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Faculty Detail    
Name ZSUZSANNA BEBOK
M.D.		  
Campus Address MCLM 360 Zip 0005
Phone  (205) 975-5449
E-mail  bebok@uab.edu
Other websites
     

Education
Medical School  University of Pecs, Medical School    1984  M.D. 
Residency  University of Pecs, Medical School and Haynal Imre University of Health Sciences, Budapest    1988  Pathologist and Histopathologist 

Certifications
Pathology and Histopathology  1988 


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Associate Professor
Center  Comprehensive Diabetes Center  Comprehensive Diabetes Center Associate Professor
Center  Cystic Fibrosis Research Center  Cystic Fibrosis Research Center Associate Professor
Center  GL Ctr for Craniofacial, Oral, & Dental Disorders  GL Ctr for Craniofacial, Oral, & Dental Disorders Associate Professor
Center  General Clinical Research Center  Nephrology Research & Training Center Associate Professor

Graduate Biomedical Sciences Affiliations
Cell, Molecular, & Developmental Biology 
Genetics, Genomics and Bioinformatics 
Medical Scientist Training Program 
Pathobiology and Molecular Medicine 

Biographical Sketch 
Dr Bebok completed her medical degree and a residency program in Pathology and Histopathology at the University Medical School of Pecs, Hungary. As a student and later as faculty member, she worked under the guidance of Dr. Peter Nemeth at the Department of Immunology at the University Medical School of Pecs, Hungary. In 1993, she started a postdoctoral fellowship at the Department of Physiology, University of Alabama at Birmingham under the mentorship of Dr. Eric Sorscher. As junior faculty at the Department of Medicine at UAB, and associate scientist of the Cystic Fibrosis Research Center, she worked on the cellular and molecular mechanisms underlying cystic fibrosis. She joined the Department of Cell Biology in 2002. Dr. Bebok's research concentrates on cellular and molecular mechanisms by which cellular stress responses contribute to the development of human disorders. In addition to research, she has a passion for teaching and mentoring students. Dr. Bebok has decades of experience teaching at UAB. She lectured and directed courses in the Schools of Medicine, Dentistry, Optometry and Health Professions. She serves as co-director of the UAB General Biomedical Sciences (GBS), Genetics, Genomics and Bioinformatics (GGB) PhD Theme since 2016. At the national level she serves on Scientific Review Panels for the National Institute of Health.



Research/Clinical Interest
Title
Molecular mechanisms by which cellular stress responses such as the unfolded protein response (UPR) contribute to the pathology of human disorders.
Description
Our earlier studies concentrated on 1) cellular mechanisms that reduce endoplasmic reticulum (ER) protein load during the unfolded protein response (UPR) to alleviate ER stress and 2) how mutations and single nucleotide polymorphism affect mRNA structure and co-translational protein folding. ER stress and activation of the UPR contribute to the pathogenesis of a wide range of human disorders including cystic fibrosis, chronic obstructive pulmonary diseases (COPD), diabetes mellitus, and chronic kidney disorders. Thus, understanding the molecular pathways of cellular stress responses will provide important clues for the development of molecular therapies. Our second project investigated how synonymous mutations such as single nucleotide polymorphisms (SNPs) affect mRNA structure, co-translational protein folding and consequently protein function. We have demonstrated that one synonymous change in the CFTR gene alters mRNA structure and affects translation. Our recent studies concentrate on the mechanisms by which cellular stress responses are communicated between cells in different tissues and how they contribute to disease pathogenesis.

Selected Publications 
Publication PUBMEDID
Targets for cystic fibrosis therapy: proteomic analysis and correction of mutant cystic fibrosis transmembrane conductance regulator.  20653506 
A synonymous codon change alters the drug sensitivity of F508-del cystic fibrosis transmembrane conductance regulator.  26336913  
Limited ATF4 Expression in Degenerating Retinas with Ongoing ER Stress Promotes Photoreceptor Survival in a Mouse Model of Autosomal Dominant Retinitis Pigmentosa.  27144303 
Mechanistic Approaches to Improve Correction of the Most Common Disease-Causing Mutation in Cystic Fibrosis.  27214033 
miR-200b downregulates CFTR during hypoxia in human lung epithelial cells.  29167681 
Influenza virus M2 targets cystic fibrosis transmembrane conductance regulator for lysosomal degradation during viral infection.  25795456 
The silent codon change I507-ATC->ATT contributes to the severity of the F508-del CFTR channel dysfunction.  23907436 
Influenza virus M2 targets cystic fibrosis transmembrane conductance regulator for lysosomal degradation during viral infection.  25795456 
A synonymous single nucleotide polymorphism in F508-del CFTR alters the secondary structure of the mRNA and the expression of the mutant protein.   20628052 
The unfolded protein response (UPR)-activated transcription factor XBP1 induces micro-RNA-346 expression that Targets the human antigen peptide transporter 1 (TAP1) mRNA and governs immune regulatory genes.   22002058 
Methods to Study Membrane Protein Expression Regulation by the Unfolded Protein Response. Methods in Enzymology, UPR and Cellular Stress.   21329791 
Activation of the unfolded protein response by F508-del CFTR.   18458236 
The mechanism of CFTR transcriptional repression during the unfolded protein response.   18319256 
Endoplasmic reticulum stress and the unfolded protein response regulate genomic cystic fibrosis transmembrane conductance regulator expression.   16987996 
Decoding mechanisms by which silent codon changes influence protein biogenesis and function.  25817479 
 

Keywords
membrane proteins, ER stress, UPR, SNP, mutation, CFTR, micro-RNA