Our research delves into how ING proteins modulate chromatin remodeling and gene expression, serving as pivotal epigenetic regulators in cellular aging and cancer.
We study the dynamics of telomeres and their critical role in cellular aging, using models to unravel their impact on cell longevity and cancer.
Our research focuses on understanding how epigenetic modifications control gene expression and contribute to cancer development. We explore the complex interplay between chromatin remodeling proteins and their impact on tumor suppressor genes and oncogenes.
HATs are crucial enzymes that acetylate lysine residues on histone proteins, leading to a relaxed chromatin structure and increased gene transcription. In cancer, aberrant activity of HATs can lead to the overexpression of oncogenes. Our studies aim to understand these mechanisms to potentially target HATs in cancer therapy.
Conversely, HDACs remove acetyl groups from histone tails, resulting in a condensed chromatin state and decreased gene expression. Dysregulation of HDAC activity is common in various cancers, leading to the silencing of tumor suppressor genes. We investigate HDAC inhibitors as a therapeutic strategy to reactivate these suppressed genes.
The ING family of proteins, which we were first to identify, are crucial in regulating cell growth, senescence, and apoptosis, contributing significantly to cancer suppression. These proteins interact with both HATs and HDACs, positioning them as key players in epigenetic regulation.
ING proteins function as readers of the histone code, interacting with histone marks through their PHD domains to modulate chromatin structure and gene expression. This regulation is crucial for maintaining genomic stability and responding to DNA damage, pivotal in aging and cancer.
By targeting the regulatory activities of ING proteins, particularly their interactions with epigenetic modifiers, we explore innovative approaches to cancer treatment that disrupt pathological gene regulation patterns.
Our research delves into the role of telomeres in cellular aging and longevity. Telomeres are repetitive nucleotide sequences at the ends of chromosomes that protect them from deterioration or fusion with neighboring chromosomes. Over time, due to repeated cell divisions, telomeres shorten, leading to cellular senescence or apoptosis when they reach a critical length.
We study how differing telomere lengths affect various cellular pathways and contribute to the aging process. Our research utilizes advanced models to explore the dynamics of telomeres, aiming to understand their critical role in cellular aging and the onset of age-related diseases.
Telomere dynamics also play a significant role in cancer development. Shortened telomeres can lead to genomic instability, promoting tumorigenesis. By unraveling the complex relationships between telomere length, cellular pathways, and cancer, we aim to advance the understanding of cancer biology.
© 2024 Riabowol Lab
An Aging & Cancer Research Lab based at the University of Calgary
Arnie Charbonneau Cancer Institute
3280 Hospital Dr NW
Calgary, AB T2N 4Z6
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