Klemens J Hertel

picture of Klemens J Hertel

Professor, Microbiology & Molecular Genetics
School of Medicine

Associate Dean for Graduate Studies and Postdoctoral Affairs
School of Medicine

Vice Chair, Microbiology & Molecular Genetics
School of Medicine

B.A., Colorado College
PH.D., University of Colorado, Boulder

Phone: (949) 824-2127
Fax: (949) 824-8598
Email: khertel@uci.edu

University of California, Irvine
B233 Med Sci I
Mail Code: 4025
Irvine, CA 92697
Research Interests
Alternative pre-mRNA splicing, regulation of gene expression, splicing regulation, bioinformatics, deep sequencing, Spinal Muscular Atrophy, human genetic disease, molecular therapy, stem cells, colon cancer
Research Abstract
With the completion of the human genome project, it has become clear that the sheer number of genes cannot account for the complexity of the human proteome. Among several proposed mechanisms, alternative pre-mRNA splicing is considered to be one of the most efficient and widespread avenues to generate multiple protein isoforms from individual genes. Current estimates indicate that over 90% of all human genes undergo alternative splicing, thus greatly increasing the coding potential of our genome. In addition, defects in splicing have been linked with a variety of human genetic diseases. Understanding the basic mechanisms of pre-mRNA splicing and splice site recognition is therefore fundamental to understanding the expression of genes and human diseases.

Research in the Hertel laboratory focuses on elucidating the mechanisms of splice site selection with the long-term goal to generate a splicing code that permits alternative splicing predictions based on sequence analysis. We are taking a number of biochemical and computational approaches (1) to determine the mechanisms whereby the binding location of splicing regulatory proteins positively or negatively influence exon recognition, (2) to derive methods to determine if single nucleotide changes elicit differences in exon selection and inclusion, and (3) to test the hypothesis that aberrant expression of splicing regulators trigger cancer-specific alternative splicing.

Our long-term goals are to use the knowledge of splice-site recognition mechanisms to classify intronic and exonic mutations, thus paving the way for the design of therapeutic approaches to combat splicing-associated disease.
A current list of publications can be found in PubMed
Research in the Hertel laboratory is supported by grants from the National Institute of Health and UC Cancer Research Coordinating Committee
Professional Societies
RNA Society
International Society for Computational Biology
Graduate Programs
Cellular and Molecular Biosciences

Mathematical and Computational Biology

Research Center
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