Researcher:
Güner, Gökhan

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Master Student

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Gökhan

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Güner

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Güner, Gökhan

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2014 - 201922020 - 20211

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Researcher Of Publications: search.filters.isAuthorOfPublication.0c77aa78-ef52-4972-92fe-4f0d06590bc4

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    Roles of nelavl in Kif2a pre-mrna splicing and functional roles of KIF2A protein isoforms
    (Wiley-Blackwell, 2014) Bayam, Emrah; N/A; N/A; N/A; Department of Molecular Biology and Genetics; Akkaya, Cansu; Güner, Gökhan; Dunn, Gülayşe İnce; PhD Student; Master Student; Other; Department of Molecular Biology and Genetics; Graduate School of Sciences and Engineering; Graduate School of Sciences and Engineering; College of Sciences; N/A; N/A; N/A
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    NEUROD2 regulates stim1 expression and store-operated calcium entry in cortical neurons
    (Soc Neuroscience, 2017) N/A; N/A; N/A; N/A; N/A; N/A; N/A; N/A; Department of Physics; Department of Molecular Biology and Genetics; Güner, Gökhan; Güzelsoy, Gizem; İşleyen, Fatma Sadife; Şahin, Gülcan Semra; Akkaya, Cansu; Bayam, Efil; Kotan, Ilgın Eser; Kabakçıoğlu, Alkan; Dunn, Gülayşe İnce; Master Student; Master Student; Master Student; Master Student; PhD Student; Researcher; Master Student; Faculty Member; Other; Department of Physics; Department of Molecular Biology and Genetics; Graduate School of Sciences and Engineering; Graduate School of Sciences and Engineering; Graduate School of Sciences and Engineering; Graduate School of Sciences and Engineering; Graduate School of Sciences and Engineering; Graduate School of Sciences and Engineering; Graduate School of Sciences and Engineering; College of Sciences; College of Sciences; N/A; N/A; N/A; N/A; N/A; N/A; N/A; 49854; N/A
    Calcium signaling controls many key processes in neurons, including gene expression, axon guidance, and synaptic plasticity. In contrast to calcium influx through voltage- or neurotransmitter-gated channels, regulatory pathways that control store-operated calcium entry (SOCE) in neurons are poorly understood. Here, we report a transcriptional control of Stim1 (stromal interaction molecule 1) gene, which is a major sensor of endoplasmic reticulum (ER) calcium levels and a regulator of SOCE. By using a genome-wide chromatin immunoprecipitation and sequencing approach in mice, we find that NEUROD2, a neurogenic transcription factor, binds to an intronic element within the Stim1 gene. We show that NEUROD2 limits Stim1 expression in cortical neurons and consequently fine-tunes the SOCE response upon depletion of ER calcium. Our findings reveal a novel mechanism that regulates neuronal calcium homeostasis during cortical development.
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    Roles of developmentally regulated KIF2A alternative isoforms in cortical neuron migration and differentiation
    (The Company of Biologists, 2021) N/A; N/A; N/A; N/A; N/A; N/A; N/A; Department of Molecular Biology and Genetics; N/A; Akkaya, Cansu; Atak, Dila; Kamacıoğlu, Altuğ; Akarlar, Büşra; Güner, Gökhan; Bayam, Efil; Taşkın, Ali Cihan; Dunn, Gülayşe İnce; PhD Student; PhD Student; Master Student; Other; Master Student; Researcher; Other; Faculty Member; Other; Department of Molecular Biology and Genetics; N/A; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); Graduate School of Sciences and Engineering; Graduate School of Sciences and Engineering; Graduate School of Sciences and Engineering; N/A; Graduate School of Sciences and Engineering; N/A; N/A; College of Sciences; N/A; N/A; N/A; N/A; N/A; N/A; N/A; 291296; 105301; N/A
    KIF2A is a kinesin motor protein with essential roles in neural progenitor division and axonal pruning during brain development. However, how different KIF2A alternative isoforms function during development of the cerebral cortex is not known. Here, we focus on three Kif2a isoforms expressed in the developing cortex. We show that Kif2a is essential for dendritic arborization in mice and that the functions of all three isoforms are sufficient for this process. Interestingly, only two of the isoforms can sustain radial migration of cortical neurons; a third isoform, lacking a key N-terminal region, is ineffective. By proximity-based interactome mapping for individual isoforms, we identify previously known KIF2A interactors, proteins localized to the mitotic spindle poles and, unexpectedly, also translation factors, ribonucleoproteins and proteins that are targeted to organelles, prominently to the mitochondria. In addition, we show that a KIF2A mutation, which causes brain malformations in humans, has extensive changes to its proximity-based interactome, with depletion of mitochondrial proteins identified in the wild-type KIF2A interactome. Our data raises new insights about the importance of alternative splice variants during brain development.