Bio
Dr. Mona Abdelrahman Mohamed Khaier is a dedicated researcher and academic from Sudan, currently affiliated with the College of Veterinary Medicine at the University of Bahri, where she serves as Head of the Department of Molecular Biology and Bioinformatics. She earned her PhD in Genetics and Molecular Biology from the University of Khartoum in 2002, specializing in molecular parasitology and bioinformatics. With a career spanning over two decades, Dr. Khaier has made significant contributions to computational biology, particularly through her work on non-synonymous single nucleotide polymorphisms (nsSNPs) in the HGD gene, as demonstrated in her prominent paper published in a Global Journal. She has published 27 scientific works, accumulating 28 citations, with an h-index of 3 and an i10-index of 0. Her research integrates molecular biology, bioinformatics, and population genetics to address health and disease challenges. Dr. Khaier is also an active peer reviewer for several international journals and holds ORCID ID 0000-0001-9260-3105 and an OpenAlex author profile (A5055730649). Her expertise and leadership continue to influence the next generation of scientists in Sudan and beyond.
Educational Journey
University of Khartoum
PhD in genetics and molecular biology • Zoology department
2002University of Bahri
University of Bahri, College of Veterinary Medicine, Department of Molecular Biology and Bioinformatics
Experience
Head of the department
2018 - 2024 • Molecular Biology and BioinformaticsAffiliations
University of Bahri
university board member, faculty board research member
Member since 2018Research
Computational Analysis of Possibly Pathogenic Non-Synonymous Single Nucleotide Polymorphisms Variants in HGD Gene
Alkaptonuria (AKU) is an autosomal recessive disorder caused by mutations in the homogentisate-1,2-dioxygenase (HGD) gene leading to the deï¬ciency of HGD enzyme activity. The aim of this study was to use some computational bioinformatics tools to predict the most pathogenic non- synonymous mutations in the HGD gene. The data was retrieved from the SNPs database of the National Center for Biotechnology Information (dbSNPs) (Oct. 2021). The primary sequence of the protein was obtained from the UniProt database (Oct. 2021). The pathogenic effect on the protein structure and function was predicted by GeneMANIA, SIFT, Provean, Polyphen-2, I-Mutant, and Project Hope software. The human HGD gene comprises a total of 423SNPs out of that 348 were found to be synonymous, 75 were missense SNPs (nsSNPs). Analysis of the nsSNPs by SIFT predicts 35 as deleterious and 40 as tolerated ones. Using Provean only 30 were deleterious while 5 SNPs were neutral. Taking the deleterious nsSNPSs to Polyphen-2, 25 nsSNPs were damaging (22 were probably damaging and 3 2 were possibly damaging), while 5 were benign. Using SNPs&GO 11 nsSNPs were predicted as disease-related while 14 were predicted to be neutral. Project Hope analysis the mutations according to their size, charge, hydrophobicity, and conservancy. In conclusion, 7 of the predicted mutations were not reported before according to the ClinVar database while the remaining 4 were reported from patients through DNA sequencing. More research is needed to confirm these new mutations in patients.
