 3c, 3d, 3f, 3g, 5c, 5d, 5f, 5g, 6b–g) and twelve known (2b, 2e, 2f, 3b, 3e, 4a–c, 4e, 4f, 5b, 5e) compounds were shown to contain phytosphingosine-type backbones i-t17:0 (1), n-t17:0 (2), i-t18:0 (3), n-t18:0 (4), i-t19:0 (5), or ai-t19:0 (6), N-acylated with saturated (2R)-2-hydroxy C21 (a), C22 (b), C23 (c), i-C23 (d), C24 (e), C25 (f), or C26 (g) acids. The used combination of the instrumental and chemical methods permitted the more detailed investigation of the sponge ceramides than previously reported. It was found that the cytotoxic effect of crambescidin 359 (alkaloid from M. clathrata) and cisplatin decreased after pre-incubation of MDA-MB-231 and HL-60 cells with the investigated phytoceramides. In an in vitro paraquat model of Parkinson’s disease, the phytoceramides decreased the neurodegenerative effect and ROS (reactive oxygen species) formation induced by paraquat in neuroblastoma cells. In general, the preliminary treatment (for 24 or 48 h) of the cells with the phytoceramides of M. clathrata was necessary for their cytoprotective functions, otherwise the additive damaging effect of these sphingolipids and cytotoxic compounds (crambescidin 359, cisplatin or paraquat) was observed.
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Yamada, T., N. Kubushiro, K. Shigemasa, T. Ikeda, and M. Takagi. "Effects of Transforming Growth Factor-β1 on Decorin Expression by Undifferentiated Osteoblastic Cells." Microscopy and Microanalysis 3, S2 (August 1997): 187–88. http://dx.doi.org/10.1017/s1431927600007820.

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Decorin is the predominant proteoglycan isolated from bone of several animal species. Bone matrix decorin appears to bind transforming growth factor β (TGF-β) and enhances its bioactivity. TGF-β is stored in bone matrix in abundant amounts and modulates the synthesis of bone matrix proteins by osteoblasts. Thus it appears to play a role in regulation of bone formation during the bone remodeling process. The effect of TGF-β on decorin expression in bone cells has been evaluated in murine osteoblastic cells, but the results are divergent depending on the experimental conditions and cell types used. The present study investigated the effect of TGF-βl on the expression of decorin mRNA in two clonal rat osteoblastic cell lines with different stages of differentiation, ROS-C26 (C26) and ROS-C20 (C20); C26 is a potential osteoblast precursor cell line that is also capable of differentiating into muscle cells and adipocytes; C20 is a more differentiated osteoblastic cell line.
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Eisenkolb, Marlis, Christoph Zenzmaier, Erich Leitner, and Roger Schneiter. "A Specific Structural Requirement for Ergosterol in Long-chain Fatty Acid Synthesis Mutants Important for Maintaining Raft Domains in Yeast." Molecular Biology of the Cell 13, no. 12 (December 2002): 4414–28. http://dx.doi.org/10.1091/mbc.e02-02-0116.

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Fungal sphingolipids contain ceramide with a very-long-chain fatty acid (C26). To investigate the physiological significance of the C26-substitution on this lipid, we performed a screen for mutants that are synthetically lethal with ELO3. Elo3p is a component of the ER-associated fatty acid elongase and is required for the final elongation cycle to produce C26 from C22/C24 fatty acids.elo3Δ mutant cells thus contain C22/C24- instead of the natural C26-substituted ceramide. We now report that under these conditions, an otherwise nonessential, but also fungal-specific, structural modification of the major sterol of yeast, ergosterol, becomes essential, because mutations in ELO3 are synthetically lethal with mutations in ERG6. Erg6p catalyzes the methylation of carbon atom 24 in the aliphatic side chain of sterol. The lethality of an elo3Δ erg6Δ double mutant is rescued by supplementation with ergosterol but not with cholesterol, indicating a vital structural requirement for the ergosterol-specific methyl group. To characterize this structural requirement in more detail, we generated a strain that is temperature sensitive for the function of Erg6p in an elo3Δ mutant background. Examination of raft association of the GPI-anchored Gas1p and plasma membrane ATPase, Pma1p, in the conditional elo3Δ erg6 ts double mutant, revealed a specific defect of the mutant to maintain raft association of preexisting Pma1p. Interestingly, in an elo3Δ mutant at 37°C, newly synthesized Pma1p failed to enter raft domains early in the biosynthetic pathway, and upon arrival at the plasma membrane was rerouted to the vacuole for degradation. These observations indicate that the C26 fatty acid substitution on lipids is important for establishing raft association of Pma1p and stabilizing the protein at the cell surface. Analysis of raft lipids in the conditional mutant strain revealed a selective enrichment of ergosterol in detergent-resistant membrane domains, indicating that specific structural determinants on both sterols and sphingolipids are required for their association into raft domains.
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SCHNEITER, Roger, Britta BRÜGGER, Clare M. AMANN, Glenn D. PRESTWICH, Raquel F. EPAND, Günther ZELLNIG, Felix T. WIELAND, and Richard M. EPAND. "Identification and biophysical characterization of a very-long-chain-fatty-acid-substituted phosphatidylinositol in yeast subcellular membranes." Biochemical Journal 381, no. 3 (July 27, 2004): 941–49. http://dx.doi.org/10.1042/bj20040320.

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Morphological analysis of a conditional yeast mutant in acetyl-CoA carboxylase acc1ts/mtr7, the rate-limiting enzyme of fatty acid synthesis, suggested that the synthesis of C26 VLCFAs (very-long-chain fatty acids) is important for maintaining the structure and function of the nuclear membrane. To characterize this C26-dependent pathway in more detail, we have now examined cells that are blocked in pathways that require C26. In yeast, ceramide synthesis and remodelling of GPI (glycosylphosphatidylinositol)-anchors are two pathways that incorporate C26 into lipids. Conditional mutants blocked in either ceramide synthesis or the synthesis of GPI anchors do not display the characteristic alterations of the nuclear envelope observed in acc1ts, indicating that the synthesis of another C26-containing lipid may be affected in acc1ts mutant cells. Lipid analysis of isolated nuclear membranes revealed the presence of a novel C26-substituted PI (phosphatidylinositol). This C26-PI accounts for approx. 1% of all the PI species, and is present in both the nuclear and the plasma membrane. Remarkably, this C26-PI is the only C26-containing glycerophospholipid that is detectable in wild-type yeast, and the C26-substitution is highly specific for the sn-1 position of the glycerol backbone. To characterize the biophysical properties of this lipid, it was chemically synthesized. In contrast to PIs with normal long-chain fatty acids (C16 or C18), the C26-PI greatly reduced the bilayer to hexagonal phase transition of liposomes composed of 1,2-dielaidoyl-sn-glycero-3-phosphoethanolamine (DEPE). The biophysical properties of this lipid are thus consistent with a possible role in stabilizing highly curved membrane domains.
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Rodolfo, M., C. Zilocchi, C. Melani, B. Cappetti, I. Arioli, G. Parmiani, and M. P. Colombo. "Immunotherapy of experimental metastases by vaccination with interleukin gene-transduced adenocarcinoma cells sharing tumor-associated antigens. Comparison between IL-12 and IL-2 gene-transduced tumor cell vaccines." Journal of Immunology 157, no. 12 (December 15, 1996): 5536–42. http://dx.doi.org/10.4049/jimmunol.157.12.5536.

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Abstract We have compared the therapeutic activity and characterized the antitumor response induced by IL-12 and IL-2 gene-transduced tumor cell vaccines. Mice bearing lung metastases of the BALB/c colon carcinoma C51 were treated with syngenic, histologically related, and antigenically cross-reacting irradiated IL-12 (C26/IL12) or IL-2 (C26/IL2) gene-transduced C26 tumor cells given s.c. Vaccination with C26/IL12 cells cured 40% of mice, while vaccination with C26/IL2 cells reduced the number of metastatic nodules without affecting survival. Despite this difference, similar antitumor CTL activation was shown in mice treated with C26/IL12 or C26/IL2 cells. The lytic pattern of CTL was shown to be directed to tumor-associated Ags (TAA) shared between the colon carcinomas C51, C26, and CC36 as well as with other syngenic tumors. Both treatments induced anti-TAA Abs, but only sera from mice treated with C26/IL12 contained Ab that lysed tumor cells in a C-dependent cytotoxicity assay. Early infiltration of activated T cells was found in the lungs of mice vaccinated with C26/IL12. CD4+ lymphocytes purified from the lymph nodes draining the vaccination site or from the spleen showed a higher production of IFN-gamma in response to anti-CD3 mAb in C26/IL12 vaccinated mice, while a higher production of IL-4 was shown in mice vaccinated with C26/IL2 cells. These results indicate that the better therapeutic efficacy of vaccination with C26/IL12 is associated with the production of C-binding Ab, an early infiltration of the metastatic lungs by activated T lymphocytes and a predominant systemic activation of Th1 more than Th2 cells.
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Smakman, Niels, Diana J. M. van den Wollenberg, Inne H. M. Borel Rinkes, Rob C. Hoeben, and Onno Kranenburg. "Sensitization to Apoptosis Underlies KrasD12-Dependent Oncolysis of Murine C26 Colorectal Carcinoma Cells by Reovirus T3D." Journal of Virology 79, no. 23 (December 15, 2005): 14981–85. http://dx.doi.org/10.1128/jvi.79.23.14981-14985.2005.

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ABSTRACT Reovirus T3D is an oncolytic agent that preferentially targets tumor cells expressing an activated Ras oncogene. Ras signaling interferes with the cellular stress response that inhibits translation of reovirus RNAs. Murine C26 colorectal carcinoma cells express a mutant KrasD12 gene. Reovirus T3D efficiently kills C26 cells, but not C26 cells in which the KrasD12 mRNA is stably repressed by expression of KrasD12-directed short-hairpin RNAs. Surprisingly, neither reovirus T3D protein synthesis nor T3D virus yields were suppressed by deletion of KrasD12. Rather, reovirus-induced tumor cell apoptosis was completely abrogated as a result of Kras knockdown. We conclude that sensitization of C26 tumor cells to reovirus-induced apoptosis underlies the Ras dependency of reovirus T3D oncolysis.
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Dissertations / Theses on the topic "C26 cells"

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Chaouki, Ghita. "Etude du rôle de la voie de signalisation eIF2αATF4 au cours des états inflammatoires, dans le cadre du stress mitochondrial et de l’anorexie associée à la pathologie." Electronic Thesis or Diss., Université Clermont Auvergne (2021-...), 2022. http://www.theses.fr/2022UCFAC109.

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La voie de signalisation eIF2α-ATF4 est activée dans les cellules en réponse à un large éventail de stress cellulaires. Son activation conduit à une inhibition de la synthèse protéique globale et la régulation de l’expression de gènes cibles du facteur de transcription ATF4. Cette voie est sollicitée en réponse au déficit en acides aminés indispensables, au stress mitochondrial, au stress du réticulum endoplasmique ou encore aux infections virales. Elle déclenche des mécanismes adaptatifs, à l’échelle cellulaire (tels que l’inhibition de la synthèse protéique et l’augmentation du niveau d’autophagie) et de l’organisme entier (comme la régulation du métabolisme, l’inflammation, l’immunité et la prise alimentaire). Les résultats précédents générés par notre laboratoire ainsi que les données de la littérature nous ont amenés à étudier le rôle de la signalisation eIF2α-ATF4 dans deux contextes différents. Dans une première partie, nous avons exploré le rôle de la signalisation eIF2α-ATF4 dans l’anorexie associée aux pathologies cataboliques inflammatoires (sepsis et cancer). Nous avons émis l’hypothèse que cette voie de signalisation pourrait contribuer à l’inhibition de prise alimentaire par une action directe au niveau central et/ou en stimulant l’expression de cytokines anorexigènes, dont GDF15, en périphérie (foie, intestin). Nous avons utilisé deux modèles expérimentaux reproduisant une anorexie associée à la pathologie chez la souris : un modèle d’inflammation systémique aigue de type sepsis (administration unique de lipopolysaccharide bactérien) et un modèle de souris porteuses d’une tumeur de cellules de carcinome de colon C26. Ces deux modèles ont été caractérisés en phase précoce de l’anorexie, par une inflammation aux niveaux périphérique et central (hypothalamus), une augmentation des niveaux circulants d’IL-6 et de GDF15, une profonde modification du métabolisme des acides aminés, et une activation de la voie de signalisation eIF2α-ATF4 dans l’hypothalamus et dans le foie. Ensuite, la réponse de modèles inductibles de perte de fonction d’ATF4 a été testée dans le modèle de sepsis. L’invalidation d’ATF4 au niveau du foie et de l’intestin n’a pas eu d’impact ni sur l’anorexie, ni sur l’induction de la production de GDF15. L’invalidation constitutive de GDF15 a également été sans effet sur l’inhibition de prise alimentaire induite par l’administration de LPS. Le rôle de la fonction ATF4 au niveau central n’a pas pu être testée et devra faire l’objet d’expérimentations futures. L’analyse des échantillons des souris invalidées pour la fonction d’ATF4 au niveau hépatique nous permettra d’évaluer son implication dans les réorientations du métabolisme des AA (transport, biosynthèse, autophagie). Dans le modèle de cancer C26, le passage du stade de pré-anorexie au stade de début d’anorexie a été associé à une activation de la voie signalisation eIF2αATF4 aux niveaux hépatique et hypothalamique, et une approche fonctionnelle pharmacologique sera prochainement mise en place à l’aide de l’ISRIB (ISR Inhibitor) pour étudier son implication dans la régulation de l’appétit et du métabolisme des AA (dans ce modèle les invalidations géniques ne sont pas possibles). Dans une deuxième partie, nous nous sommes intéressés au dysfonctionnement mitochondrial, qui représente une menace majeure pour l'homéostasie cellulaire, favorise l'apparition de nombreux troubles métaboliques et joue un rôle crucial dans la pathogenèse du sepsis. Compte-tenu du rôle joué par la voie de signalisation eIF2α-ATF4 dans la réponse adaptative au stress mitochondrial, nous avons cherché à savoir si un prétraitement activateur de cette voie pourrait être un moyen d'augmenter la résilience du pool mitochondrial lors d'événements stressants ultérieurs. (...)
The eIF2α-ATF4 signaling pathway is activated in cells in response to a wide range of cellular stresses. Its activation leads to the inhibition of the global protein synthesis and the regulation of the transcription factor ATF4 target genes expression. This pathway is activated in response to essential amino acid deficiency, mitochondrial stress, endoplasmic reticulum stress or viral infections. Its activation triggers adaptive mechanisms, both at the cellular level (such as inhibition of protein synthesis and increased autophagy) and at the whole organism level (such as regulation of metabolism, inflammation, immunity and food intake). Previous results generated by our laboratory as well as data from the scientific literature led us to investigate the role of eIF2α-ATF4 signaling in two different contexts. Firstly, we explored the role of eIF2α-ATF4 signaling in anorexia associated with catabolic inflammatory pathologies (sepsis and cancer). We hypothesized that this signaling pathway could contribute to the inhibition of food intake by its direct action at the central level and/or by stimulating the expression of anorectic cytokines, including GDF15, in the periphery (liver, intestine). We used two experimental models reproducing pathology-associated anorexia in mice: a sepsis model of acute and systemic inflammation (single administration of bacterial lipopolysaccharide) and a model of mice carrying a C26 colon carcinoma cell tumor. Both models were characterized in the early phase of anorexia by inflammation at the peripheral and central (hypothalamus) levels, increased circulating levels of IL-6 and GDF15, profound alterations in amino acid metabolism, and activation of the eIF2αATF4 signaling pathway in the hypothalamus and liver. Afterwards, the response of inducible models of ATF4 loss-of-function was tested in the sepsis model. ATF4 knock-out in the liver and intestine had no impact on either anorexia or the induction of GDF15 production. Constitutive invalidation of GDF15 also had no effect on the inhibition of food intake induced by LPS administration. The role of ATF4 function at the central level could not be tested and should be the subject of future experiments. The analysis of samples from mice knocked-out for ATF4 at the hepatic level, will allow us to evaluate ATF4 involvement in the reorientation of AA metabolism (transport, biosynthesis, autophagy). In the C26 cancer model, the transition from pre-anorexia to early anorexia was associated with an activation of the eIF2α-ATF4 signaling pathway at the hepatic and hypothalamic levels, and a pharmacological approach using ISRIB (ISR Inhibitor) will soon be implemented to study the involvement of the ISR in the regulation of appetite and AA metabolism (in this model, genes knock-out is not possible) Secondly, we focused on mitochondrial dysfunction, which represents a major threat to cellular homeostasis, promotes the development of many metabolic disorders and plays a crucial role in the pathogenesis of sepsis. Given the role played by the eIF2α-ATF4 signaling pathway in the adaptive response to mitochondrial stress, we investigated whether a pretreatment activating this pathway could be a way to increase the resilience of the mitochondrial pool during subsequent stressful events. We demonstrated in mice that a pretreatment activating the GCN2-eIF2α-ATF4 pathway upstream of inflammatory stress (LPS administration) counteracted some of the effects of this stress on mitochondrial homeostasis in the liver, an organ playing a major role in the metabolic and immune response to endotoxic stress. These results are presented as an article that will be submitted soon for publication
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Enyindah-Asonye, Gospel. "PATHOPHYSIOLOGICAL ROLE OF CD6 AND ITS NEW LIGAND IN DISEASES." Case Western Reserve University School of Graduate Studies / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=case1491389112552353.

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Falkenberg, Christiane. "Optimizing Organic Solar Cells." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2012. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-89214.

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This thesis deals with the characterization and implementation of transparent electron transport materials (ETM) in vacuum deposited p-i-n type organic solar cells (OSC) for substituting the parasitically absorbing standard ETM composed of n-doped C60. In addition to transparency in the visible range of the sun spectrum, the desired material properties include high electron mobility and conductivity, thermal and morphological stability, as well as good energy level alignment relative to the adjacent acceptor layer which is commonly composed of intrinsic C60. In this work, representatives of three different material classes are evaluated with regard to the above mentioned criteria. HATCN (hexaazatriphenylene hexacarbonitrile) is a small discoid molecule with six electron withdrawing nitrile groups at its periphery. It forms smooth thin films with an optical energy gap of 3.3eV, thus being transparent in the visible range of the sun spectrum. Doping with either 5wt% of the cationic n-dopant AOB or 7wt% of the proprietary material NDN1 effectively increases the conductivity to 7.6*10^-6 S/cm or 2.2*10^-4 S/cm, respectively. However, the fabrication of efficient OSC is impeded by the exceptionally high electron affinity (EA ) of approximately 4.8eV that causes the formation of an electron injection barrier between n-HATCN and intrinsic C60 (EA=4.0eV). This work presents a strategy to remove the barrier by introducing doped and undoped C60 intermediate layers, thus demonstrating the importance of energy level matching in a multi-layer structure and the advantages of Fermi level control by doping. Next, a series of six Bis-Fl-NTCDI (N,N-bis(fluorene-2-yl)-naphthalenetetracarboxylic diimide) compounds, which only differ by the length of the alkyl chains attached to the C9 positions of the fluorene side groups, is examined. When increasing the chain length from 0 to 6 carbon atoms, the energy levels remain nearly unchanged: We find EA=3.5eV as estimated from cyclic voltammetry, an ionization potential (IP ) in the range between 6.45eV and 6.63eV, and Eg,opt=3.1eV which means that all compounds form transparent thin films. Concerning thin film morphology, the addition of side chains results in the formation of amorphous layers with a surface roughness <1nm on room temperature glass substrates, and (1.5+/-0.5)nm for deposition onto glass substrates heated to 100°C. In contrast, films composed of the side chain free compound Bis-HFl-NTCDI exhibit a larger surface roughness of (2.5+/-0.5)nm and 9nm, respectively, and are nanocrystalline already at room temperature. Moreover, the conductivity achievable by n-doping is very sensitive to the side chain length: Whereas doping of Bis-HFl-NTCDI with 7wt% NDN1 results in a conductivity in the range of 10^-4 S/cm, the attachment of alkyl chains causes a conductivity which is more than three orders of magnitude smaller despite equal or slightly higher doping concentrations. The insufficient transport properties of the alkylated derivatives lead to the formation of pronounced s-kinks in the jV -characteristics of p-i-n type OSC while the use of n-Bis-HFl-NTCDI results in well performing devices. The last material, HATNA-Cl6 (2,3,8,9,14,15- hexachloro-5,6,11,12,17,18-hexaazatrinaphthylene), exhibits Eg,opt=2.7eV and is therefore not completely transparent in the visible range of the sun spectrum. However, its energy level positions of EA=4.1eV and IP=7.3eV are well suited for the application as ETM in combination with i-C60 as acceptor. The compound is dopable with all available n-dopants, resulting in maximum conductivities of sigma=1.6*10^-6, 3.5*10^-3, and 7.5*10^-3 S/cm at 7.5wt% AOB, Cr2(hpp)4, and NDN1, respectively. Applying n-HATNA-Cl6 instead of the reference ETM n-C60 results in a comparable or improved photocurrent density at an ETM thickness d(ETM)=40nm or 120nm, respectively. At d(ETM)=120nm, the efficiency eta is more than doubled as it increases from eta(n-C60)=0.4% to eta(n-HATNA-Cl6)=0.9% . Optical simulations show that the replacement of n-C60 by n-Bis-HFl-NTCDI, n-HATNA-Cl6, or the previously studied n-NTCDA (naphthalenetretracarboxylic dianhydride) in p-i-n or n-i-p type device architectures is expected to result in an increased photocurrent due to reduced parasitic absorption. For quantifying the gain, the performance of p-i-n type OSC with varying ETM type and thickness is evaluated. Special care has to be taken when analyzing devices comprising the reference ETM n-C60 as its conductivity is sufficiently large to extend the area of the aluminum cathode and thus the effective device area which may lead to distorted results. Overall, the experiment is able to confirm the trends predicted by the optical simulation. At large ETM thickness in the range between 60 and 120nm, the window layer effect of the ETM is most pronounced. For instance, at d(ETM)=120nm, eta(C60) is more than doubled using n-HATNA-Cl6 and even more than tripled using n-Bis-HFl-NTCDI or n-NTCDA. At optimized device geometry the photocurrent gain is slightly less than expected but nonetheless, the efficiency is improved from eta(max)=2.1% for n-C60 and n-HATNA-Cl6 solar cells to eta(max)=2.3, and 2.4% for n-Bis-HFl-NTCDI and n-NTCDA devices, respectively. This development is supported by generally higher Voc and FF in solar cells with transparent ETM. Finally, p-i-n type solar cells with varying ETM are aged at a temperature of 50°C and an illumination intensity of approximately 2 suns. Having extrapolated lifetimes t(80) of 36, 500, and 14000h and nearly unchanged jV-characteristics after 2000h, n-C60 and n-Bis-HFl-NTCDI devices exhibit the best stability. In contrast, n-NTCDA devices suffer from a constant decrease in Isc while n-HATNA-Cl6 solar cells show a rapid dscegradation of both Isc and FF associated with a decomposition of the material or a complete de-doping of the ETM. Here, lifetimes of only 4500h and 445hare achieved.
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Chang, Shang-wen. "Cu₂S/ZnCdS thin film heterojunction solar cell studies." Diss., Virginia Polytechnic Institute and State University, 1985. http://hdl.handle.net/10919/54740.

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Cu₂S/CdS solar cells have been studied extensively for the past two decades due to their potentially high efficiencies per unit cost. The operation and characteristics of Cu₂S/CdS solar cells are fairly well understood. However, the properties of the newer Cu₂S/ZnCdS cell type are not well understood. The main goals of this thesis were to compare Cu₂S/CdS and Cu₂S/ZnCdS cells using Cu₂S/CdS cells as a reference, and to understand the operation and properties of Cu₂S/ZnCdS cells in order to improve cell performance. Four different measurements were used in this research to achieve these goals. They were; electrical, spectral, capacitance and deep trap measurements. I-V measurements give important electrical parameters of the cells; cell efficiency, fill factor, short circuit current, open circuit voltage, shunt resistance and series resistance are reported. From a In(ISC) versus VOC measurement, the diode factor, A, was found to be about 1 for Cu₂S/CdS, Cu₂S/Zn0.11Cd0.89S, and about 1.2 for Cu₂S/Zn0.25Cd0.75S cells. The relation between In(Joo) (current density) and ϕ (potential barrier height) is linear for both types of cells. The slope of this linear relationship increases as the content of Zn increases in ZnxCd1-xS. Under air mass 1 (100 mW/cm²) illumination, it was found that VOC decays and capacitance increases for Cu₂S/ZnCdS cells. This is attributed to electron relaxation from deep traps near the junction. Spectral response with and without bias light were measured for both Cu₂S/CdS and Cu₂S/ZnCdS cells. White and blue bias light enhance the spectral response, while red bias light quenches the response. This is attributed to ionization and filling of deep traps near the junction. Capacitance measurements on both cell types show that 1/C² versus voltage is quite flat, which indicates the existence of an i-layer (insulation layer) in the CdS or ZnCdS near the junction. Three methods–photocapacitance, space-charge-limited current, and thermally stimulated. current techniques–were used for deep trap measurements. Photocapacitance measurements indicate one deep donor energy and two deep acceptor energy levels. These trap energies become larger as the content of Zn in ZnCdS increases. Space-charge-limited current measurements give a trap density of the order of 10¹⁶ cm³ for both cell types. The shallow energy trap is found to be 0.26 eV below the conduction band edge of CdS. The occurrence of a current-saturated region for Cu₂S/ZnCdS is attributed to the filling of the interface traps near the junction. Thermally stimulated current measurements give two energy levels below the conduction band of CdS; 0.05 eV and 0.26 eV. From the above results, several differences between the Cu₂S/CdS and the Cu₂S/ZnCdS cells can be seen. The Cu₂S/ZnCdS cells show stronger red quenching, smaller electron lifetime at the interface near the junction, and deeper traps than the Cu₂S/CdS cells. These differences can account for the decline of ISC and the VOC decay. The smaller ISC for the Cu₂S/ZnCdS cells can also possibly result from smaller electron lifetime at the interface, larger interface recombination velocity, different deep trap levels, and enhanced Zn concentration near the junction. The VOC decay for the Cu₂S/ZnCdS cells is mostly due to long decay of charge. Longer decay could be attributed to deeper traps.
Ph. D.
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Allen, Frederick Jr. "CCL3 Augments Antitumor Responses in CT26 by Enhancing Cellular Trafficking and Interferon-Gamma Expression." Case Western Reserve University School of Graduate Studies / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=case1513124234665339.

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Hassan, Namir. "Interactions of the leukocyte cell-surface proteins CD5 and CD6." Thesis, University of Oxford, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398158.

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Yeh, Ming-Hsin. "Identification of CD8+ T cell-stimulating shared antigens that are uncovered in CT26 vaccinated mice in the absence of CD25+ regulatory T cells." Thesis, University of Southampton, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.431953.

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Liu, Gin-Yun. "Analysis of the effects of Leptomycin B on Cells Exiting Mitosis." The Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=osu1153488860.

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Alam, Israt Shamima. "Imaging tumour cell death using the C2A domain of Synaptotagmin-I." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609494.

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Lau, Mike Rudi. "Characterisation of the class II phosphoinositide 3-kinase, PI 3K-C2β." Thesis, Institute of Cancer Research (University Of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.342221.

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Book chapters on the topic "C26 cells"

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van de Beek, Malu-Clair, Inge M. E. Dijkstra, and Stephan Kemp. "Method for Measurement of Peroxisomal Very Long-Chain Fatty Acid Beta-Oxidation and De Novo C26:0 Synthesis Activity in Living Cells Using Stable-Isotope Labeled Docosanoic Acid." In Methods in Molecular Biology, 45–54. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6937-1_5.

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Sen, Dipankar. "Whole-Cell Protein Profiles of Soil Bacteria by Gel Electrophoresis." In SSSA Book Series, 619–34. Madison, WI, USA: Soil Science Society of America, 2018. http://dx.doi.org/10.2136/sssabookser5.2.c29.

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Dübendorfer, A. "Feedback-Regulation of Ecdysone C20-Hydroxylation in Primary Cell Cultures from Drosophila Embryos." In Invertebrate and Fish Tissue Culture, 39–42. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73626-1_10.

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Morschhauser, Franck, and Pier Luigi Zinzani. "Indolent Lymphomas." In The EBMT/EHA CAR-T Cell Handbook, 83–86. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-94353-0_15.

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AbstractIndolent non-Hodgkin lymphoma (iNHL), including follicular (FL) and marginal zone (MZL) lymphoma, now enjoy durable disease control with first-line immunochemotherapy, with a median overall survival (OS) of over 15 years in most series (Kahl and Yang 2016). However, iNHL is still widely considered incurable in most cases, and disease history remains characterized by a relapsing and remitting course, with each remission period shorter than the previous one, and OS and progression-free survival (PFS) decrease with each subsequent line of conventional therapy (Batlevi et al. 2020). Patients with unmet needs include approximately 20% of FL patients who experience disease progression within 24 months (POD24) after initial chemoimmunotherapy (with a 5-year OS of 48% (Casulo et al. 2015)—although it remains unclear how much this worse outcome is driven by misdiagnosed transformed follicular lymphoma (Freeman et al. 2019)) and those who fail multiple regimens (5-year PFS of 23%) (Rivas-Delgado et al. 2019) have double refractory disease (Gopal et al. 2017) or experience relapse after autologous stem cell transplantation (ASCT) (Sesques et al. 2020). Although promising results were obtained with an immunomodulatory regimen combining anti-C20 Moab and lenalidomide (Leonard et al. 2019; Morschhauser et al. 2019), most current approved therapies do not overcome incremental disease resistance, resulting in multiple lines of treatment with cumulative toxicity over a patient’s lifetime. The autologous anti-CD19 chimeric antigen receptor T cell (CAR-T) therapies tisa-cel and axi-cel, which are now approved for patients with relapsed/refractory (r/r) large B cell lymphoma (LBCL), have also been tested in iNHL, with promising results.
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Aktories, K. "C2 toxin (Clostridium botulinum type C and D)." In Guidebook to Protein Toxins and Their Use in Cell Biology, 66–68. Oxford University PressOxford, 1997. http://dx.doi.org/10.1093/oso/9780198599555.003.0023.

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Abstract C2 toxin is binary in structure and consists of a binding component (C211, 100 kDa) and an enzyme component (C2I, 50 kDa) (Aktories et al. 1992). Both components are separated proteins. The gene of the enzyme compo¬ nent has been cloned recently (Fujii et al. 1996; EMBL Data Library D63903). C2II has to be activated by trypsin treatment to release an 75 kDa active fragment. C2II binds to a membrane receptor (not identified), which is present on all cell types studied so far. Binding of C2II induces a binding site for C21. The toxin is taken-up by receptor-mediated endocytosis (Simpson 1989) (see Fig. 1). In artificial membranes, C2II induces cation selective and voltage-dependent channels (Schmid et al. 1994).
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Turk, Seyhan. "The Impact of Biochemical Alterations in the Tumor Microenvironment on Cancer Progression and Treatment." In Current Researches in Health Sciences-II. Özgür Yayınları, 2023. http://dx.doi.org/10.58830/ozgur.pub128.c626.

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The tumor microenvironment (TME) plays a critical role in cancer progression and treatment response. Recent studies have revealed that biochemical alterations within the TME can significantly influence tumor behavior and therapeutic outcomes. Alterations in the TME, such as changes in pH, hypoxia, and nutrient availability, have been shown to promote cancer cell survival and growth. Acidic pH conditions within the TME enhance tumor invasiveness and metastasis while conferring resistance to conventional therapies. Hypoxia, caused by insufficient oxygen supply, not only promotes genetic instability and immune evasion but also induces resistance to radiation and certain chemotherapeutic agents. Additionally, nutrient deprivation within the TME can activate survival pathways in cancer cells, leading to treatment resistance. Understanding the biochemical alterations in the TME has led to the development of novel therapeutic approaches. Strategies to modulate the TME, such as targeting angiogenesis, reversing immunosuppression, and normalizing the microenvironment, have shown promise in preclinical and clinical studies. Combining conventional therapies with agents targeting the TME holds potential to overcome treatment resistance and improve patient outcomes. In conclusion, the biochemical alterations within the TME significantly impact cancer progression and treatment response. Recognizing these alterations and their influence on therapeutic outcomes is crucial for developing effective treatment strategies. Continued research in this area is vital to unravel the complexity of the TME and identify novel therapeutic targets for improving cancer patient outcomes.
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Zinola, C. "The Electrochemical Fuel Cell Reactor." In Surfactant Science, 385–402. CRC Press, 2010. http://dx.doi.org/10.1201/9781420045451-c16.

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Weete, J., and S. Gandhi. "Enhancement of C20 Polyunsaturated Fatty Acid Production in Pythium ultimum." In Industrial Applications of Single Cell Oils. AOCS Publishing, 1992. http://dx.doi.org/10.1201/9781439821855.ch6.

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Bowen, Phyllis. "Lycopene Oxidation, Uptake, and Activity in Human Prostate Cell Cultures." In Carotenoids, 437–64. CRC Press, 2009. http://dx.doi.org/10.1201/9781420052312-c21.

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"CHAPTER 22. The Vision in the Penitentiary Cell." In Prison Blossoms, 199–203. Harvard University Press, 2011. http://dx.doi.org/10.4159/harvard.9780674066618.c23.

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Conference papers on the topic "C26 cells"

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Angelotti, Austin, Rachel Cole, Amy Webb, Maciej Pietrzak, and Martha Belury. "Diet-induced Gene Expression Changes of Cachectic Muscle, Adipose, and Liver." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/gvbe2596.

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Cancer cachexia is a systemic disease characterized by muscle and adipose loss that cannot be reversed by increasing caloric intake. Our previous research has shown insulin resistance precedes cancer cachexia in the C26 mouse model of cachexia, and a diet high in linoleic acid, the essential omega-6 polyunsaturated fatty acid, attenuates the C26-induced insulin resistance. Therefore, to better understand how dietary linoleic acid is improving insulin sensitivity, we characterized gene expression changes in three major tissues responsible for controlling insulin sensitivity: skeletal muscle, adipose, and liver. To do this male CD2F1 (Charles River, MA) were randomized to semi-purified diet (24% fat by weight) containing fat prominently from lard, or containing fat prominently from safflower oil (a linoleic acid-rich oil). One week after diet randomization, mice were inoculated with colon-26 (C26) adenocarcinoma cells (1.0E6 cells). 13 days after inoculation mice were euthanized and gastrocnemius skeletal muscle, epididymal white adipose tissue, and liver tissue were collected for total transcriptome analysis using poly-A enriched next generation RNA-sequencing. Differentially expressed genes were selected based on p-values < 0.05. There were no detectable differences in body weight or food intake between the two diets in mice with C26 tumors. Between the two diets 12 genes were differentially expressed in the muscle, while 57 genes were differentially expressed in the liver, and 314 genes were differentially expressed in adipose. A linoleic acid enriched diet had little effect on the skeletal muscle transcriptome but induced larger transcriptome changes in liver and adipose. This could suggest dietary linoleic acid increases insulin sensitivity through affecting metabolism in adipose and liver, rather than skeletal muscle. Determining these diet-induced transcriptome changes allows us to better target tissue-specific molecular mechanisms of linoleic acid in future research.
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Benedicto, Aitor, Joana Marquez, Elvira Olaso, and Beatriz Arteta. "Abstract B10: LFA-1/ICAM-1 interaction switches on an orchestrated prometastatic microenvironmental shift during experimental liver metastasis of colon C26 cancer cells." In Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; February 26 — March 1, 2014; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-b10.

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Leyva Gutierrez, Francisco, and Tong Wang. "Crystallography and Functionality of Natural Waxes: Insights for the Development of Tailored Lipid Materials." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/nyok4571.

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Natural waxes are valuable industrial products consisting of complex chemical mixtures. To probe the structure−function role of select constituents, model n-alkanes, alcohols, aldehydes, and fatty acids of C18−19, C22−23, and C26−27 carbon chain lengths were synthesized and analyzed via calorimetry and X-ray powder diffraction. Pure compounds and binary mixtures crystallized into monoclinic (M), triclinic (T), and orthorhombic (O) lattices or combinations thereof. The C26 aldehyde formed an O lattice and exhibited one solid−solid phase transition similar to n-alkanes. The water vapor permeability (WVP) of model systems cast as films was determined. For pure compounds, WVP decreased in the following order: fatty acid > even n-alkane > odd n-alkane > alcohol > aldehyde. Increasing carbon chain length, which translates to increasing unit cell volume, decreased WVP. Binary mixtures generally exhibited a more complex relationship with WVP. These findings may be applicable to the agricultural postharvest, pharmaceutical, and paperboard coating industries.
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Franich, Andjela, Ivana Vasić, Snežana Rajković, Aleksandar Arsenijević, Marija Milovanović, Nebojša Arsenijević, Jelena Milovanović, and Marija Živković. "CYTOTOXICITY OF CATIONIC DINUCLEAR PLATINUM(II) COMPLEXES IN AN EXPERIMENTAL MODEL OF MOUSE COLON CANCER." In 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac, 2021. http://dx.doi.org/10.46793/iccbi21.293f.

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The series of nine dinuclear platinum(II) complexes, [{Pt(L)Cl}2(μ-X)]2+ (where L is two NH3 or bidentantly coordinated diamine ligand – ethylenediamine, en; (±)-1,2-propylenediamine, 1,2-pn; isobutylenediamine, ibn; trans-(±)-1,2-diaminocyclohexane, dach; 1,3-propylenediamine, 1,3-pd; 2,2- dimethyl-1,3-propylenediamine, 2,2-diMe-1,3-pd; (±)-1,3-pentanediamine,1,3-pnd, and X is a bridging pyrazine (pz) or pyridazine (pydz) ligand) have been synthesized and characterized. The antitumor potential of these complexes against CT26 cells were determined by in vitro and in vivo assays. A murine model of heterotopic colon cancer tumor was induced in immunocompetent BALB/c mice for investigating antitumor potential of the Pt(II) complexes in vivo. It was found that complexes Pt1, Pt2 and Pt7 shows significant in vitro cytotoxic activity against mouse colon carcinoma CT26 cells, while all these complexes show moderate apoptotic effect. Complexes Pt1 and Pt7 arrested CT26 cells in G2/M phase of cell cycle, while complexes Pt5 and Pt6 exerted the highest antiproliferative effect which was evaluated by detection of Ki67 expressing cells. Complexes Pt1 and Pt2 performed significant in vivo antitumor effects reducing the growth of primary tumor and the incidence of lung and liver metastases without causing the significant hepato- and nephro- toxicity.
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Holliday, Michael W., Steven B. Cox, Min H. Kang, and Barry J. Maurer. "Abstract 4661: Levels of C22:0- and C24:0-dihydroceramide correlate with cytotoxicity in T-cell acute lymphoblastic leukemia cell lines." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4661.

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Larrouilh, B., K. Mogensen, and A. Dehane. "Very Rich Laboratory Data Set Paves the Way for Miscible Gas Injection Evaluation Onshore Abu Dhabi." In ADIPEC. SPE, 2023. http://dx.doi.org/10.2118/216680-ms.

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Abstract Phase equilibrium calculations require experimental lab data to constrain component properties in an equation of state (EOS) model. In this work, we evaluated the miscibility behavior of four different injection gases for a reservoir onshore Abu Dhabi containing medium-light oil. The extensive experimental program included swelling and slimtube experiments using CO2 as well as three hydrocarbon gases, in addition to conventional black-oil experiments. Based on the large company PVT database, gas additions in the swelling experiment were carefully designed to reduce uncertainty on the transition point where the swollen fluid type changes from oil to gas. We developed several fully tuned EOS models by gradually lumping down while monitoring the match quality. Due to the richness of the injection gases, C2 (15 mol%), C3 (15 mol%), C4 (10 mol%) and CO2 were kept as separate components resulting in a 10-component final EOS description. The compositional data showed a distinct tail effect above C20, which we believe is a lab artifact. The plus fraction was therefore lumped back from C36 to C20 to characterize the composition from C20 up to C80. This step improved the match of the dead oil properties. While the swelling data were matched well, the slimtube recovery data yielded some uncertainty on the MMP estimate, especially for the CO2 test. We made use of the reported effluent gas composition to show that one of the points denoted as immiscible in the lab report is most likely miscible. We tested several EOS-based MMP algorithms and found them to give similar MMP estimates for the hydrocarbon gases whereas the CO2 MMP was predicted with a much larger spread. Our view is that for CO2 flooding, cell-based simulations capture the dynamic behavior of miscible displacement better than the key tie-line approach. The tuned EOS model reproduced the single-phase density very accurately, which is important for the saturation estimation in the transition zone. Several injection gases appear suitable for miscible flooding and further screening studies are now ongoing.
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Kolev, Vihren, Yan Wang, Kam Sprott, Irina Shapiro, Jennifer Ring, Jonathan Pachter, and David Weaver. "Abstract C29: FAK inhibition targets cancer stem cells." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-c29.

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Ibrahim, Omar, Stephen G. Grant, Nicole T. Myers, Amie B. Courtney, Nancy A. lalanne, and Jean J. Latimer. "Abstract C26: Analysis of stem cell number & potency in African-American breast tissue." In Abstracts: Ninth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; September 25-28, 2016; Fort Lauderdale, FL. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7755.disp16-c26.

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Kim, Jeong‐Ah, Wonshik Han, Eun‐Mi Jung, Ki‐Tae Hwang, and Dong‐Young Noh. "Abstract C26: Nuclear factor I/B regulates cell proliferation of ER negative breast cancer." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-c26.

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An, Ho Jung, Eun Kyoung Choi, Jin-Sun Kim, Seung-Woo Hong, Jai-Hee Moon, Jae-Sik Shin, Seung-Hee Ha, et al. "Abstract C276: Ruxolitinib induces apoptotic cell death through the suppression of pJAK1 in human colon cancer cells." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-c276.

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Reports on the topic "C26 cells"

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Gafni, Yedidya, Moshe Lapidot, and Vitaly Citovsky. Dual role of the TYLCV protein V2 in suppressing the host plant defense. United States Department of Agriculture, January 2013. http://dx.doi.org/10.32747/2013.7597935.bard.

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TYLCV-Is is a major tomato pathogen, causing extensive crop losses in Israel and the U.S. We have identified a TYLCV-Is protein, V2, which acts as a suppressor of RNA silencing. Intriguingly, the counter-defense function of V2 may not be limited to silencing suppression. Our recent data suggest that V2 interacts with the tomato CYP1 protease. CYP1 belongs to the family of papain-like cysteine proteases which participate in programmed cell death (PCD) involved in plant defense against pathogens. Based on these data we proposed a model for dual action of V2 in suppressing the host antiviral defense: V2 targets SGS3 for degradation and V2 inhibits CYP1 activity. To study this we proposed to tackle three specific objectives. I. Characterize the role of V2 in SGS3 proteasomal degradation ubiquitination, II. Study the effects of V2 on CYP1 maturation, enzymatic activity, and accumulation and, III. Analyze the effects of the CYP1-V2 interaction on TYLCV-Is infection. Here we describe results from our study that support our hypothesis: the involvement of the host's innate immune system—in this case, PCD—in plant defense against TYLCV-Is. Also, we use TYLCV-Is to discover the molecular pathway(s) by which this plant virus counters this defense. Towards the end of our study we discovered an interesting involvement of the C2 protein encoded by TYLCV-Is in inducing Hypersensitive Response in N. benthamianaplants which is not the case when the whole viral genome is introduced. This might lead to a better understanding of the multiple processes involved in the way TYLCV is overcoming the defense mechanisms of the host plant cell. In a parallel research supporting the main goal described, we also investigated Agrobacteriumtumefaciens-encoded F-box protein VirF. It has been proposed that VirF targets a host protein for the UPS-mediated degradation, very much the way TYLCV V2 does. In our study, we identified one such interactor, an Arabidopsistrihelix-domain transcription factor VFP3, and further show that its very close homolog VFP5 also interacted with VirF. Interestingly, interactions of VirF with either VFP3 or VFP5 did not activate the host UPS, suggesting that VirF might play other UPS-independent roles in bacterial infection. Another target for VirF is VFP4, a transcription factor that both VirF and its plant functional homolog VBF target to degradation by UPS. Using RNA-seqtranscriptome analysis we showed that VFP4 regulates numerous plant genes involved in disease response, including responses to viral and bacterial infections. Detailed analyses of some of these genes indicated their involvement in plant protection against Agrobacterium infection. Thus, Agrobacterium may facilitate its infection by utilizing the host cell UPS to destabilize transcriptional regulators of the host disease response machinery that limits the infection.
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