In Silico Bioinformatic Analysis of Glucose Transporter 1 (GLUT1/SLC2A1) Gene in Vitiligo
Emam, A., Gomaa, A., Tawfik, N., Abd El-Fadeal, N., Eyada, M. (2025). In Silico Bioinformatic Analysis of Glucose Transporter 1 (GLUT1/SLC2A1) Gene in Vitiligo. EKB Journal Management System, 28(7), 35-41. doi: 10.21608/scumj.2025.440935
Amira A.M. Emam; Amal H.A. Gomaa; Noha Z. Tawfik; Noha M. Abd El-Fadeal; Moustafa M. K. Eyada. "In Silico Bioinformatic Analysis of Glucose Transporter 1 (GLUT1/SLC2A1) Gene in Vitiligo". EKB Journal Management System, 28, 7, 2025, 35-41. doi: 10.21608/scumj.2025.440935
Emam, A., Gomaa, A., Tawfik, N., Abd El-Fadeal, N., Eyada, M. (2025). 'In Silico Bioinformatic Analysis of Glucose Transporter 1 (GLUT1/SLC2A1) Gene in Vitiligo', EKB Journal Management System, 28(7), pp. 35-41. doi: 10.21608/scumj.2025.440935
Emam, A., Gomaa, A., Tawfik, N., Abd El-Fadeal, N., Eyada, M. In Silico Bioinformatic Analysis of Glucose Transporter 1 (GLUT1/SLC2A1) Gene in Vitiligo. EKB Journal Management System, 2025; 28(7): 35-41. doi: 10.21608/scumj.2025.440935

In Silico Bioinformatic Analysis of Glucose Transporter 1 (GLUT1/SLC2A1) Gene in Vitiligo

Suez Canal University Medical Journal
Article 5, Volume 28, Issue 7, July 2025, Page 35-41  XML PDF (446.15 K)
Document Type: Original Article
DOI: 10.21608/scumj.2025.440935
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Authors
Amira A.M. Emam email orcid 1; Amal H.A. Gomaaorcid 1; Noha Z. Tawfikorcid 1; Noha M. Abd El-Fadeal2; Moustafa M. K. Eyadaorcid 3
1Department of Dermatology, Venereology and Andrology Faculty of Medicine, Suez Canal University, Ismailia, Egypt
2Department of Medical Biochemistry and Molecular Biology, Faculty of Medicine, Suez Canal University, Ismailia, Egypt Biochemistry Department, Ibn Sina National College for Medical Studies, Jeddah, Saudi Arabia.
31Department of Dermatology, Venereology and Andrology Faculty of Medicine, Suez Canal University, Ismailia, Egypt
Abstract
Background: Vitiligo is a common autoimmune dermatological disorder characterized by the progressive loss of pigmentation in the skin and/or mucosal surfaces. Recent advances in research have focused on elucidating the molecular mechanisms underlying vitiligo pathogenesis, with particular emphasis on epidermal–immune cell interactions, structural alterations in cutaneous cellular components, and dysregulation of immune cell metabolism. Glucose transporter 1 (GLUT1), a key mediator of cellular glucose uptake, has been increasingly recognized for its elevated expression in proinflammatory and autoimmune conditions. Notably, upregulation of GLUT1 has been documented in diseases such as rheumatoid arthritis, systemic lupus erythematosus, psoriasis, vitiligo and chronic spongiotic dermatitis, suggesting a potential role in the immunopathogenesis of these disorders. Methods: This study assesses the role of GLUT1 (encoded by SLC2A1) in vitiligo as an example of autoimmune skin disorders via in silico bioinformatic analysis, integrating gene expression, genetic polymorphisms, and inflammatory signaling correlations. Conclusion: Our findings highlight elevated GLUT1 expression in vitiligo regulatory impacts of pro-inflammatory cytokines on melanocyte, keratinocyte, fibroblast and immune cells GLUT1 expression, and the potential functional impact of intragenic SNPs on gene regulation, underscoring GLUT1 as a promising target for novel therapeutic interventions
Keywords
GLUT1; SLC2A1; Vitiligo; Bioinformatics
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