Utz Herbig, Ph.D.
Human somatic cells do not have the ability to proliferate indefinitely. Instead, these cells arrest irreversibly by a process called replicative senescence after undergoing 60-80 cell divisions. Already over 50 years ago, it was speculated that this limited replicative potential served one major purpose: to limit uncontrolled cellular proliferation of cancer cells. It was also proposed that this potential tumor suppressing mechanism would ultimately prevent somatic cells from regenerating our tissues and thereby contribute to aging of humans. These predictions, however, remained untested for decades as the molecular trigger of replicative senescence was unknown. Over the past years, work in our laboratory has revealed that the molecular trigger of replicative senescence is telomere dysfunction (Figure 1), provided evidence that Telomere Dysfunction-Induced Senescence (TDIS) promotes aging, and demonstrated that TDIS indeed suppresses cancer growth in humans. More recently, we discovered another unexpected role for TDIS: that of promoting tissue repair during wound healing. Current research in the laboratory focuses of exploring the causes for telomere erosion, telomere attrition, and telomere dysfunction in addition to characterizing the contributions of TDIS to tumor suppression, aging, and wound healing in humans.
1999 Ph.D. in Molecular Biology, Vanderbilt University, Nashville, TN
1995 Hauptdiplom (Masters of Science) in Chemistry/Biochemistry, Ludwig Maximilians University, Munich, Germany
2013-present Associate Professor, Microbiology, Biochemistry & Molecular Genetics, Rutgers Biomedical and Health Sciences, Rutgers, The State University of New Jersey
2006-2013 Assistant Professor, Microbiology & Molecular Genetics, University of Medicine and Dentistry of New Jersey (UMDNJ)
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