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Relevant bibliographies by topics / Neuro 2a Cell Line

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Academic literature on the topic 'Neuro 2a Cell Line'

Author: Grafiati

Published: 7 September 2023

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Journal articles on the topic "Neuro 2a Cell Line"

1

Petrossian, G., and J. A. Oliver. "Synthesis of angiotensinogen by renin-containing neuroblastomas." American Journal of Physiology-Cell Physiology 257, no. 2 (August 1, 1989): C185—C189. http://dx.doi.org/10.1152/ajpcell.1989.257.2.c185.

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Angiotensinogen in plasma is of hepatic origin, but many organs possess the ability to synthesize this protein because messenger RNA for angiotensinogen is widely distributed in the body. The cell types responsible for the extrahepatic synthesis of angiotensinogen remain to be identified. To examine whether renin-containing cells synthesize angiotensinogen, we have utilized a polyclonal antibody to angiotensinogen and immunoprecipitated metabolically labeled cells of two neuroblastomas known to contain renin. The results indicate that the cell line Neuro 2a synthesizes and releases a protein with a molecular mass of 57 kDa that is specifically recognized by the angiotensinogen antibody, indicating that Neuro 2a synthesizes angiotensinogen. Similarly, the cell line NB41A3 was also found to synthesize a protein specifically recognized by the antibody to angiotensinogen.

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2

Bauer, David F., Larisa Pereboeva, G. Yancey Gillespie, Gretchen A. Cloud, Osama Elzafarany, Catherine Langford, James M. Markert, and Lawrence S. Lamb Jr. "Effect of HSV-IL12 Loaded Tumor Cell-Based Vaccination in a Mouse Model of High-Grade Neuroblastoma." Journal of Immunology Research 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/2568125.

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We designed multimodal tumor vaccine that consists of irradiated tumor cells infected with the oncolytic IL-12-expressing HSV-1 virus, M002. This vaccine was tested against the syngeneic neuroblastoma mouse model Neuro 2a injected into the right caudate nucleus of the immunocompetent A/J mice. Mice were vaccinated via intramuscular injection of multimodal vaccine or uninfected irradiated tumor cells at seven and 14 days after tumor establishment. While there was no survival difference between groups vaccinated with cell-based vaccine applied following tumor injection, a premunition prime/boost vaccination strategy produced a significant survival advantage in both groups and sustained immune response to an intracranial rechallenge of the same tumor. The syngeneic but unrelated H6 hepatocellular tumor cell line grew unrestricted in vaccinated mice, indicative of vaccine-mediated specific immunity to Neuro 2a tumors. Longitudinal analyses of tumor-infiltrating lymphocytes revealed a primary adaptive T cell response involving both CD4+ and CD8+ T cell subsets. Spleen cell mononuclear preparations from vaccinated mice were significantly more cytotoxic to Neuro 2a tumor cells than spleen cells from control mice as demonstrated in a four-hourin vitrocytotoxicity assay. These results strongly suggest that an irradiated whole cell tumor vaccine incorporating IL-12-expressing M002 HSV can produce a durable, specific immunization in a murine model of intracranial tumor.

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3

van Zoelen, E. J., W. J. van de Ven, H. J. Franssen, T. M. van Oostwaard, P. T. van der Saag, C. H. Heldin, and S. W. de Laat. "Neuroblastoma cells express c-sis and produce a transforming growth factor antigenically related to the platelet-derived growth factor." Molecular and Cellular Biology 5, no. 9 (September 1985): 2289–97. http://dx.doi.org/10.1128/mcb.5.9.2289-2297.1985.

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Mouse neuroblastoma Neuro-2A cells produce transforming growth factors during exponential growth in a defined hormone-free medium, which, on Bio-Gel columns in 1 M HAc, elute at a molecular size of 15 to 20 kilodaltons (kDa). These neuroblastoma-derived transforming growth factors have strong mitogenic activity, but they do not compete with epidermal growth factor for receptor binding (E. J. J. van Zoelen, D. R. Twardzik, T. M. J. van Oostwaard, P. T. van der Saag, S. W. de Laat, and G. J. Todaro, Proc. Natl. Acad. Sci. U.S.A. 81:4085-4089, 1984). In this study approximately 80% of the mitogenic activity was immunoprecipitated by antibodies raised against platelet-derived growth factor (PDGF). Immunoblotting indicated a true molecular size of 32 kDa for this PDGF-like growth factor. Analysis of poly(A)+ RNA from Neuro-2A cells demonstrated the expression of the c-sis oncogene in this cell line, whereas in vitro translation of the RNA yielded a 20-kDa protein recognized by anti-PDGF antibodies. Separation by reverse-phase high-pressure liquid chromatography demonstrated the presence of two distinct mitogenic activities in neuroblastoma-derived transforming growth factor preparations, one of which is antigenically related to PDGF. Both activities had the ability to induce anchorage-independent growth in normal rat kidney cells, both in the presence and in the absence of epidermal growth factor. It is concluded that Neuro-2A cells express c-sis with concomitant production and secretion of a PDGF-like growth factor, which plays a role in the induction of phenotypic transformation on normal rat kidney cells.

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4

Bamberger, Ana-Maria, Le-Ping Pu, David R. Cool, and Y. Peng Loh. "The Neuro-2a neuroblastoma cell line expresses [Met]-enkephalin and vasopressin mRNA and peptide." Molecular and Cellular Endocrinology 113, no. 2 (September 1995): 155–63. http://dx.doi.org/10.1016/0303-7207(95)03625-h.

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5

Sakaguchi, Minoru, Kouichi Murayama, Kozue Yabe, Motonobu Satoh, Masao Takeuchi, and Eiko Matsumura. "β-Casomorphin-5 stimulates neurite outgrowth in a mouse neuroblastoma cell line (Neuro-2a)." Neuroscience Letters 251, no. 2 (July 1998): 97–100. http://dx.doi.org/10.1016/s0304-3940(98)00500-x.

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6

Matten, W. T., and P. F. Maness. "V max. activation of pp60c-src tyrosine kinase from neuroblastoma neuro-2A." Biochemical Journal 248, no. 3 (December 15, 1987): 691–96. http://dx.doi.org/10.1042/bj2480691.

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A kinetic analysis of the tyrosine-specific protein kinase of pp60c-src from the C1300 mouse neuroblastoma cell line Neuro-2A and pp60c-src expressed in fibroblasts was carried out to determine the nature of the increased specific activity of the neuroblastoma enzyme. In immune-complex kinase assays with ATP-Mn2+ and the tyrosine-containing peptide angiotensin I as phosphoacceptor substrate, pp60c-src from the neuroblastoma cell line was characterized by a maximum velocity (Vmax.) that was 7-15-fold greater than the Vmax. of pp60c-src from fibroblasts. The neuroblastoma enzyme exhibited Km values for ATP (16 +/- 3 microM) and angiotensin I (6.8 +/- 2.6 mM) that were similar to Km values for ATP (25 +/- 3 microM) and angiotensin I (6.5 +/- 1.7 mM) of pp60c-src from fibroblasts. pp60v-src expressed in Rous-sarcoma-virus-transformed cells exhibited an ATP Km value (25 +/- 4 microM) and an angiotensin I Km value (6.6 +/- 0.5 mM) that approximated the values determined for pp60c-src in neuroblastoma cells and fibroblasts. These results indicate that the pp60c-src kinase from neuroblastoma cells has a higher turnover number than pp60c-src kinase from fibroblasts, and that the neural form of the enzyme would be expected to exhibit increased catalytic activity at the saturating concentrations of ATP that are found intracellularly.

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7

Wu, Po-Ming, Hsin-Yen Cho, Chi-Wu Chiang, Tzu-Hsien Chuang, Sheng-Nan Wu, and Yi-Fang Tu. "Characterization in Inhibitory Effectiveness of Carbamazepine in Voltage-Gated Na+ and Erg-Mediated K+ Currents in a Mouse Neural Crest-Derived (Neuro-2a) Cell Line." International Journal of Molecular Sciences 23, no. 14 (July 17, 2022): 7892. http://dx.doi.org/10.3390/ijms23147892.

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Carbamazepine (CBZ, Tegretol®) is an anticonvulsant used in the treatment of epilepsy and neuropathic pain; however, several unwanted effects of this drug have been noticed. Therefore, the regulatory actions of CBZ on ionic currents in electrically excitable cells need to be reappraised, although its efficacy in suppressing voltage-gated Na+ current (INa) has been disclosed. This study was undertaken to explore the modifications produced by CBZ on ionic currents (e.g., INa and erg-mediated K+ current [IK(erg)]) measured from Neuro-2a (N2a) cells. In these cells, we found that this drug differentially suppressed the peak (transient, INa(T)) and sustained (late, INa(L)) components of INa in a concentration-dependent manner with effective IC50 of 56 and 18 μM, respectively. The overall current–voltage relationship of INa(T) with or without the addition of CBZ remained unchanged; however, the strength (i.e., ∆area) in the window component of INa (INa(W)) evoked by the short ascending ramp pulse (Vramp) was overly lessened in the CBZ presence. Tefluthrin (Tef), a synthetic pyrethroid, known to stimulate INa, augmented the strength of the voltage-dependent hysteresis (Hys(V)) of persistent INa (INa(P)) in response to the isosceles-triangular Vramp; moreover, further application of CBZ attenuated Tef-mediated accentuation of INa(P)’s Hys(V). With a two-step voltage protocol, the recovery of INa(T) inactivation seen in Neuro-2a cells became progressively slowed by adding CBZ; however, the cumulative inhibition of INa(T) evoked by pulse train stimulation was enhanced during exposure to this drug. Neuro-2a-cell exposure to CBZ (100 μM), the magnitude of erg-mediated K+ current measured throughout the entire voltage-clamp steps applied was mildly inhibited. The docking results regarding the interaction of CBZ and voltage-gate Na+ (NaV) channel predicted the ability of CBZ to bind to some amino-acid residues in NaV due to the existence of a hydrogen bond or hydrophobic contact. It is conceivable from the current investigations that the INa (INa(T), INa(L), INa(W), and INa(P)) residing in Neuro-2a cells are susceptible to being suppressed by CBZ, and that its block on INa(L) is larger than that on INa(T). Collectively, the magnitude and gating of NaV channels produced by the CBZ presence might have an impact on its anticonvulsant and analgesic effects occurring in vivo.

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8

van Zoelen, E. J., W. J. van de Ven, H. J. Franssen, T. M. van Oostwaard, P. T. van der Saag, C. H. Heldin, and S. W. de Laat. "Neuroblastoma cells express c-sis and produce a transforming growth factor antigenically related to the platelet-derived growth factor." Molecular and Cellular Biology 5, no. 9 (September 1985): 2289–97. http://dx.doi.org/10.1128/mcb.5.9.2289.

Full text

Abstract:

Mouse neuroblastoma Neuro-2A cells produce transforming growth factors during exponential growth in a defined hormone-free medium, which, on Bio-Gel columns in 1 M HAc, elute at a molecular size of 15 to 20 kilodaltons (kDa). These neuroblastoma-derived transforming growth factors have strong mitogenic activity, but they do not compete with epidermal growth factor for receptor binding (E. J. J. van Zoelen, D. R. Twardzik, T. M. J. van Oostwaard, P. T. van der Saag, S. W. de Laat, and G. J. Todaro, Proc. Natl. Acad. Sci. U.S.A. 81:4085-4089, 1984). In this study approximately 80% of the mitogenic activity was immunoprecipitated by antibodies raised against platelet-derived growth factor (PDGF). Immunoblotting indicated a true molecular size of 32 kDa for this PDGF-like growth factor. Analysis of poly(A)+ RNA from Neuro-2A cells demonstrated the expression of the c-sis oncogene in this cell line, whereas in vitro translation of the RNA yielded a 20-kDa protein recognized by anti-PDGF antibodies. Separation by reverse-phase high-pressure liquid chromatography demonstrated the presence of two distinct mitogenic activities in neuroblastoma-derived transforming growth factor preparations, one of which is antigenically related to PDGF. Both activities had the ability to induce anchorage-independent growth in normal rat kidney cells, both in the presence and in the absence of epidermal growth factor. It is concluded that Neuro-2A cells express c-sis with concomitant production and secretion of a PDGF-like growth factor, which plays a role in the induction of phenotypic transformation on normal rat kidney cells.

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9

Ledreux, Aurélie, Sophie Krys, and Cécile Bernard. "Suitability of the Neuro-2a cell line for the detection of palytoxin and analogues (neurotoxic phycotoxins)." Toxicon 53, no. 2 (February 2009): 300–308. http://dx.doi.org/10.1016/j.toxicon.2008.12.005.

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10

Dickey, Amy, Stephen Schleicher, Kathleen Leahy, Rong Hu, Dennis Hallahan, and Dinesh Kumar Thotala. "GSK-3β inhibition promotes cell death, apoptosis, and in vivo tumor growth delay in neuroblastoma Neuro-2A cell line." Journal of Neuro-Oncology 104, no. 1 (December 16, 2010): 145–53. http://dx.doi.org/10.1007/s11060-010-0491-3.

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Dissertations / Theses on the topic "Neuro 2a Cell Line"

1

Ebrahimian, Venus. ""Characterization of Red Diamondback Rattlesnake Venom Proteins on Cell Death and Function"." Wright State University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=wright1389638004.

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2

Alaei, Sarah Rose. "C-terminal lysines modulate Connexin32 turnover and its ability to suppress growth of Neuro-2a cell cultures." Thesis, 2013. https://doi.org/10.7916/D8FN15M4.

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The extent of gap junction (GJ)-mediated coupling can be modulated through GJ channel gating. However, the amount of connexin protein available for incorporation into GJ, efficiency of channel assembly, trafficking to the cell surface, and disassembly also contribute to the regulation of cell-cell communication. In addition to their function in GJ, connexins also regulate a variety of physiological processes by forming hemichannels that are involved in paracrine signaling (Sanchez, Orellana et al. 2009) and through interactions with other proteins in the cytoplasm(Francis, Xu et al. 2011) and at the plasma membrane(Fowler, Akins et al. 2013). These other connexin functions are also likely to be influenced by the channel assembly dynamics, trafficking, and fast turnover of connexin proteins. The aim of this work was to determine if post-translational modifications, such as lysine acetylation, regulate connexin function through the fine-tuning of protein turnover or some other aspect of GJ dynamics. We chose to focus specifically on Cx32 for several reasons. Cx32 is an important regulator of neuronal myelination and loss of Cx32 GJ function is a common cause of the demyelinating neuropathy, Charcot-Marie-Tooth disease. Most studies addressing post-translational modifications of connexins focus on Cx43, which shares little sequence homology with Cx32 in the domains that are most-often subject to post-translational modification. We surmised that our results could be compared to what is known about Cx43 in order to determine if shared post-translational modifications regulate evolutionarily divergent connexins in similar ways. Here we show that Cx32 is an acetylated protein and that acetylated Cx32 is found in the cytoplasm and in the plasma membrane, where it is incorporated into GJ. For many proteins, acetylation has been implicated in pathways that modulate protein turnover(Caron, Boyault et al. 2005), thus we tested whether acetylation could regulate Cx32 protein level, resulting in the modulation of Cx32 functions. Our results demonstrate that acetylation is a positive regulator of Cx32 protein level, which increases the amount of Cx32 at the cell surface. Inhibition of the cytoplasmic deacetylase, HDAC6, results in hyperacetylation and accumulation of Cx32, which is dependent upon cytoplasmic C-terminal lysines. Mutational analysis revealed that these C-terminal lysines influence the ubiquitination and turnover rate of Cx32 protein. Comparison of the subcellular localization of WT Cx32 to that of mutants that either abolish acetylation sites while maintaining the original amino acid charge (K → R) or mimic constitutive acetylation (K → Q) suggests that acetylation does not simply alter lysine occupancy, thus preventing Cx32 ubiquitination and subsequent turnover. Instead, it seems likely that acetylation modulates protein-protein interactions that influence the amount of Cx32 in the plasma membrane and the role of Cx32 as a regulator of growth of cell cultures. K → Q Cx32 accumulates at the cell-surface more than WT Cx32, while K → R behavior resembles that of WT. Further, K → Q Cx32 suppresses the expansion of N2a cell cultures, whereas WT and K → R Cx32 do not. Interestingly, none of the mutations resulted in detectable alterations of cell-cell communication, suggesting that the suppression of cell culture growth observed when cells expressed the K → Q mutant may be independent of cell-cell communication. These results suggest that Cx32 acetylation is a positive regulator of Cx32 mediated suppression of proliferation or enhancement of pro-apoptotic signaling and provide rationale for future studies to determine which protein-protein interactions are modulated through Cx32 acetylation.

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3

Sung, Po-yu, and 宋伯瑜. "A Stable HeLa Cell Line That Inducibly Expresses 2A Protease of Enterovirus 71: Effects on Cell Apoptosis." Thesis, 2002. http://ndltd.ncl.edu.tw/handle/44048610083760400143.

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4

Chang, Chia-Cheng, and 張家誠. "The Cytotoxic Studies of Nano-size Titanium Dioxide on Central Nervous System Series Cell (Neuro-2a, Microglia, and Astrocyte)." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/32t9r8.

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碩士
國立清華大學
生醫工程與環境科學系
102
With the development of nanotechnology, more and more nanomaterials have been produced. Titanium dioxide (TiO2) nanoparticle (NP) is one of the important nanoscale materials. Though TiO2 nanoparticles (NPs) have been widely used in industry and biomedical field, they would have some potential risk to human health. Furthermore, animal and cell experiments were found NPs can induce toxic effects against central nervous system, such as cell death, inflammation, and oxidative stress ... etc. In this study, we exposed central nervous system cells (Neuro-2a cell line (N2A), microglial cell line (BV-2), and astrocytes (ALT)) w/wo endotoxin (lipopolysaccharide (LPS)) to TiO2 NPs (5 nm and 30 nm) to investigate the direct effect of neurotoxicity of TiO2 on cells. We also established the co-culture/tri-culture systems, co-existence of two or three cell lines by transwell assay. Then, one of the cells (ALT or BV-2) were treated with TiO2 NPs to study the effects of cell-cell interaction through secreted cytokines and chemokines. The results show that TiO2 NPs induce CNS series cells to generate inflammatory substances, and high concentration of TiO2 NPs have more cytotoxic to ALT and BV2 than N2A. Uptake ability of TiO2 NPs were BV-2 > N2A > ALT, so we speculate that BV-2 microglia is principal cells of uptaking TiO2 NPs in the brain. LPS pre-treatment can activate cells, especially BV-2 which can ingest more nanoparticles and result in more serious damage to the cells, such as cell death, inflammation, oxidative stress... etc. TiO2 NPs in smaller size can induce CNS series cell to release more inflammatory substances. Therefore, we will use 3-5 nm TiO2 NPs to do indirect effect of subsequent experiments. We found that only direct contact with nanoparticles, the declined phenomenon in cell viability was observed except for BV2-N2A co-culture system. In terms of uptake of nanoparticles, the SSC value of the cells also only in contact with the nanoparticles have increased significantly. When exposed to TiO2 NPs and LPS, glia cells generate inflammatory substances and ROS, and these inflammatory substances affect other kinds of cells, such as glia cells and neuron, leading to cell morphology changed, inflammatory substances increased, oxidative stress, and even cells death. We believe that when TiO2 NPs passed into the central nervous system, TiO2 NPs were ingested by ALT or BV-2 cells causing cell death, oxidative stress, inflammation, and these conditions may cause damage to the central nervous system and lead to the generation of neurodegenerative diseases (such as Alzheimer's disease, Parkinson's s disease) . This study provides important information for nano titanium dioxide effects on the central nervous system series cells, and the results can supply a reference for future animal and human experiments.

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Chen, Ying-Duan, and 陳映端. "Study of retinoic acid activating Rac1, Akt and anti-oxidant enzymes to induce survival ofNeuro-2a cell line." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/12935328527180686427.

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碩士
國立高雄大學
生物科技研究所
100
Akt plays an important role in neuronal survival, especially phosphorylated Akt. Additionally, there are reports that excess ROS (reactive oxygen species) can damage neuronal cells. However, the damage can be prevented by anti-oxidant enzymes such as SOD (superoxide dismutase), Catalase, and glutathione peroxidase. In order to realize the relationship between anti-oxidant enzymes and survival signal, Neuro-2a cell line was used in this research. Three different Rac1 genes were transfected into cells, including wild type Rac1, constitutive activated G12V, and dominant negative T17N. After transfecting, 10μM Retinoic acid (RA) was treated to induce neurite outgrowth. In this research, neurite outgrowth was found in Rac1 wild type and G12V, but not T17N. Protein expressions of p-Akt, SOD1 and Catalase were increased in all transfection treatments, but not Akt and SOD2. In the assay of immunoprecipitation, Rac1 could bind to Akt and induced neurite outgrowth. RA-induced Rac1 enhanced its binding with Catalase. Furthermore, Akt was associated with SOD1 via c-Src. In summary, RA-induced neurite outgrowth was regulated by Akt/ Rac1 pathway. SOD1 and Catalase involved in RA-induced neurite outgrowth. The relationship between survival pathway and anti-oxidant enzymes relied on the association of Rac1 and Catalase.

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6

You, Sheng-Jie, and 游勝傑. "The influence of endogenous β-amyloid on mitochondria and expression of heat shock protein in Neuro 2a cells bearing the amyloid precursor protein and primary neuron cell." Thesis, 2007. http://ndltd.ncl.edu.tw/handle/42546933042973511737.

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碩士
中國醫藥大學
醫學研究所碩士班
95
Aβ accumulation to oligomers is a kind of stress which can cause cell damage by inducing oxidative stress in vitro studies. Heat shock proteins (HSPs) induced by stress. The relationship between endogenous Aβ and HSP expression remains uncleaer. In our study, APPwt transfected neuro 2a (N-wt) and APPsw gene transfected neuro 2a (N-sw) cells and primary neuron were used. We evaluated viability of N-wt and N-sw via trypan blue stain. We found the cell viability was decreased compared with control. Result of cell cycle showed that sub G1 peak of N-wt and N-sw was increased compared with control. DNA fragmentations showed apoptotic features in N-wt, N-sw. JC-1 stain(mitochondrial membrane potential), mitotracker stain(ROS level), Fluo-3A (Ca2+ level) stain and cytochrome c oxidase assay showed mitochondrial function impared. Western blot showed expression of pro-apoptotic protein Bid and cytochrome c increased while expression of anti-apoptotic protein Bcl-2 compared with control, respectively. Increased expression of HSP70, HSP60, and HSP27 were in N-wt, N-sw while HSP90, HSP32 were decreased in N-wt, N-sw compared with control, respectively. Similar results were found in primary neuron; Aβs decreased cell viability of neuronal cell and influenced mitochondria function. Increased expression of pro-apoptotic related protein, Bid, cytochrome c while expression of anti-apoptotic protein Bcl-2 was decreased compared with control. Increased expression of HSP90, HSP70, HSP60, HSP27 while HSP32 decreased compared with control. This is the first study of the correlation between Aβs and HSP. Aβs is a potent source of oxidative stress, but expression of HSP induced by Aβs remains unclear. We respect expression of HSP up regulated, but HSP 90 in N-wt, N-sw and HSP 32 are down regulated. HSP induced by stress and could protect cell, but in this study, the viability of neurons were decreased compare with control. The neuron protection of HSP while Aβs exists needs further investigation.

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Book chapters on the topic "Neuro 2a Cell Line"

1

Drexler, Hans G. "Mac-2A." In The Leukemia-Lymphoma Cell Line FactsBook, 495–96. Elsevier, 2001. http://dx.doi.org/10.1016/b978-012221970-2/50314-4.

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2

Drexler, Hans G. "RC-2A." In The Leukemia-Lymphoma Cell Line FactsBook, 599. Elsevier, 2001. http://dx.doi.org/10.1016/b978-012221970-2/50386-7.

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Conference papers on the topic "Neuro 2a Cell Line"

1

Fomenko, A. N., and M. S. Korovin. "Comparative analysis of the effect of low-dimensional alumina structures on cell lines L929 and Neuro-2a." In PHYSICS OF CANCER: INTERDISCIPLINARY PROBLEMS AND CLINICAL APPLICATIONS (PC’16): Proceedings of the International Conference on Physics of Cancer: Interdisciplinary Problems and Clinical Applications 2016. Author(s), 2016. http://dx.doi.org/10.1063/1.4960234.

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