User:C15677434/N2a cell
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Differentiation Properties
Originating from a mouse, the N2a cell line has a neuronal and amoeboid stem cell morphology, allowing it to differentiate in response to environmental factors. The differentiated cells have many properties of neurons, including neurofilaments. The differentiation of N2a cells is caused by activation of the mitogen-activated protein kinase/extracellular-signal regulated kinase (MAPK/ERK) and the phosphoinositide-3-kinase/protein kinase B (PI3K/Akt) signaling pathways.[1] The cells, due to passaging since initial collection, can exhibit responses to toxins that differ from those of neuronal cells in a live organism.[2] Synthesizing large amounts of microtubules, N2a cells are susceptible to viruses (such as herpes simplex and poliovirus) that can alter cell morphology and physiology.
Factors that Affect Differentiation of N2a Cells
Promoting Factors
- Emodin causes N2a differentiation and growth through activation of the PI3K/Akt pathway. It does so by activating Akt while inactivating glycogen synthase kinase-3β (GSK-3β), an inhibitor of the Akt pathway. Emodin specifically causes phosphorylation of cAMP-responsive element binding protein (CREB), an important molecule in the differentiation of neurons.[3]
- β-Hydroxy-β-methylbutyrate (HMB) causes N2a growth through activation of the PI3K/Akt and MAPK/ERK signaling pathways.[4]
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References
- https://www.sciencedirect.com/science/article/pii/S0165027009006025
- https://www.jbc.org/article/S0021-9258(20)88936-4/fulltext
- https://www.sciencedirect.com/science/article/pii/S0011224015002424
- https://www.mdpi.com/1422-0067/23/2/1006
- https://www.science.org/doi/full/10.1126/scisignal.254cm1
- https://www.sciencedirect.com/science/article/pii/S0024320514006195?casa_token=c8-w211pzzUAAAAA:fATpGqDUxyZ5k8QfTNaKdc6CJAEzw2E1ajnFRzBLkS9olTShZdjyCF2eObkHW8e1S7AdLxJUgQ
- https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0135614
- https://www.aging-us.com/article/100131/text
- https://www.dl.begellhouse.com/journals/7b004699754c9fe6,4158286763abf5e8,32bb22b358744318.html
- https://www.pnas.org/doi/full/10.1073/pnas.1324035111
- https://www.sciencedirect.com/science/article/pii/S0165027020301643
- https://www.nature.com/articles/1208494
- ^ Salto, Rafael; Vílchez, Jose D.; Girón, María D.; Cabrera, Elena; Campos, Nefertiti; Manzano, Manuel; Rueda, Ricardo; López-Pedrosa, Jose M. (2015-08-12). "β-Hydroxy-β-Methylbutyrate (HMB) Promotes Neurite Outgrowth in Neuro2a Cells". PLOS ONE. 10 (8): e0135614. doi:10.1371/journal.pone.0135614. ISSN 1932-6203. PMC 4534402. PMID 26267903.
{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link) - ^ LePage KT, Dickey RW, Gerwick WH, Jester EL, Murray TF (2005). "On the use of neuro-2a neuroblastoma cells versus intact neurons in primary culture for neurotoxicity studies". Critical Reviews in Neurobiology. 17 (1): 27–50. doi:10.1615/critrevneurobiol.v17.i1.20. PMID 16307526.
- ^ Park, Shin-Ji; Jin, Mei Ling; An, Hyun-Kyu; Kim, Kyoung-Sook; Ko, Min Jung; Kim, Cheol Min; Choi, Young Whan; Lee, Young-Choon (2015-02-19). "Emodin induces neurite outgrowth through PI3K/Akt/GSK-3β-mediated signaling pathways in Neuro2a cells". Neuroscience Letters. 588: 101–107. doi:10.1016/j.neulet.2015.01.001. ISSN 0304-3940.
- ^ Salto, Rafael; Vílchez, Jose D.; Girón, María D.; Cabrera, Elena; Campos, Nefertiti; Manzano, Manuel; Rueda, Ricardo; López-Pedrosa, Jose M. (2015-08-12). "β-Hydroxy-β-Methylbutyrate (HMB) Promotes Neurite Outgrowth in Neuro2a Cells". PLOS ONE. 10 (8): e0135614. doi:10.1371/journal.pone.0135614. ISSN 1932-6203. PMC 4534402. PMID 26267903.
{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link)