Karl Riabowol

Professor

Biochemistry & Molecular Biology

Hon BSc, PhD


Contact information

Phone

Office: 403-220-8695

Web presence

PubMed

ACHRI

Location

Office : HMRB 388

Preferred method of communication

ADMIN ASSISTANT

Benedicta Odame-Ankrah

Email: b.odameankrah@ucalgary.ca

Office: 403-220-3029


Research and teaching

Area of Focus

  • Epigenetics and telomere dynamics in cancer and aging

Summary of Research

Our laboratory studies mechanisms that are critical for enforcing the state of cellular senescence in normal human cells, to determine how these mechanisms are eluded during the process of cancer cell immortalization.  We examine the roles of tumour suppressors, telomeres and transcription factors in these processes. Several years ago we discovered a novel tumour suppressor we called ING1 for INhibitor of Growth that is intimately involved in cell aging, the Hutchinson-Gilford progeria syndrome (HGPS) form of childhood accelerated aging, and cell immortalization leading to cancer. The ING genes encode a family of proteins that contain plant homeodomains (PHDs) that interact specifically with epigenetic histone marks and a LID domain that interacts with nuclear lamin proteins that when mutated, cause HGPS. These proteins also regulate apoptosis through their ability to transduce phospholipid-mediated stress signals resulting from DNA damage and to affect the DNA repair process. The ING proteins act as epigenetic regulators through their targeting of histone acetyltransferase (HAT) and histone deacetylase (HDAC) complexes that regulate chromatin structure and gene expression. Our ongoing research program focuses upon determining how we can regulate the normal activity of these tumour suppressors to block the growth of cancer cells and to extend the replicative lifespan of normal cells through epigenetic modification.  We also hope to help define how mutation of the lamin A gene and its association with ING proteins causes HGPS accelerated aging in children. Work in our laboratory also includes examination of telomere biology and the role of replicative senescence in aging and age-related diseases, focusing upon aspects of chromatin remodelling and functions of the ING family of type II tumour suppressors. We are also establishing a new and powerful canine model for studying cell and organismal aging in which telomere length very strongly correlates to breed lifespan.


Biography

Dr. Riabowol is a full tenured Professor at the University of Calgary where he heads the Aging and Immortalization Laboratory within the Robson DNA Sciences Centre. Following training at Simon Fraser University, the University of Southern California, University of Arkansas for Medical Sciences and Cold Spring Harbor Laboratory, he held a staff position at Cold Spring Harbor Lab before joining the Cancer Biology Research Group at the University of Calgary in 1991. He served two terms as the Head of the Cancer Biology Group in the University of Calgary's Faculty of Medicine and as Vice Director of the Southern Alberta Cancer Research Institute. 

His group discovered the first member of the INhibitor of Growth (ING) family of epigenetic regulators and they remain at the forefront of ING research, examining their roles in growth control, cancer, aging and stem cell maintenance. He has published over 125 papers and numerous chapters and reviews, as well as 10 patents dealing with cell cycle regulation and the ING family. His work has been recognized by numerous awards including the Leukemia Society of America's Special Fellowship, The President's Award for Creative Activity Excellence, The Noble Foundation Award for Research and most recently the Killam Annual Professor Award for Excellence in Research, Teaching and Service. 

His laboratory provided the first definitive evidence for the inheiritance of telomere length through the male germ line and has provided some of the strongest evidence to date for the contribution of telomere length to lifespan. His group continues to focus on understanding the links between cancer and aging, particularly regarding how telomere dynamics and epigenetic remodelling may contribute to this relationship.