Relevant bibliographies by topics / SH-SY5Y cell

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  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'SH-SY5Y cell'

Author: Grafiati
Published: 4 June 2021
Last updated: 14 March 2023

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Journal articles on the topic "SH-SY5Y cell"

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Lee, Hyun-Su, Eun-Nam Kim, and Gil-Saeng Jeong. "Lupenone Protects Neuroblastoma SH-SY5y Cells Against Methamphetamine-Induced Apoptotic Cell Death via PI3K/Akt/mTOR Signaling Pathway." International Journal of Molecular Sciences 21, no. 5 (February 27, 2020): 1617. http://dx.doi.org/10.3390/ijms21051617.

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Methamphetamine (METH) is an addictive psychostimulant showing neurotoxicity through neuronal apoptosis and the neuro-inflammatory pathway. Lupenone, a lupane triterpenoid, is an isolated compound exhibiting anti-oxidative, anti-inflammation, and anti-diabetic activities. However, whether lupenone plays a protective role against apoptosis induced by METH in SH-SY5y neuroblastoma cells remains unknown. In the present study, we elucidated that lupenone had no toxicity to SH-SY5y cells at different concentrations. On the other hand, we found that the treatment of SH-SY5y cells with an optimal concentration of lupenone could lead to protection against cell death induced by METH. AnnexinV/PI apoptosis analysis revealed a dramatically reduced level of the apoptotic cell population in lupenon and METH treated SH-SY5y cells. Moreover, diminished expression of anti-apoptotic proteins, including Bcl-2, Caspase3, Caspase7, and Caspase8 in METH-exposed SH-SY5y cells, was significantly recovered by treatment with lupenone. This protection in the expression of anti-apoptotic proteins was due to an increased phosphorylation level of PI3K/Akt in METH-treated SH-SY5y cells pre-incubated with lupenone. These findings suggest that lupenone can protect SH-SY5y cells against METH-induced neuronal apoptosis through the PI3K/Akt pathway.
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An, Xinfang, Zixing Fu, Chendi Mai, Weiming Wang, Linyu Wei, Dongliang Li, Chaokun Li, and Lin-Hua Jiang. "Increasing the TRPM2 Channel Expression in Human Neuroblastoma SH-SY5Y Cells Augments the Susceptibility to ROS-Induced Cell Death." Cells 8, no. 1 (January 8, 2019): 28. http://dx.doi.org/10.3390/cells8010028.

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Human neuroblastoma SH-SY5Y cells are a widely-used human neuronal cell model in the study of neurodegeneration. A recent study shows that, 1-methyl-4-phenylpyridine ion (MPP), which selectively causes dopaminergic neuronal death leading to Parkinson’s disease-like symptoms, can reduce SH-SY5Y cell viability by inducing H2O2 generation and subsequent TRPM2 channel activation. MPP-induced cell death is enhanced by increasing the TRPM2 expression. By contrast, increasing the TRPM2 expression has also been reported to support SH-SY5Y cell survival after exposure to H2O2, leading to the suggestion of a protective role for the TRPM2 channel. To clarify the role of reactive oxygen species (ROS)-induced TRPM2 channel activation in SH-SY5Y cells, we generated a stable SH-SY5Y cell line overexpressing the human TRPM2 channel and examined cell death and cell viability after exposure to H2O2 in the wild-type and TRPM2-overexpressing SH-SY5Y cells. Exposure to H2O2 resulted in concentration-dependent cell death and reduction in cell viability in both cell types. TRPM2 overexpression remarkably augmented H2O2-induced cell death and reduction in cell viability. Furthermore, H2O2-induced cell death in both the wild-type and TRPM2-overexpressing cells was prevented by 2-APB, a TRPM2 inhibitor, and also by PJ34 and DPQ, poly(ADP-ribose) polymerase (PARP) inhibitors. Collectively, our results show that increasing the TRPM2 expression renders SH-SY5Y cells to be more susceptible to ROS-induced cell death and reinforce the notion that the TRPM2 channel plays a critical role in conferring ROS-induced cell death. It is anticipated that SH-SY5Y cells can be useful for better understanding the molecular and signaling mechanisms for ROS-induced TRPM2-mediated neurodegeneration in the pathogenesis of neurodegenerative diseases.
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Song, Zurong, and Ali Tao. "The Neuroprotective Effects of Astragaloside IV against H2O2-Induced Damage in SH-SY5Y Cells are Associated with Synaptic Plasticity." Journal of Chemistry 2020 (May 13, 2020): 1–7. http://dx.doi.org/10.1155/2020/5343619.

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The aim of this study was to investigate whether the neuroprotective effects of astragaloside IV (AS-IV) against hydrogen peroxide (H2O2)-induced damage on human neuroblastoma cell line (SH-SY5Y) are associated with synaptic plasticity. The concentration screening of AS-IV and H2O2 on SH-SY5Y cells and the protective effects of AS-IV on SH-SY5Y cells under H2O2 stress were all determined by MTT assay. The expression of postsynaptic density 95 (PSD-95) and growth-associated protein 43 (GAP-43) were measured by western blot (WB) and inmunofluorescence staining assay under the same treatment conditions. According to the MTT results, the concentration of H2O2 at 50 μmol/L for 3 h was used for the cell damage model, and various concentrations of AS-IV (0.1, 0.2, 0.3, and 0.4 μmol/L) were used to affect SH-SY5Y cells. The MTT results showed that pretreatment of SH-SY5Y cells with AS-IV (0.1, 0.2, 0.3, and 0.4 μmol/L) attenuated the damage induced by H2O2 (50 μmol/L, 51.62% cell viability) and increased cell viability to 64.19, 63.48, 65.86, and 65.81%, respectively. Western blot analysis and immunofluorescence staining showed that the protective effects of AS-IV against SH-SY5Y cell damage caused by H2O2 resulted in reduced expression of PSD-95 and increased expression of GAP-43 in comparison with the H2O2 treatment group. The conclusion shows that AS-IV protected SH-SY5Y cells and enhanced their viability under H2O2 stress. AS-IV may facilitate presynaptic and postsynaptic plasticity to exert protective effects against oxidative damage of SH-SY5Y cells.
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Qin, Chunlian, Saisai Zhang, Qunchen Yuan, Mengxue Liu, Nan Jiang, Liujing Zhuang, Liquan Huang, and Ping Wang. "A Cell Co-Culture Taste Sensor Using Different Proportions of Caco-2 and SH-SY5Y Cells for Bitterness Detection." Chemosensors 10, no. 5 (May 5, 2022): 173. http://dx.doi.org/10.3390/chemosensors10050173.

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Bitter taste receptors (T2Rs) are involved in bitter taste perception, which is one of the five basic taste modalities in mammals. In this study, a cell co-culture taste sensor using different proportions of Caco-2 cells and SH-SY5Y cells was proposed. Caco-2 cells, which endogenously expressed the human T2R38 receptor, and SH-SY5Y cells, which endogenously expressed the human T2R16 receptor, were co-cultured. Using Caco-2 cells and SH-SY5Y cells at a constant total concentration of 40 K/mL, we designed seven mixtures with [Caco-2]/([Caco-2] + [SH-SY5Y]) ratios of 0, 20, 40, 50, 60, 80, and 100%. These mixtures were then seeded on the 16 E-plates of the electric cell-substrate impedance sensor (ECIS) for bitterness detection. Theoretically, after T2R38 ligands activation, continuous evolution profiles (CEP), with [Caco-2]/([Caco-2] + [SH-SY5Y]) ratios as the x-axis and ΔCI (Max) as the y-axis, would exhibit positive correlation property. After T2R16 ligands activation, the CEP would show negative correlation property. However, when stimulated with compounds that could activate both T2R16 and T2R38, it would show different response patterns.
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Ahmad, Faizan. "Inflammatory response of stem cell secreting conditioned media in SH-SY5Y cell line." Bionatura 5, no. 3 (August 15, 2020): 1243–45. http://dx.doi.org/10.21931/rb/2020.05.03.13.

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Mesenchymal stem cells (MSCs) are reported to secrete anti-inflammatory cytokines and growth factors, which makes MSCs a promising candidate in the treatment of various neurodegenerative diseases. SH-SY5Y show extreme inflammatory response under LPS and an inadequate inflammatory response when treated with Wharton's jelly, conditioned media. This study mainly focuses on the inflammatory (pro and anti-inflammatory) response of SH-SY5Y by gene expression study. SH-SY5Y cell line used for cell culture and RT- q PCR was done with 5 different primers. In this article, lipopolysaccharides (LPS) show a significant result in pro-inflammatory and pro-apoptotic. In this article, we focus on the therapeutic approach of stem cells, which reduce inflammation by secreting stem cell factors to cure various neurodegenerative diseases.
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Xu, Xiaonan, Chengle Zhuang, Zimu Wu, Hongyan Qiu, Haixia Feng, and Jun Wu. "LincRNA-p21 Inhibits Cell Viability and Promotes Cell Apoptosis in Parkinson’s Disease through Activating α-Synuclein Expression." BioMed Research International 2018 (December 25, 2018): 1–10. http://dx.doi.org/10.1155/2018/8181374.

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Long intergenic noncoding RNA-p21 (lincRNA-p21) has been reported to be increased in Parkinson’s disease (PD). However, the function and underlying mechanisms of lincRNA-p21 remain not clear. In order to explore the role of lincRNA-p21 in PD, we used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to induce in vivo PD model (C57BL/6 mice) and utilized N-methyl-4-phenylpyridinium (MPP+) to create in vitro PD model (SH-SY5Y cells). Results showed that the expression level of lincRNA-p21 was increased significantly in PD models. High abundance of lincRNA-p21 inhibited viability and promoted apoptosis markedly in SH-SY5Y cells treated with MPP+. Mechanistically, further experiments demonstrated that upregulation of lincRNA-p21 could sponge miR-1277-5p and indirectly increase the expression of α-synuclein to suppress viability and activate apoptosis in SH-SY5Y cells. In short, our study illustrated that lincRNA-p21/miR-1277-5p axis regulated viability and apoptosis in SH-SY5Y cells treated with MPP+ via targeting α-synuclein. LincRNA-p21 might be a novel target for PD.
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Pires, Ana O., Andreia Neves-Carvalho, Nuno Sousa, and António J. Salgado. "The Secretome of Bone Marrow and Wharton Jelly Derived Mesenchymal Stem Cells Induces Differentiation and Neurite Outgrowth in SH-SY5Y Cells." Stem Cells International 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/438352.

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The goal of this study was to determine and compare the effects of the secretome of mesenchymal stem cells (MSCs) isolated from human bone-marrow (BMSCs) and the Wharton jelly surrounding the vein and arteries of the umbilical cord (human umbilical cord perivascular cells (HUCPVCs)) on the survival and differentiation of a human neuroblastoma cell line (SH-SY5Y). For this purpose, SH-SY5Y cells were differentiated with conditioned media (CM) from the MSCs populations referred above. Retinoic acid cultured cells were used as control for neuronal differentiated SH-SY5Y cells. SH-SY5Y cells viability assessment revealed that the secretome of BMSCs and HUCPVCs, in the form of CM, was able to induce their survival. Moreover, immunocytochemical experiments showed that CM from both MSCs was capable of inducing neuronal differentiation of SH-SY5Y cells. Finally, neurite lengths assessment and quantitative real-time reverse-transcription polymerase chain reaction (RT-PCR) analysis demonstrated that CM from BMSCs and HUCPVCs differently induced neurite outgrowth and mRNA levels of neuronal markers exhibited by SH-SY5Y cells. Overall, our results show that the secretome of both BMSCs and HUCPVCs was capable of supporting SH-SY5Y cells survival and promoting their differentiation towards a neuronal phenotype.
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Wei, Bo, Gui-rong Xiao, Cheng-long Wu, and Yi-qin Xu. "HAGLR promotes neuron differentiation through the miR-130a-3p-MeCP2 axis." Open Medicine 16, no. 1 (January 1, 2021): 1121–31. http://dx.doi.org/10.1515/med-2021-0301.

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Abstract Parkinson’s disease (PD) is a prevalent neurodegenerative disease. Currently, the molecular mechanisms underlying the progressions of PD are not fully understood. The human neuroblastoma cell line SH-SY5Y has been widely used as an in vitro model for PD. This study aims to investigate the molecular mechanisms of the non-coding RNA-mediated SH-SY5Y differentiation induced by retinoic acid (RA). By microArray analysis, lncRNA HAGLR was observed to be significantly upregulated during the RA-induced SH-SY5Y differentiation. Silencing HAGLR blocked the RA-induced SH-SY5Y differentiation. Moreover, bioinformatical analysis illustrated that miR-130a-3p contains binding sites for HAGLR. The RNA-pull down assay and luciferase assay demonstrated that HAGLR functioned as a ceRNA of miR-130a-3p in SH-SY5Y cells. Overexpression of miR-130a-3p effectively inhibited SH-SY5Y differentiation. We identified MeCP2, a vital molecule in neuronal diseases, to be a direct target of miR-130a-3p in SH-SY5Y cells by western blot and luciferase assays. The rescue experiments verified that recovery of miR-130a-3p in HAGLR-overexpressing SH-SY5Y cells could successfully overcome the RA-induced SH-SY5Y differentiation by targeting MeCP2. In summary, this study reveals a potential molecular mechanism for the lncRNA-HAGLR-promoted in vitro neuron differentiation by targeting the miR-130a-3p-MeCP2 axis, contributing to the understanding of the pathogenesis and progression of PD.
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Zhang, Yuan, Tun Sun, Meng Li, Yanling Lin, Yue Liu, Shusheng Tang, and Chongshan Dai. "Ivermectin-Induced Apoptotic Cell Death in Human SH-SY5Y Cells Involves the Activation of Oxidative Stress and Mitochondrial Pathway and Akt/mTOR-Pathway-Mediated Autophagy." Antioxidants 11, no. 5 (May 5, 2022): 908. http://dx.doi.org/10.3390/antiox11050908.

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Ivermectin (IVM) could cause potential neurotoxicity; however, the precise molecular mechanisms remain unclear. This study explores the cytotoxicity of IVM in human neuroblastoma (SH-SY5Y) cells and the underlying molecular mechanisms. The results show that IVM treatment (2.5–15 μM) for 24 h could induce dose-dependent cell death in SH-SY5Y cells. Compared to the control, IVM treatment significantly promoted the production of ROS, mitochondrial dysfunction, and cell apoptosis. IVM treatment also promoted mitophagy and autophagy, which were charactered by the decreased expression of phosphorylation (p)-Akt and p-mTOR proteins, increased expression of LC3II, Beclin1, ATG5, PINK, and Pakin1 proteins and autophagosome formation. N-acetylcysteine treatment significantly inhibited the IVM-induced production of ROS and cell death in SH-SY5Y cells. Autophagy inhibitor (e.g., 3-methyladenine) treatment significantly inhibited IVM-induced autophagy, oxidative stress, and cell apoptosis. Taken together, our results reveal that IVM could induce autophagy and apoptotic cell death in SH-SY5Y cells, which involved the production of ROS, activation of mitochondrial pathway, and inhibition of Akt/mTOR pathway. Autophagy inhibition improved IVM-induced oxidative stress and apoptotic cell death in SH-SY5Y cells. This current study provides new insights into understanding the molecular mechanism of IVM-induced neurotoxicity and facilitates the discovery of potential neuroprotective agents.
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Lavrin, Teja, Tilen Konte, Rok Kostanjšek, Simona Sitar, Kristina Sepčič, Sonja Prpar Mihevc, Ema Žagar, et al. "The Neurotropic Black Yeast Exophiala dermatitidis Induces Neurocytotoxicity in Neuroblastoma Cells and Progressive Cell Death." Cells 9, no. 4 (April 14, 2020): 963. http://dx.doi.org/10.3390/cells9040963.

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The neurotropic and extremophilic black yeast Exophiala dermatitidis (Herpotrichellaceae) inhabits diverse indoor environments, in particular bathrooms, steam baths, and dishwashers. Here, we show that the selected strain, EXF-10123, is polymorphic, can grow at 37 °C, is able to assimilate aromatic hydrocarbons (toluene, mineral oil, n-hexadecane), and shows abundant growth with selected neurotransmitters (acetylcholine, gamma-aminobutyric acid, glycine, glutamate, and dopamine) as sole carbon sources. We have for the first time demonstrated the effect of E. dermatitidis on neuroblastoma cell model SH-SY5Y. Aqueous and organic extracts of E. dermatitidis biomass reduced SH-SY5Y viability by 51% and 37%, respectively. Melanized extracellular vesicles (EVs) prepared from this strain reduced viability of the SH-SY5Y to 21%, while non-melanized EVs were considerably less neurotoxic (79% viability). We also demonstrated direct interactions of E. dermatitidis with SH-SY5Y by scanning electron and confocal fluorescence microscopy. The observed invasion and penetration of neuroblastoma cells by E. dermatitidis hyphae presumably causes the degradation of most neuroblastoma cells in only three days. This may represent a so far unknown indirect or direct cause for the development of some neurodegenerative diseases such as Alzheimer’s.
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Dissertations / Theses on the topic "SH-SY5Y cell"

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Belbaraka, Loubaba. "Growth, differentiation and cell-cell coupling in the human neuroblastoma cell line SH-SY5Y." Thesis, University of Ottawa (Canada), 2002. http://hdl.handle.net/10393/6112.

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Neuroblastoma is one of the most common paediatric solid tumours, frequently occurring in infancy with the primary lesion in the adrenal gland and sympathetic nervous system. It originates from primitive neural crest cells. In rare cases, this tumour regresses spontaneously to a more benign ganglioneuroma probably by neuronal differentiation or apoptosis. We investigated the role of induction of neuronal differentiation and apoptosis in vitro in SH-SY5Y neuroblastoma cells. A variety of agents that are known to induce neuronal differentiation including retinoic acid, nerve growth factor (NGF), protein kinase C (PKC) inhibitors and a cAMP-dependent protein kinase A (PKA) activator were tested solely or in combination for their capacity to induce terminal differentiation. The cells were characterised for markers of differentiation as well as their ability to withdraw from the cell cycle. We found that the combination of 8-Br-cAMP (PKA activator) with NGF in the presence of the cell cycle inhibitor aphidicolin was the best treatment to induce terminal differentiation in SH-SY5Y cells. Treated cells showed long neurites resembling those of neurones. They expressed markers characteristic of the cytoskeleton (NF200, NF68) and of neuronal function (tyrosine hydroxylase, choline acetyltransferase and the neurone-specific enolase) and showed an increase in the expression of TrkA, the receptor for NGF. Furthermore, the expression of the N-myc oncogene that is normally overexpressed in these cells decreased. Since neurones are dependent on NGF for survival, we tested the ability of terminally differentiated SH-SY5Y cells to survive in the absence of NGF. We found that the cells became NGF-survival dependent and that deprivation from this neurotrophic factor induced programmed cell death. We also tested the effect of PKC specific and non-specific inhibitors on cell proliferation, differentiation and apoptosis in SH-SY5Y cells. We found that only the non-specific PKC inhibitors staurosporine and H7 induced morphological and molecular differentiation as well as decreased N-myc amplification followed by apoptosis. The effect of differentiation induction on p53 sub-localisation was also investigated in undifferentiated and differentiated SH-SY5Y cells. p53 immunostaining showed that p53 was sequestered in the cytoplasm in undifferentiated SH-SY5Y cells and that the induction of differentiation resulted in the partial transfer of p53 to the nucleus where it probably became able to regulate the cell cycle and apoptosis since p53 is not mutated in neuroblastoma. Gap junction intercellular communication (GJIC) is known to be involved in the regulation of cell growth and homeostasis and has been shown to contribute to many diseases including cancer. We investigated the role of GJIC in neuroblastoma. We found that SH-SY5Y cells have altered GJIC due to an aberrant localisation in the perinuclear region of connexin 43 (Cx43), one of the proteins of GJIC normally present at the plasma membrane. GJ channel formation and gating is regulated by PKC, PKA and/or MAPK. We found that induction of differentiation using the PKA activator 8-Br-cAMP relocalised Cx43 to the plasma membrane region and restored GJIC. Furthermore, inhibition of p38 MAPK induced a block of cell proliferation associated with GJIC proficiency while inhibition of the subfamily of MAPK, Erk1/Erk2, likely promoted the degradation of Cx43.
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Song, Juxian, and 宋聚先. "Protective effects of chrysotoxine on Parkinsonian neurotoxins induceddopaminergic neuronal cell death in SH-SY5Y cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47150129.

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Samms, Warren C. "Catecholamine disturbance and SH-SY5Y cell toxicity of halogenated 3-amino-2 phenylpropenes." Diss., Wichita State University, 2009. http://hdl.handle.net/10057/2378.

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Parkinson’s disease (PD) is a progressive neurodegenerative disease that affects between 1% and 2% of the population over age 65. Despite decades of research and the development of many molecular models of PD, there is far from a consensus as to the etiology of this disease. Current molecular models, such as the role of the quaternary ammonium ion MPP+ and its effect on cell death, in the presence/absence of monoamine transporters as opposed to distinct intracellular activity are still disputed. The 3-amino-2-phenylpropene (APP) class of compounds has been previously characterized as reversible inhibitors for the bovine adrenal chromaffin granule vesicular monoamine transporter (VMAT) as well as potent irreversible dopamine-β- monooxygenase (DβM) and monoamine oxidase (MAO) inhibitors. These effects result in perturbation of catecholamine uptake, storage and/or metabolism, leading to the potential for increased oxidative stress. Herein, we report that halogen substitution on the 4'-position of the aromatic ring gradually increases VMAT inhibition potency from 4'-F to 4'-I, parallel to the hydrophobicity of the halogen. We show that these derivatives are taken up into both neuronal and non-neuronal cells, and into resealed chromaffin granule ghosts efficiently through passive diffusion. In addition, these derivatives are highly toxic to human neuroblastoma SH-SY5Y cells, they are not toxic to several non-neuronal cell lines at similar concentrations. These compounds drastically perturb DA uptake and metabolism in SH-SY5Y cells under sub-lethal conditions, and are able to deplete both viii vesicular and cytosolic catecholamines similar to amphetamines. Additionally, (4'-iodo) 3-amino-2-phenylpropene (4'-IAPP) treatment significantly increases intracellular reactive oxygen species (ROS) and decreases glutathione reduced form (GSH) levels in SH-SY5Y cells, and cell death is significantly attenuated by the common antioxidants α- tocopherol, N-acetyl-L-cysteine (NAC) and glutathione (GSH). This suggests that ROS production is intricately involved with the mechanism of cell death. Although DNA fragmentation analysis supports that apoptosis occurs, the fact that a non-specific caspase inhibitor provided no significant protection suggests that that cell death is likely due to a caspase-independent ROS-mediated apoptotic pathway. Based on these and other findings, we propose that drastic perturbation of DA metabolism in SH-SY5Y cells by 4'-halo APP derivatives causes increased oxidative stress leading to apoptotic cell death. These compounds, which induce catecholaminespecific neurotoxic effects following nonspecific cellular entry may be a unique resource in the modeling of PD both in vitro and in vivo.
Thesis (Ph.D.)--Wichita State University, College of Liberal Arts and Sciences, Dept. of Chemistry
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Lin, Shu-Ting. "Effects of inclusion body formationand alpha-synuclein on apoptotic cell death in SH-SY5Y." Thesis, King's College London (University of London), 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.417323.

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FERNANDEZ, ABASCAL JESUS. "Role of cytochrome P450 against toxic insult in neuroblastoma SH-SY5Y cells." Doctoral thesis, Università di Siena, 2018. http://hdl.handle.net/11365/1051261.

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Cytochrome P450 (CYP) is one of the main metabolic systems involved in xenobiotic clearance in live organisms. Its activity is mainly carried out at hepatic level, but in the last two decades, its function has been also reported to be important in other extrahepatic tissues, especially in the central nervous system. In brain, CYP isoenzymes vary their expression depending on the brain area and the cell type. However, the role of the different isoforms is not yet well characterized. Some of them have been involved in detoxification and/or toxic activation of xenobiotics; while other have been related with production of oxidative stress through the metabolism of endogenous compounds. Therefore, the presence and the function of the CYP in the brain has been related with neurodegenerative diseases such as Parkinson’s Disease (PD). On the other hand, the study of the degeneration of dopaminergic neurons in vitro has been carried out by the use of several toxins that promote apoptosis and similar pathological features that the observed in PD. Among these xenobiotics, 1-methyl-4-phenylpyridinium (MPP+), rotenone, and paraquat are the most used because they are able to promote neurodegeneration of dopaminergic cells by directly targeting complex I of mitochondria. Recently, it has been reported that some CYP isoforms, such as CYP 2D6, can be involved in the development of this neurodegenerative disease. To better characterize this role, we have studied the induction of some isoforms in an in vitro system. Undifferentiated SH-SY5Y cells were treated with well-known inducers of CYP for 48 hours, namely β-naphtoflavone (β-NF), ethanol (EtOH), and cyclophosphamide (CPA); and qRT-PCR, Western Blot (WB) and confocal microscopy analysis were performed. CPA increased the mRNA levels of CYP 1A1, 2D6 and 2E1, while the other inducers promoted a slight increase on these isoforms compared to CPA. WB analysis confirmed the induction promoted by CPA in CYP 1A1 and 2D6, and revealed that CYP 2D6 was also inducible by EtOH. Moreover, CYP 2E1 was increased by β-NF and EtOH treatments. In differentiated SH-SY5Y cells, a preliminary WB analysis of CYP 2D6 and 2E1 was also performed. The results suggested a change in the regulation of the expression of CYP 2D6 when treated with β-NF, and also of CYP 2E1 levels when treated with β-NF and CPA. Immunohistochemistry analysis confirmed the inducibility of CYPs and showed a co-localization of CYP 2D6 with mitochondria. These data indicate that CYP can be induced in both undifferentiated and differentiated neuroblastoma cells, and underline the possibility to use this in vitro system for studying the role of CYPs in neurodegeneration. Moreover, as showed by our group and others, β-naphtoflavone and ethanol have the ability to induce the expression of some CYP isoforms. In order to study the possible role of CYP induction in neurodegeneration, we have use the same in vitro model than before, where undifferentiated neuroblastoma SH-SY5Y cells have been treated with these inducers separately previous and during exposure of MPP+. In both experimental conditions, the toxic effect of MPP+ was partially reverted. MTT assays showed an increase in cell viability of approximately 17% in β-NF treatment, while EtOH showed an increase between 13-15%. The analysis of apoptotic population by flow cytometry showed that both treatments were able to restore the populations to control values compared to the toxic effect of MPP+. The mitochondrial fission-fusion kinetics revealed that both treatments were able to avoid the impairment of this mitochondrial motility after exposure to the toxin. Finally, this neuroprotection was confirmed by a lowest effect of MPP+ upon complex I activity when cells were preincubated with the inducers. These results bring new insights about the possible role of CYPs, specially CYP 2D6, in neuroprotection and possible development of therapeutic drugs.
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Klein, Juliane. "Amyloid precursor protein (APP) and copper homeostasis in the human neuroblastoma cell line SH-SY5Y." Thesis, University of Newcastle upon Tyne, 2011. http://hdl.handle.net/10443/1201.

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Alzheimer’s disease (AD) is characterised by cerebellar accumulation and aggregation of amyloid beta (Aβ), a cleavage product of the transmembrane amyloid precursor protein (APP). APP contains a range of functional domains in its large extracellular portion, among which are two copper-binding motifs and one zinc-binding motif. The copper-binding motifs are present in the amino-terminal region of APP and within the Aβ region of the protein and readily reduce Cu(II) to Cu(I), thus APP and its cleavage products are linked to copper metabolism and have been hypothesised to participate in cellular copper homeostasis. In this project human neuroblastoma cell lines SH-SY5Y were utilised to determine the effect of expressing a familial AD mutation on intracellular copper concentrations and possible functional alterations or deficits of enzymes that require copper as a co-factor. The familial AD mutation first found in a Swedish population was previously shown to increase the total amount of released Aβ. Direct phenotypic comparison between SH-SY5Y APPWT cell lines expressing endogenous levels of APP and APPswe Coupling native two dimensional liquid chromatography with metal analysis, SDS-PAGE and Principal Component Analysis identified one major copper and zinc containing pool as copper-zinc superoxide dismutase (SOD1) in soluble whole cell protein extracts. Comparative analysis of metal content between APP cell lines overexpressing APP carrying the Swedish mutation was performed in standard culture and manipulated copper concentrations. WT and APPswe cultures indicated a difference in metallation of SOD1 with copper. APPswe cultures displayed reduced metallation of SOD1, whereas SOD1 metallation with zinc remained unaltered. Functional analysis of copper-binding enzymes, such as SOD1 and cytochrome c oxidase (CCO), using standard biochemical approaches, identified lower activities for both enzymes during standard cell culture in APPswe cells. Upon treatment of cultures with increasing concentrations of exogenous copper APPWT enzyme activities remained unaltered but enzyme activities in APPswe cultures increased in direct correlation with increasing copper concentrations. Combined with phenotypic analysis of growth, survival and intracellular metal content it appears that APPswe cultures are copper deficient, but this can be overcome by copper supplementation. Lower copper accumulation also enables greater survival of APP swe Overall, these data suggest that APP cells in elevated copper. swe overexpression in SH-SY5Y cells results in functional copper deficiency which can be rescued by supplementation of cultures with exogenous copper. APPswe further confers resistance to copper toxicity not only via increased Aβ release, but also via increased copper delivery to enzymatic target proteins improving cellular antioxidant response and energy metabolism. These data are consistent with a function of APP in copper efflux either in a regulatory capacity or directly contributing to copper egress.
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Lau, Kwok-wai. "Evaluation of using all-trans-retinoic acid to differentiate human neuroblastoma SH-SY5Y cells in neurodegeneration research." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/HKUTO/record/B39557339.

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Lau, Kwok-wai, and 劉國威. "Evaluation of using all-trans-retinoic acid to differentiate human neuroblastoma SH-SY5Y cells in neurodegeneration research." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39557339.

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Fjæraa, Alfredsson Christina. "Effects of ellagic acid in human neuroblastoma cells." Doctoral thesis, Karlstads universitet, Institutionen för hälsovetenskaper, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:kau:diva-29905.

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A diet rich in polyphenols has been proposed to have beneficial health effects and to reduce risk of disease. Ellagic acid, a polyphenol common in red berries and pomegranates, has potential anti-tumorigenic effects that make it interesting to further study in different cancer cell systems. Neuroblastoma is a childhood cancer that arises during development of the peripheral nervous system. Neuroblastoma, being an embryonal tumor, show loss of function of genes controlling differentiation and apoptosis. Neuroblastoma is a heterogenic tumor disease, and highly malignant neuroblastomas are difficult to treat despite different treatment modalities, identifying a need for new and combinatory treatments. A common model for human neuroblastoma is the SH-SY5Y cell line resembling immature neuroblasts that can be differentiated in vitro with several agents including the phorbol ester 12-O-tetradecanoylphorbol-13-acetate and the vitamin A-derivative all-trans retinoic acid. Here, the effect of ellagic acid on proliferation, cell detachment and apoptosis in non-differentiated and in vitro-differentiated SH-SY5Y cells were studied with the aim of identifying cellular target mechanisms and a possible therapeutic potential for ellagic acid. In non-differentiated cells, ellagic acid reduced cell number, inhibited cell cycle activity, and induced cell detachment and apoptosis. Apoptosis was partly mediated by the intrinsic pathway. 12-O-tetradecanoylphorbol-13-acetate and all-trans retinoic acid both induced morphological differentiation, while only the latter induced G0/G1-arrest. Single-cell analysis revealed that 12-O-tetradecanoylphorbol-13-acetate-treated cells continued cycling during neuritogenesis while these two read-outs were mutually exclusive in all-trans retinoic acid-treated cells. 12-O-tetradecanoylphorbol-13-acetate- and especially all-trans retinoic acid-differentiated cells showed lower sensitivity to ellagic acid-dependent cell detachment and apoptosis.

Artikel 4 ("Altered sensitivity...") ingick som manuskript i avhandlingen, nu publicerad.

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Sadideen, Doraid, and Doraid Sadideen. "Exploring G-Protein-Coupled Receptors Regulation, Specificity and Controllability of Exosomes Release in the Neuronal Cell Line SH-SY5Y." Thesis, The University of Arizona, 2016. http://hdl.handle.net/10150/621166.

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Parkinson's disease is a neurodegenerative disease characterized by the buildup of aggregated and spread of misfolded alpha-synuclein. How the misfolded alpha-synuclein contributing to the toxicity and death of neuronal cells has been the focal point of research. The spread of alpha-synuclein has been attributed to many mechanisms, one of which is via cell-derived vesicles called exosomes. This project aims to examine the controllability of exosome release. SH-SY5Y, MCF-7 and CHO-K1 cells were transfected with dopamine receptor 3-green fluorescent protein, G-protein receptor 143 or green fluorescent protein and treated with either dopamine or L-DOPA. Medium was harvested and subjected to ultracentrifugation and a silver stain and western blot were performed. There was no significant difference in the total protein in the exosome fraction lanes between the treatment groups or within them. Another aim was to test the specificity of exosomes. Exosomes isolated from SH-SY5Y or MCF-7 were labeled with Exo-Red dye and introduced to wells containing SH-SY5Y, MCF-7 and CHO-K1 cells at room temperature and -4C. At room temperature, exosomes were observed intercellular in all of the cell lines, however, they did not deliver their content. At -4C exosome uptake was halted and they remained on the surface of the cells. Exo-Red labeled SH-SY5Y exosomes were treated with proteinase K and were introduced to CHO-K1 cells at -4C and room temperature. CHO-K1 did not take up exosomes, suggesting exosomes contain one or more necessary proteins needed to interact with the cellular membrane to initiate internalization. CHO-K1 cells were treated with versene to examine the involvement of integrin proteins. Exo-Red labeled SH-SY5Y exosomes were trapped on the surface of CHO-K1 after versene treatment. Lastly, Exo-Red labeled SH-SY5Y exosomes were biotinylated and magnetically captured then introduced to SH-SY5Y and MCF-7 cells and a silver stain and a biotinylated blot were performed. MCF-7 bound more Exo-Red labeled SH-SY5Y exosomes.
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Books on the topic "SH-SY5Y cell"

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Olsson, Anna-Karin. Ras-Mapk Signaling on Differentiating Sh-Sy5Y Human Neuroblastoma Cells. Uppsala Universitet, 2000.

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Book chapters on the topic "SH-SY5Y cell"

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Annuario, Emily, Kristal Ng, and Alessio Vagnoni. "High-Resolution Imaging of Mitochondria and Mitochondrial Nucleoids in Differentiated SH-SY5Y Cells." In Methods in Molecular Biology, 291–310. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-1990-2_15.

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AbstractMitochondria are highly dynamic organelles which form intricate networks with complex dynamics. Mitochondrial transport and distribution are essential to ensure proper cell function, especially in cells with an extremely polarised morphology such as neurons. A layer of complexity is added when considering mitochondria have their own genome, packaged into nucleoids. Major mitochondrial morphological transitions, for example mitochondrial division, often occur in conjunction with mitochondrial DNA (mtDNA) replication and changes in the dynamic behaviour of the nucleoids. However, the relationship between mtDNA dynamics and mitochondrial motility in the processes of neurons has been largely overlooked. In this chapter, we describe a method for live imaging of mitochondria and nucleoids in differentiated SH-SY5Y cells by instant structured illumination microscopy (iSIM). We also include a detailed protocol for the differentiation of SH-SY5Y cells into cells with a pronounced neuronal-like morphology and show examples of coordinated mitochondrial and nucleoid motility in the long processes of these cells.
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Kovalevich, Jane, and Dianne Langford. "Considerations for the Use of SH-SY5Y Neuroblastoma Cells in Neurobiology." In Neuronal Cell Culture, 9–21. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-640-5_2.

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Gutul, T., A. Dimoglo, and T. Mironic. "Copper-Containing Polyoxometalates: Syntheses and Anticancer Activity against the SH-SY5Y Human Neuroblastoma Cell Line." In 3rd International Conference on Nanotechnologies and Biomedical Engineering, 292–96. Singapore: Springer Singapore, 2016. http://dx.doi.org/10.1007/978-981-287-736-9_71.

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Forsby, Anna. "Neurite Degeneration in Human Neuronal SH-SY5Y Cells as an Indicator of Axonopathy." In Neuromethods, 255–68. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-077-5_12.

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Maruyama, W., M. Shamoto-Nagai, Y. Akao, P. Riederer, and M. Naoi. "The effect of neuromelanin on the proteasome activity in human dopaminergic SH-SY5Y cells." In Parkinson’s Disease and Related Disorders, 125–32. Vienna: Springer Vienna, 2006. http://dx.doi.org/10.1007/978-3-211-45295-0_20.

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Isoda, Hiroko, Junkyu Han, and Hideyuki Shigemori. "Protective Effect of Di-O-Caffeoylquinic Acid on Human-Derived Neurotypic SH-SY5Y Cells Against Alzheimer’s Disease Amyloid-Beta-Induced Toxicity." In Cells and Culture, 755–57. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-3419-9_131.

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Chen, H. Y., and Y. Chang. "Study the Impact of the SH-SY5Y Cells under the Magnetic Stimulation with Different Frequency and Duration." In IFMBE Proceedings, 241–43. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-12262-5_67.

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Teppola, Heidi, Jertta-Rinna Sarkanen, Tuula Orvokki Jalonen, and Marja-Leena Linne. "Impacts of laminin and polyethyleneimine surface coatings on morphology of differentiating human SH-SY5Y cells and networks." In EMBEC & NBC 2017, 298–301. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-5122-7_75.

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Glaß, Marco, Heinz-Georg Jahnke, and Andrea A. Robitzki. "Reverse Transcription PCR Screening of different neuronal guiding cues and their receptors in human staurosporine differentiated SH-SY5Y cells." In IFMBE Proceedings, 98–101. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-03900-3_29.

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Kim, Yon-Suk, Eun-Kyung Kim, Jin-Woo Hwang, Jin-Soo Kim, Woen-Bin Shin, Xin Dong, Weligala Pahalagedara Amila Srilal Nawarathna, Sang-Ho Moon, Byong-Tae Jeon, and Pyo-Jam Park. "Neuroprotective Effect of Taurine-Rich Cuttlefish (Sepia officinalis) Extract Against Hydrogen Peroxide-Induced Oxidative Stress in SH-SY5Y Cells." In Advances in Experimental Medicine and Biology, 243–54. Dordrecht: Springer Netherlands, 2017. http://dx.doi.org/10.1007/978-94-024-1079-2_22.

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Conference papers on the topic "SH-SY5Y cell"

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Li, Rui, Xuefei Lv, and Yulin Deng. "NOA 81 fabricated microfluidic chip for SH-SY5Y cell culture." In 2015 IEEE International Conference on Mechatronics and Automation (ICMA). IEEE, 2015. http://dx.doi.org/10.1109/icma.2015.7237621.

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Piah, Nur Hana Md, Sharil Sarman, Khairul Aizat Mohd Sharin, and Mazatulikhma Mat Zain. "Potential neuroprotective effect of herbal extracts (NHA56) on hydrogen peroxide-induced SH-SY5Y cell lines." In its Applications (CSPA). IEEE, 2010. http://dx.doi.org/10.1109/cspa.2010.5545217.

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"Effect of DNA-hydrolyzing catalytic IgGs from schizophrenia patients on cell viability of the SH-SY5Y cell line." In Bioinformatics of Genome Regulation and Structure/Systems Biology (BGRS/SB-2022) :. Institute of Cytology and Genetics, the Siberian Branch of the Russian Academy of Sciences, 2022. http://dx.doi.org/10.18699/sbb-2022-452.

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Mohan, Nishant, Naren L. Banik, and Swapan K. Ray. "Abstract 2139: 4-HPR and apigenin together suppressed autophagy and cell survival pathways to increase apoptosis in human malignant neuroblastoma SH-SY5Y cells." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2139.

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Wissel, K., K. Kreisköther, A. Warnecke, P. Behrens, and T. Lenarz. "Gene expression analysis to examine the adhesion of the human neuroblastoma cell line SH-SY5Y growing on gold surfaces coated with L1CAM." In Abstract- und Posterband – 89. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Forschung heute – Zukunft morgen. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1640695.

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Gonulalan, E., O. Bayazeid, E. Nemutlu, F. Yalçın, and Ö. Demirezer. "The correlation between BDNF in SH-SY5Y cell lines and GC-MS metabolomic profiling of Melissa officinalis, Hypericum perforatum and Passiflora incarnata." In GA 2017 – Book of Abstracts. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1608271.

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Rao, Ling, Fu-Tao Li, Fei-Yi Sun, Jian-Feng Li, and Hong Ma. "Expression of Mutant But Not Wild-Type α-synuclein in SH-SY5Y Cells Induces Apoptosis and Autophagy: Implication for Regulation of Cell Death in Parkinson's Disease." In 2015 International Conference on Medicine and Biopharmaceutical. WORLD SCIENTIFIC, 2016. http://dx.doi.org/10.1142/9789814719810_0010.

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Teschner, M., W. Nuss, G. Brandes, A. Warnecke, T. Lenarz, and K. Wissel. "Influence of omega-3 fatty acids and L-carnitine on the metabolic activity of the human neuroblastoma (SH-SY5Y) and the mouse organ of Corti (HEI-OC1) cell lines." In Abstract- und Posterband – 91. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Welche Qualität macht den Unterschied. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1711158.

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Teschner, M., K. Wissel, G. Brandes, T. Lenarz, and W. Nuss. "Omega-3 fatty acids combined with L-carnitine have an effect on the metabolic activity of the human neuroblastoma (SH-SY5Y) and the murine organ of Corti (HEI-OC1) cell lines." In 100 JAHRE DGHNO-KHC: WO KOMMEN WIR HER? WO STEHEN WIR? WO GEHEN WIR HIN? Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1728464.

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Wang, Xingyue, Cuihua Hu, Jianjun Dong, Kaige Qu, Rui Wang, Zuobin Wang, and Baohua Jia. "Effect of VC on Living SH-SY5Y Cells Studied by Atomic Force Microscopy." In 2022 IEEE International Conference on Manipulation, Manufacturing and Measurement on the Nanoscale (3M-NANO). IEEE, 2022. http://dx.doi.org/10.1109/3m-nano56083.2022.9941568.

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Reports on the topic "SH-SY5Y cell"

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Marmol, Frederic. Effects of lithium treatment on oxidative stress markers in mitochondrial complex I and complex III inhibition and after CO2 exposure in SH-SY5Y cells. Science Repository OÜ, February 2019. http://dx.doi.org/10.31487/j.nnb.2019.01.001.

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