Seyrantepe, Volkan
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Seyrantepe, V
Seyrantepe, V.
Seyrantepe, V.
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volkanseyrantepe@iyte.edu.tr
Main Affiliation
04.03. Department of Molecular Biology and Genetics
Status
Current Staff
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Sustainable Development Goals
1NO POVERTY
0
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2ZERO HUNGER
0
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3GOOD HEALTH AND WELL-BEING
6
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4QUALITY EDUCATION
2
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5GENDER EQUALITY
0
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6CLEAN WATER AND SANITATION
0
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7AFFORDABLE AND CLEAN ENERGY
0
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8DECENT WORK AND ECONOMIC GROWTH
0
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9INDUSTRY, INNOVATION AND INFRASTRUCTURE
7
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10REDUCED INEQUALITIES
0
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11SUSTAINABLE CITIES AND COMMUNITIES
0
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12RESPONSIBLE CONSUMPTION AND PRODUCTION
0
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13CLIMATE ACTION
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14LIFE BELOW WATER
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15LIFE ON LAND
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16PEACE, JUSTICE AND STRONG INSTITUTIONS
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17PARTNERSHIPS FOR THE GOALS
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Documents
49
Citations
1792
h-index
21
Documents
62
Citations
1621
Scholarly Output
72
Articles
26
Views / Downloads
92014/15206
Supervised MSc Theses
19
Supervised PhD Theses
6
WoS Citation Count
273
Scopus Citation Count
302
Patents
0
Projects
22
WoS Citations per Publication
3.79
Scopus Citations per Publication
4.19
Open Access Source
37
Supervised Theses
25
| Journal | Count |
|---|---|
| Molecular Genetics and Metabolism | 7 |
| FEBS Open Bio | 6 |
| European Journal of Human Genetics | 4 |
| Frontiers in Molecular Biosciences | 2 |
| PLoS Genetics | 2 |
Current Page: 1 / 6
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72 results
Scholarly Output Search Results
Now showing 1 - 10 of 72
Article Citation - WoS: 14Citation - Scopus: 15Neuraminidase-1 Contributes Significantly To the Degradation of Neuronal B-Series Gangliosides but Not To the Bypass of the Catabolic Block in Tay-Sachs Mouse Models(Elsevier Ltd., 2015) Timur, Zehra Kevser; Akyıldız Demir, Seçil; Marsching, C.; Sandhoff, R.; Seyrantepe, VolkanTaySachs disease is a severe lysosomal storage disorder caused bymutations in the HEXA gene coding for? subunit of lysosomal β-Hexosaminidase A enzyme, which converts GM2 to GM3 ganglioside. HexA mice, depleted of the β-Hexosaminidase A iso-enzyme, remain asymptomatic up to 1 year of age because of a metabolic bypass by neuraminidase(s). These enzymes remove a sialic acid residue converting GM2 to GA2,which is further degraded by the still intact β-Hexosaminidase B iso-enzyme into lactosylceramide. A previously identified ganglioside metabolizing neuraminidase, Neu4, is abundantly expressed in the mouse brain and has activity against gangliosides like GM2 in vitro. Neu4 mice showed increased GD1a and decreased GM1 ganglioside in the brain suggesting the importance of the Neu4 in ganglioside catabolism. Mice with targeted disruption of both HexA and Neu4 genes showed accumulating GM2 ganglioside and epileptic seizures with 40% penetrance, indicating that the neuraminidase Neu4 is a modulatory gene, but may not be the only neuraminidase contributing to the metabolic bypass in HexA mice. Therefore, we elucidated the biological role of neuraminidase-1 in ganglioside degradation in mouse. Analysis of HexANeu1 and HexANeu4Neu1 mice models showed significant contribution of neuraminidase-1 on B-series ganglioside degradation in the brain. Therefore, we speculate that other neuraminidase/neuraminidases such as Neu2 and/or Neu3 might be also involved in the ganglioside degradation pathway in HexA mice.Conference Object Human Neu3 Sialidase Reduces GM2 Ganglioside Accumulation in Neuroglia Cells of Tay-Sachs Disease Mice Model(Springernature, 2024) Basirli, Hatice Hande; Ozgur, Melike Can; Seyrantepe, VolkanMaster Thesis Identification of Neuroinflammatory Markers in a Mouse Model With a Deficiency of Neu1(01. Izmir Institute of Technology, 2024) Seyrantepe, Volkan; Ada, Ebru; Seyrantepe, VolkanLysosomal neuraminidase 1 is responsible for sialic acid removal from oligosaccharides and glycoconjugates. Neu1 sialidase forms enzyme complex with protective protein cathepsin A, and glycosidase β-galactosidase. Mutations in Neu1 sialidase cause sialidosis, and Neu1-/- mice show symptoms of sialidosis patients. GM3 ganglioside is defined as substrate of lysosomal sialidase in vitro, and marked increase in GM3, GD3, and GM4 ganglioside levels in brain, spleen and liver autopsy tissues of sialidosis patients. Additionally, it was monitored that Neu1 has regulatory roles in immune response; expression of interleukins, activation of Toll-like receptor, and production of NF-kB in immune cells. However, relationship between inflammatory pathways and secondary lipid metabolisms in Neu1 sialidase deficiency remains unclear. Here, we aimed to investigate secondary lipid alterations and inflammatory response in tissues of Neu1-/- mice. In this study, lipidomic, molecular, histological and immunohistochemical analyses were performed in brain, spleen and kidney tissues of 2- and 5-month-old Neu1-/- mice. Decreasing levels of secondary lipids (phosphotidylcholine, phosphatidylethanolamine, and phosphotidylinositol) and elevated levels of pro-inflammatory cytokines, glycoconjugate accumulations, morphological degenerations, oligodendrocyte and neuronal loss, astrogliosis, and microgliosis were observed in brain, spleen and kidney of 2- and 5-month-old Neu1-/- mice. In the light of our findings, reduced levels of glycerophospholipids may be considered as biomarkers of activated inflammatory response in Type II sialidosis mice model. In the future studies, novel therapeutic strategies can target these altered glycerophospholipids, and their regulation can be crucial for alleviation of pathogenesis in sialidosis patients.Conference Object Investigation of the Regulatory Role of Lysosomal Cathepsin a in the Autophagy(Springernature, 2024) Yanbul, Selman; Seyrantepe, VolkanArticle Mass Spectrometric Profiling Reveals Alterations in N-Glycans and O-Glycans in Tay-Sachs Disease Under Autophagy-Induced Conditions(Springer, 2025) Can, Melike; Basirli, Hande; Jin, Chunsheng; Karlsson, Niclas G.; Bojar, Daniel; Seyrantepe, VolkanTay-Sachs disease is a rare neurodegenerative disorder caused by mutations in the HEXA gene. The HEXA gene encodes the alpha-subunit of the enzyme beta-hexosaminidase A, which degrades GM2 ganglioside. Previously, we identified impaired autophagy in the brains of a mouse model of Tay-Sachs disease, which exhibited neuropathological and clinical abnormalities. Moreover, we demonstrated autophagosome clearance in Tay-Sachs cells under lithium-induced conditions. Here, we further aimed to evaluate N- and O-glycan changes in these cells and examine whether glycan alterations are linked to ER stress. The profiles of N- and O-glycans were analyzed using LC-MS/MS in fibroblasts and neuroglial cells from 5-month-old Hexa-/-Neu3-/- mice and neuroglial cells from Tay-Sachs patients under lithium induction and nutrient deprivation. The expression levels of ER stress-related markers were assessed using qRT-PCR and Western blot analyses. We demonstrated higher levels of high mannose and lower levels of complex types of N-glycans, along with increased O-glycan levels in Tay-Sachs cells. Compared to control groups, we observed upregulated expression of endoplasmic reticulum (ER) stress-related markers, CHOP and ATF-6, in Tay-Sachs cells. Our study demonstrated that autophagy induction causes the degradation of accumulated high-mannose N-glycans and O-glycans, which is associated with the downregulation of ER stress-related genes in Tay-Sachs cells. Our study is the first to show this phenomenon in Tay-Sachs cells and suggests the presence of ER stress-mediated autophagy. Therefore, targeting glycans through autophagy induction could offer therapeutic benefits to patients with Tay-Sachs disease in future studies.Master Thesis Investigation of the Molecular and Genetic Response in Enterocytes of Duodenum During Elevated Intracellular Glucose Level(Izmir Institute of Technology, 2016) Boztepe, Tuğçe; Güleç, Şükrü; Seyrantepe, VolkanGlucose is one of the nutritional factor that involves in developing of obesity and type 2 diabetes in human. The studies indicated that enterocyte cells on intestine might play a role in dietary glucose sensing during obesity. Obese people are consumed high amount of dietary glucose and enterocyte cells consequently are exposed to high glucose. Thus, we aimed to find relevant physiological pathways and genome-wide mRNA expression profiles that can be regulated by glucose in fully differentiated human intestinal epithelial (CaCo-2). The cells were maintained two different glucose levels (5.5mM for control, 25mM for high glucose) at least three passages. The cells were grown on transwell system for 21 days to mimic human intestine system. Transepithelial electrical resistances (TEER) were measured to control monolayer formation and polarization. RNA isolation was performed and whole genome mRNA expression profile were determined following gene ontology analysis to find affected molecular pathways. Compared to control relative glucose level was found high in basolateral side of CaCo-2 cells that were under high glucose condition without effecting TEER. GLUT2, SGLT1, GLUT5 mRNA levels were significantly reduced during elevated glucose levels which is consistent with literature. Significant fold change analysis showed that 351 genes upregulated and 468 genes under high glucose condition. We found high glucose significantly leads changes of molecular pathways (downregulated; glycolysis and gluconeogenesis, adherens junction, fructose/mannose metabolism, pentose phosphate pathway and upregulated; protein export). These results provide us better understanding and open new window for glucose metabolism of enterocytes during obesity.Article Alterations in Secondary Lipids Are Associated with Neuroinflammation in the Brain of Neu1-Deficient Mice(Springer, 2026) Ada, Ebru; Seyrantepe, VolkanNeu1 (lysosomal sialidase 1) is essential for removing sialic acid from oligosaccharides and glycoconjugates. Neu1 deficiency impairs lysosomal digestion, leading to sialidosis and sialoglycoprotein accumulation. It also increases lipids, including gangliosides GM3, GD3, GM4, and LM1, in the kidney, liver, and spleen. Neu1-/- mice display symptoms resembling Type II sialidosis, including enlarged spleen and liver, kidney issues, neurological problems, spinal defects, and oligosaccharide buildup. The study examined secondary lipid alterations and inflammation in the cortex and cerebellum of these mice. Lipidomic, molecular, and immunohistochemical analyses of tissues from 2 and 5 M Neu1-/- mice revealed reduced levels of lipids, including PC, PE, PS, and CL, along with increased pro-inflammatory cytokines and loss of oligodendrocytes and neurons. Signs of astrogliosis and microgliosis emerged in specific brain regions. These results indicate that reduced levels of glycerophospholipids could serve as an indicator of inflammation in sialidosis mice. Future research should investigate therapies targeting these lipid changes, as modulating glycerophospholipids might slow disease progression in sialidosis patients.Article Citation - WoS: 2Citation - Scopus: 2Combined Treatment of Ketogenic Diet and Propagermanium Reduces Neuroinflammation in Tay-Sachs Disease Mouse Model(Springer/Plenum Publishers, 2025) Inci, Orhan Kerim; Seyrantepe, VolkanTay-Sachs disease is a rare lysosomal storage disorder caused by beta-Hexosaminidase A enzyme deficiency causing abnormal GM2 ganglioside accumulation in the central nervous system. GM2 accumulation triggers chronic neuroinflammation due to neurodegeneration-based astrogliosis and macrophage activity with the increased expression level of Ccl2 in the cortex of a recently generated Tay-Sachs disease mouse model Hexa-/-Neu3-/-. Propagermanium blocks the neuroinflammatory response induced by Ccl2, which is highly expressed in astrocytes and microglia. The ketogenic diet has broad potential usage in neurological disorders, but the knowledge of the impact on Tay-Sach disease is limited. This study aimed to display the effect of combining the ketogenic diet and propagermanium treatment on chronic neuroinflammation in the Tay-Sachs disease mouse model. Hexa-/-Neu3-/- mice were placed into the following groups: (i) standard diet, (ii) ketogenic diet, (iii) standard diet with propagermanium, and (iv) ketogenic diet with propagermanium. RT-PCR and immunohistochemistry analyzed neuroinflammation markers. Behavioral analyses were also applied to assess phenotypic improvement. Notably, the expression levels of neuroinflammation-related genes were reduced in the cortex of 140-day-old Hexa-/-Neu3-/- mice compared to beta-Hexosaminidase A deficient mice (Hexa-/-) after combined treatment. Immunohistochemical analysis displayed correlated results with the RT-PCR. Our data suggest the potential to implement combined treatment to reduce chronic inflammation in Tay-Sachs and other lysosomal storage diseases.Article A Comprehensive MicroRNA-Seq Transcriptomic Analysis of Tay-Sachs Disease Mice Revealed Distinct MiRNA Profiles in Neuroglial Cells(Springernature, 2025) Kaya, Beyza; Orhan, Mehmet Emin; Yanbul, Selman; Demirci, Muserref Duygu Sacar; Demir, Secil Akyildiz; Seyrantepe, VolkanTay-Sachs disease (TSD) is a rare lysosomal storage disorder marked by the progressive buildup of GM2 in the central nervous system (CNS). This condition arises from mutations in the HEXA gene, which encodes the alpha subunit of the enzyme beta-hexosaminidase A. A newly developed mouse model for early-onset TSD (Hexa-/-Neu3-/-) exhibited signs of neurodegeneration and neuroinflammation, evidenced by elevated levels of pro-inflammatory cytokines and chemokines, as well as significant astrogliosis and microgliosis. Identifying disease-specific microRNAs (miRNAs) may aid the development of targeted therapies. Although previous small-scale studies have investigated miRNA expression in some regions of GM2 gangliosidosis mouse models, thorough profiling of miRNAs in this innovative TSD model remains to be done. In this study, we employed next-generation sequencing to analyze the complete miRNA profile of neuroglial cells from Hexa-/-Neu3-/- mice. By comparing KEGG and Reactome pathways associated with neurodegeneration, neuroinflammation, and sphingolipid metabolism in Hexa-/-Neu3-/- neuroglial cells, we discovered new microRNAs and their targets related to the pathophysiology of GM2 gangliosidosis. For the first time, our findings showed that miR-708-5p, miR-672-5p, miR-204-5p, miR-335-5p, and miR-296-3p were upregulated, while miR-10 b-5p, miR-615-3p, miR-196a-5p, miR-214-5p, and miR-199a-5p were downregulated in Hexa-/-Neu3-/- neuroglial cells in comparison to age-matched wild-type (WT). These specific changes in miRNA expression deepen our understanding of the disease's neuropathological characteristics in Hexa-/-Neu3-/- mice. Our study suggests that miRNA-based therapeutic strategies may improve clinical outcomes for TSD patients.Master Thesis In Vitro Evaluation of Poly (2-((2 Amino) Ethyl Methacrylate) as a Potential Sirna Delivery Agent(Izmir Institute of Technology, 2015) Zelçak, Aykut; Seyrantepe, Volkan; Bulmuş Zareie, Volga; Bulmuş Zareie, Esma Volga; Seyrantepe, VolkanThe aim of this thesis is to investigate poly(2-((2-aminoethyl)amino)ethyl methacrylate) (P(AEAEMA)) as a potential siRNA carrier. For this purpose, an amine containing monomer 2-((tert-butoxycarbonyl) (2-((tert-butoxy carbonyl) amino) ethyl) amino) ethyl methacrylate (BocAEAEMA) was synthesized. Reversible addition-fragmentation chain transfer (RAFT) polymerization was performed to prepare homo- and block co-polymers of BocAEAEMA. The synthesized polymers -P(AEAEMA)19, P(AEAEMA)41 and P(PEGMA)12-b-P(AEAEMA)32- were characterized via NMR and GPC. The cytotoxicity of the polymers was investigated in vitro using ovarian cancer cell line (Skov-3-luc) via MTT assay. The polymers did not show any toxic effect on cells in 24 h. The ability of the BocAEAEMA polymers to form polyplexes with siRNA was investigated via gel electrophoresis. P(AEAEMA)19, P(AEAEMA)41 and P(PEGMA)12-b-P(AEAEMA)32 could efficiently form complexes with siRNA at an N/P ratio of 5, 2, and 2 respectively. Gel electrophoresis analysis revealed that P(AEAEMA)41 and P(PEGMA)12-b-P(AEAEMA)32 could protect siRNA against serum components at least for 6 h. Block copolymer, when complexed with siRNA at an N/P ratio of 10, could protect siRNA longer (24 h) when compared with the homopolymer. The size and surface charge of the polyplexes were investigated by DLS. The diameter of the P(AEAEMA)41-siRNA complexes was found to be lower than 110 nm at all N/P ratios tested. In contrast, P(PEGMA)12-b-P(AEAEMA)32-siRNA complexes (except the complex prepared at the N/P ratio of 2), displayed aggregation tendency. All polyplexes displayed positive zeta potential. The zeta potential of the homopolymer was found to be higher than the copolymer at the N/P ratio of 2. Finally, in order to determine siRNA transfection ability of the polymers, luciferase assay was optimized using a commercial transfection reagent lipofectamine RNAimax. The optimized assay conditions will be used in future studies to determine the transfection efficiency of the polymers.