‘Damage-eating’ protein fixes DNA harmed by aging

A toolkit of proteins that can repair breaks in strands of DNA has been discovered by scientists at the Universities of Sheffield and Oxford.

DNA can become broken and damaged through the effects of aging, but also by diseases such as motor neurone disease or interventions such as chemotherapy.

Longevity.Technology: Finding ways to repair breaks in, and damage to, DNA strands has eluded researchers, but by exploiting the voracious appetite of a certain protein, scientists on the path to a therapy that could mitigate age-related damage. 

The protein, called TEX264, works in conjunction with other enzymes, to recognise and ‘eat’ toxic proteins. These adhere to the strand of DNA, causing them to become damaged and cause aging on a cellular level. We like the idea of using nanotechnology as a non-invasive targeted delivery mechanism.


“Failure to fix DNA breaks in our genome can impact our ability to enjoy a healthy life at an old age …”


 

Professor Sherif El-Khamisy, Co-Founder and Deputy Director of the Healthy Lifespan Institute at the University of Sheffield, said: “Failure to fix DNA breaks in our genome can impact our ability to enjoy a healthy life at an old age, as well as leave us vulnerable to neurological diseases like motor neurone disease (MND).

We hope that by understanding how our cells fix DNA breaks, we can help meet some of these challenges, as well as explore new ways of treating cancer in the future [1].”

The research team will now look to research the protein TEX264 further, testing to discover if its behaviour and properties are altered in aging, or in diseases such as MND. The discovery has cancer therapy implications too, as chemotherapy is often as damaging as it is effective, and finding an alternative treatment for cancer would mitigate the dangers, improve survival rates: providing a less onerous and more reasonable way to tackle cancer.

Study co-leader Professor Kristijan Ramadan, of the University of Oxford, said: “Our finding of TEX264, a protein that forms the specialised machinery to digest toxic proteins from our DNA, significantly changes the current understanding of how cells repair the genome and so protect us from accelerated ageing, cancer and neurodegeneration.

“I believe this discovery has a great potential for cancer therapy in the future and we are already pursuing our research in this direction [2].”

[1] https://bit.ly/2IUY6h1
[2] Ibid

Image credit: lisichik from Pixabay
Eleanor Garth
Staff Writer and Community Manager Now a science and medicine journalist, Eleanor worked as a consultant for university spin-out companies and provided research support at Imperial College London and various London hospitals in a former life.

Latest articles

Evidence for tenth hallmark of aging increases with new paper

Is ten the new nine? Additional research adds weight to the argument that extracellular matrix stiffening should be considered the tenth hallmark of aging. Since...

Help us help you: Longevity biotech survey

A new survey on translational processes and hurdles to clinical trials in Longevity biotech. We're working with two MDs: Oliver Zolman and Jian Fransen, on...

First Longevity announces first investors for current round

Some news of our own: European VC fund and a Longevity innovator participate in the First Longevity funding round. Last week we announced that Tom...

GDF15 protects from age‐related metabolic phenotypes

A recent study shows an important role for GDF15 in preventing aging-induced metabolic phenotypes by modulating systemic inflammatory responses in humans and mice. Dysfunction of...