Eric Green

Physician-scientist-entrepreneur. Biotech CEO/CSO. Genetics, biotech, birds (mostly raptors), books.

[Jeremy Leipzig @jermdemo]

OK, so the $ bio ai assistants are:

Ascent Bio - https://t.co/r9XxxvizqF
Bio Protocol BIOS - https://t.co/ZlU7ueQgzT
Edison Scientific - https://t.co/qioORKVhhG
K-Dense - https://t.co/06tuwxhbsA
Potato - https://t.co/I4mcR5vhPL
SciSpace - https://t.co/4jD6wq5ufn

Did I miss any?

[FrattaLab @FrattaLab]

We find TDP-43 loss to cause presynaptic defects, which are rescued by ASOs correcting a single cryptic exon in UNC13A.
Surprising effect of just one cryptic exon and promising strategy for ALS!
Matt Keuss @PeteHarley95 in great collaboration with @jbneuro
https://t.co/zEOUW0kkJb

[Eric Green @ercgrn]

Beautiful work from Pietro Fratta, Juan Burrone groups linking TDP-43 to synaptic function with UNC13A as key mediator. Combined with human genetics, strengthens case for UNC13A as promising target for patients with ALS.

[bioRxiv @biorxivpreprint]

Loss of TDP-43 induces synaptic dysfunction that is rescued by UNC13A splice-switching ASOs https://t.co/cpRV1phU08 #bioRxiv

[Eric Green @ercgrn]

Nice example of integrating human genetics, functional genomics and protein structure to understand disease biology. Congrats @artwuster @karls_es and team.

[Art Wuster @artwuster]

There are haploinsufficiencies that are caused almost entirely by missense variants instead of truncating mutations. Those genes are more vulnerable to missense variants disrupting their function, and SLC6A1 is an example. Here's our paper: https://t.co/0IUqkHLeP3

[Eric Green @ercgrn]

Fascinating NYTimes article on quest to understand causes of Kawasaki https://t.co/SzQNjxRuHJ

[Michael Baym @baym]

If there was only one scientific practice I could teach to every scientist regardless of stage or field I think it would be: look at the data. Spot check it. Find a few data points and trace them through to see if they make sense. Look at the raw data. Don't just do analyses.

[Eric Green @ercgrn]

@RCSunlab @MazeInBiotech Great working with you over the past few years and watching metabolomics technology mature in front of our eyes.

[Eric Green @ercgrn]

@TravisHinson @ScienceTM Thanks @TravisHinson - enjoyed your new study on CRISPRa for TTN as well!

[Eric Green @ercgrn]

Now out in @ScienceTM

A novel small molecule approach to treat patients with Pompe disease (who have impaired glycogen breakdown) by blocking the production of glycogen.

https://t.co/S1oWrdJIS3

1/x

[Eric Green @ercgrn]

Complements exciting phase 1 clinical data showing gys1 inhibition reduces glycogen in muscle and peripheral blood in healthy volunteers and supports advancing to patients.

https://t.co/YMhfXlVItl

3/3

[Eric Green @ercgrn]

We show that inhibiting glycogen synthase (SRT) reduces glycogen accumulation and corrects muscle metabolism in a mouse model of Pompe, as monotherapy or combined with enzyme replacement (ERT).

2/3

[Daniel J Drucker @DanielJDrucker]

Here, substrate reduction therapy with GYS1 inhibition may be a promising therapeutic approach for Pompe disease and other glycogen storage diseases @ScienceTM https://t.co/vUe1Nw8V9U

[JASN_News @JASN_News]

A variant of APOL1, p.N264K, is associated with reduced risk of CKD and ESKD among carriers of APOL1 high risk variants to levels comparable to individuals with APOL1 low-risk genotypes https://t.co/QQP2rm571I

@DrFlashHeart @MichaelEMatheny @KSusztak @Eddiesiew2 @CassyRCohen

[Eric Green @ercgrn]

Initial data on our small molecule APOL1 pore inhibitor shared at @ASNKidney 2022 with exciting updates to come at Kidney Week 2023.

We expect to enter the clinic this year.

[Eric Green @ercgrn]

New pub from our team @MazeInBiotech with VA MVP demonstrating key piece of our approach:

human genetics -> mechanism -> medicine

See great thread below from @DrFlashHeart

[Caitlyn Vlasschaert @DrFlashHeart]

Sharing exciting new work led by Adriana Hung, Alex Bick (@AlexBickMDPhD) and Eric Green (@ercgrn):

Genetic inhibition of APOL1 Pore Forming Function Prevents APOL1-Mediated Kidney Disease

A brief 🧵:

https://t.co/JyN6HPFhNa

[Eric Green @ercgrn]

Study ids and functionalizes a renal protective variant in APOL1, implicating ion conductance as pathologic mechanism for APOL1 kidney dz.

This mechanism has been further validated by @VertexPharma POC study of APOL1 pore inhibitor in FSGS @NEJM.

[Sek Kathiresan MD @skathire]

A mutation in APOL1 that protects against kidney disease.

How does it work? Seems to reduce APOL1 pore function

Cool new work integrating human genetics with cellular APOL1 function.

👏@alexbickmdphd @ercgrn @MazeInBiotech

https://t.co/NAO8BQy5Y9

[Eric Green @ercgrn]

@skathire @MazeInBiotech @sanofi Thanks @skathire. Exciting to continue building on genetic foundations to develop medicines for rare and common disease.

[Eric Green @ercgrn]

@Dr_RajatGupta Thanks @Dr_RajatGupta ! A nice example of how we can integrate rare disease genetics (validated role of GYS1 in humans) with biobank analyses (to understand safety of modulation) to support drug discovery.

[Sasha Gusev @SashaGusevPosts]

A 🧵 on some of my intuitions/priors about the genetics of complex and molecular traits in humans (i.e. what I think of as typical), largely motivated by GWAS/QTL studies over the past decade [citing papers with nice figures where possible]