Walid Fakhouri
Associate Professor
The University of Texas Health Science Center at Houston
School of Dentistry
Department of Diagnostic and Biomedical Sciences
Dr. Fakhouri’s research focuses on elucidating the molecular and genetic mechanisms that regulate craniofacial tissue development and facial symmetry, with the goal of understanding how genetic alterations lead to craniofacial birth defects, including cleft lip and palate, facial clefts, and jaw asymmetry. His laboratory integrates mouse genetics, organ and cell based models, advanced molecular technologies, and multi omics approaches to dissect the pathways governing normal craniofacial formation and the etiology of associated disorders. A major focus of his group is the transcription factor TWIST1 and the role of its post-translational modifications, particularly phosphorylation and acetylation, in modulating epithelial to mesenchymal transition, cell migration, tissue patterning, and the establishment of facial symmetry during development. His lab investigates how disruption of these regulatory processes contributes to orofacial clefts and asymmetrical jaw formation. In parallel, the lab employs experimental datasets and bioinformatic pipelines to develop computational models that identify etiologic non-coding DNA variants implicated in cancer, including head and neck squamous cell carcinoma and breast cancer. The overarching goal of Dr. Fakhouri’s research program is to translate fundamental bench discoveries into clinical applications, improving risk assessment and advancing precision medicine. Potential rotation project: Title of the Project: Computational modeling of allelic imbalance in cis-overlapping binding motifs of P53 and bHLH family members in cancer 10-week rotation project for a graduate student: Goal: Decode the genome-wide competitive binding profile of P53 and bHLH family members at cis-overlapping binding motifs (CisOMs) and their role on transcriptional regulation of target genes in three different cancer cell lines. Establish three cancer cell line cultures and confirm the expression of P53, P63, P73, cMYC, TWIST1, and HIF-1a by western blot in Human colorectal carcinoma (HCT116), human epithelial beast cancer MCF7 and Human Burkitt lymphoma cells (Raji; CCL-86). Perform genomic ChIP for P53 and cMYC in HCT116, MCF7 and CCL-86 cells and send the samples for Next-Generation sequencing to determine the genomic binding profile (ChIP-seq) for P53 and cMYC. Validate the ChIP-seq library using ChIPqPCR for detecting the binding of these transcription factors to well-known target genes. Participate in analyzing the ChIP-seq data, if available, for each TF in all 3 cancer cell lines. Learn how to identify co-occupied regions and CisOMs and corresponding target genes using transcripts written in Python software. The students will get help from the lab members who wrote the transcripts in Python.
Education & Training
PhD, University of Hohenheim, 2002