Genome Maintenance in Cancer and Aging

Title Genome Maintenance in Cancer and Aging
Lecturer 野口 英史博士
Dr. Eishi Noguchi
Associate Professor
College of Medicine, Drexel University, USA
Language English
Date&Time 12/15/2017 (Fri) 15:00~16:00
Venue 大セミナー室

1.     Timelessタンパク質によるテロメア維持機構:Timelessがテロメア反復配列の複製を制御し、過度なDNA組換えを防ぐことによりテロメアを維持することがわかりました 。
2.     Maf1タンパク質によるゲノムの維持機構および老化防止機構: mTORの基質であるMaf1 タンパク質が、転写に依存したDNA損傷を防御することにより、寿命の延長に関わっていることを示しました。
3.     アルコールに依存したゲノムの不安定性:アルコールによるゲノム障害とその防御機構についての最近の研究成果を発表します。

Genomic instability is a hallmark of cancer and age-related diseases. Emerging evidence indicates that a variety of environmental factors and toxins damage DNA, leading to genomic instability; however, the mechanisms by which cells prevent and repair DNA damage are still elusive. Our long-term goal is to understand how cells maintain genomic integrity to regulate lifespan and avoid tumorigenesis.

1.    Role of the Timeless protein in telomere maintenance: Timeless is a component of the replication machinery and is involved in accurate genome duplication. We found that Timeless prevents repeat instability at telomeres. We show that Timeless functions as an anti-recombinase to maintain telomere length and integrity.

2.    Role of Maf1 in lifespan extension: It is widely known that mTOR regulates lifespan. However, its downstream effectors for lifespan regulation remain elusive. We provide evidence that Maf1 is a critical lifespan regulator downstream of the mTOR pathway. Our results suggest that Maf1-mediated transcriptional regulation prevents genomic instability to extend lifespan.

3.    Alcohol-induced DNA damage response: Acetaldehyde, the primary metabolite of alcohol, forms DNA adducts, resulting in genomic instability. We will discuss the role of acetaldehyde in preventing DNA replication process and dysregulating normal DNA damage response in esophageal keratinocytes.


Contact 細胞シグナル
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