Andrew Wood
@andrewwood.bsky.social
110 followers 150 following 13 posts
Research Group Leader at the University of Edinburgh. Using genome editing and targeted protein degradation to study mechanisms underlying human disease and therapy.
Posts Media Videos Starter Packs
Reposted by Andrew Wood
mrcmousenetwork.bsky.social
On 14th November, we are once again holding our Network Science Day in York, which is an exciting opportunity for Network members and non-members to engage and develop new collaborations!

The meeting is free to attend. Find out more and register by emailing us at [email protected].
andrewwood.bsky.social
Our manuscript characterising tissue-specific consequences of tagged protein fusions in CRISPR-engineered mice is now online @PLOSGenetics. journals.plos.org/plosgenetics.... Thanks again to all coauthors, reviewers and editors for a smooth publication process. Brief summary below.
andrewwood.bsky.social
Has anyone else observed significant leaky (i.e. Tir1-dependent) degradation using the AID2 system? Genuinely curious to hear whether the hive mind views this as a problem.
andrewwood.bsky.social
Disclosure: I didn’t review the paper and don’t know who did, but we covered the preprint in a lab journal club last year and flagged several of the same points.
andrewwood.bsky.social
We really appreciated your contribution to this work, and for developing DEGRONOPEDIA which we use often 🙏
Reposted by Andrew Wood
bahome.bsky.social
Oliver Smithies was born 100 years ago today. Best known for gene targeting in mice, for which he shared the 2007 Nobel, he also developed starch gel electrophoresis in the 1950s. I met him once and remember him being very gracious and thoughtful.
#genetics #OTD

www.nobelprize.org/prizes/medic...
Oliver Smithies – Facts - NobelPrize.orgOpen the search menuClose the search menuOpen the search menuClose the search menuSubmit a search termBack To Top
www.nobelprize.org
andrewwood.bsky.social
We characterise two underlying mechanisms with opposing effects on protein stability and explain their tissue-specificity, providing a rational basis for improved experimental design. Congrats to 1st author Gillian Taylor and all who contributed. Feedback welcome!
andrewwood.bsky.social
By surveying a series of CRISPR-engineered mice, we found that tags often change protein expression in some tissues but have little effect, or even opposite effects, in others. Why?
andrewwood.bsky.social
Genetic tagging is a cornerstone of modern molecular biology, but it’s no secret that tag fusion often causes unwanted changes in protein expression and function. Understanding how this happens could help us to design more refined and effective models for preclinical research.
andrewwood.bsky.social
Pleased to share our latest work and the first manuscript from the Degron Tagging Cluster in the MRC National Mouse Genetics Network. If you work with protein tags, particularly in tissue biology models, this should be of interest:

www.biorxiv.org/content/10.1...
www.biorxiv.org
Reposted by Andrew Wood
Reposted by Andrew Wood
dereklowe.bsky.social
The first bifunctional protein degrader to deliver Phase III data! It seems to work, but people were definitely expecting more:
A Bifunctional Degrader Reads Out in Phase 3
www.science.org
Reposted by Andrew Wood
behnamnabet.bsky.social
🧪 Ready, set, degrade!

So proud to share our work in the @jclinical-invest.bsky.social, establishing a versatile approach for creating transgenic dTAG mice to degrade oncoproteins. We showcase that KRAS G12V degradation triggers antitumor immunity in lung cancer.

Link: www.jci.org/articles/vie...
Reposted by Andrew Wood
scientificdiscovery.dev
Americans are now one-third less likely to die from cancer at the same ages as Americans in 1990
How has the risk of dying from cancer changed in the United States?

To understand this, we can look at national cancer death rates in the United States.

The gray line shows the crude rate, which is the rate of deaths from cancer per 100,000 people. It has risen between 1950 and 1990 and has fallen slightly since then.

However, cancer death rates rise sharply with age, and the age of the US population has increased since 1950, so we would expect cancer death rates to rise for that reason alone.

What if we adjust for the increased age of the US population?

The red line, the age-standardized rate, shows this. It shows the cancer death rate if the age structure of the US population was held constant throughout.

This shows a slight rise until 1990 and then a significant decline; rates have fallen by one-third.

This means Americans are now one-third less likely to die from cancer at the same ages as Americans in 1990.

This comes from several factors: better screening and earlier diagnosis, medical advances in cancer treatments, and public health efforts to reduce risk factors like smoking and exposure to carcinogens.