A proteomic analysis for profiling NeuroD2 related changes in N2A neuroblastoma cell line

dc.authorid0000-0002-3567-9821
dc.contributor.authorBeker, Merve
dc.contributor.authorBolat, Busenur
dc.contributor.authorAslan, Feyza Şule
dc.contributor.authorÖzbay, Elif
dc.contributor.authorKaya, Sare Burcu
dc.date.accessioned2023-06-13T10:05:06Z
dc.date.available2023-06-13T10:05:06Z
dc.date.issued2023
dc.departmentİstanbul Medipol Üniversitesi, Rektörlük, Rejeneratif ve Restoratif Tıp Araştırmaları Merkezi (REMER)
dc.departmentİstanbul Medipol Üniversitesi, Rektörlük, Sağlık Bilim ve Teknolojileri Araştırma Enstitüsü
dc.description.abstractAim: NeuroD2 transcription factor is a key regulator of neurogenin-NeuroD signaling network and induces neuronal development, differentiation, neurogenesis and calcium de- pendent signaling. NeuroD2 regulates expression of survival and plasticity related proteins in neurons. Surprisingly, inhibition of NeuroD2 causes an increase in apoptotic cell death. Even though previous studies found out important data about NeuroD2 function, molec- ular interactions of NeuroD2 behind all of these impacts remains elusive. For this reason, it was aimed to shed light on the proteome profile of NeuroD2 based changes in the N2A cell line. Materials and Methods: NeuroD2 over-expression and NeuroD2 inhibition groups were constructed via lentiviral vectors. Mouse N2A cell line was transfected with the given vectors and incubated for 6 hours. After incubation samples were prepared for proteomic analyses with Filter Aided Sample Preparation (FASP) protocol and LC-MS/MS analysis was carried out. Results: Under conditions of overexpression and inhibition, detected proteins were fil- tered according to significant cut off values. The filtered proteins were further investigated to exhibit a coherent expression in each situation. Eventually, increased NeuroD2 activity was accompanied by an increase in N-alpha-acetyltransferase 25 (NAA25), and Synapto- brevin homolog (YKT6). On the other hand, when NeuroD2 was suppressed, expression of Cytoplasmic Dynein 1 Light Intermediate Chain 1, Kinesin-Like Protein (KIF-11), Leucine-tRNA Ligase (LARS1), and Ubiquitin-Associated Protein 2 (UBA2) were found to be upregulated with a reverse action. Conclusion: Up-regulations of the proteins Cytoplasmic Dynein 1, KIF11, LARS1, and UBA2 suggested that these proteins might be controlled by inhibition of NeuroD2. In this contex it can be said that, axonal transport, neuronal signaling, and activity of PI3K/AKT pathway can be indirectly regulated by NeuroD2.
dc.identifier.citationBeker, M., Bolat, B., Aslan, F. Ş., Özbay, E. ve Kaya, S. B. (2023). A proteomic analysis for profiling NeuroD2 related changes in N2A neuroblastoma cell line. Annals of Medical Research, 30(1), 21-25. https://doi.org/10.5455/annalsmedres.2022.07.218
dc.identifier.doi10.5455/annalsmedres.2022.07.218
dc.identifier.endpage25
dc.identifier.issn2636-7688
dc.identifier.issue1
dc.identifier.startpage21
dc.identifier.trdizinid1161858
dc.identifier.urihttps://doi.org/10.5455/annalsmedres.2022.07.218
dc.identifier.urihttps://hdl.handle.net/20.500.12511/11079
dc.identifier.volume30
dc.indekslendigikaynakTR-Dizin
dc.institutionauthorÖzbay, Elif
dc.language.isoen
dc.publisherInönü University Faculty of Medicine
dc.relation.ispartofAnnals of Medical Researchen_US
dc.relation.publicationcategoryMakale - Ulusal Hakemli Dergi - İdari Personel ve Öğrenci
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International*
dc.rightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectNeurod2
dc.subjectTranscription Factors
dc.subjectGene Cloning
dc.subjectProteomics
dc.titleA proteomic analysis for profiling NeuroD2 related changes in N2A neuroblastoma cell line
dc.typeArticle

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