See you next week for Kate LeBlanc’s defense!
Title: Nuclear speckle proteins modulate tau toxicity
Lab: Kraemer Lab, VA Puget Sound
When: Monday, February 23, 3:00 p.m. PDT
Where: UW Health Sciences Building, K069 Auditorium & Zoom (email mcb@uw.edu for link)

An amazing talk from Dr. Kejia Wu in David Bakers lab at the @uwproteindesign at this year’s HD therapeutics conference in Palm Springs about her amazing designed proteins that bind intrinsically disordered peptides, including poly glutamine, which she’s working to tune to be selective for long Q’s!

Please see a collective response from an esteemed group of leaders in the dementia field to the NYT article and book “doctored” by Charles Piller. www.nytimes.com/2025/01/24/o...

Alternative 3' UTR polyadenylation is disrupted in the rNLS8 mouse model of ALS/FTLD - PubMed Recent research has highlighted widespread dysregulation of alternative polyadenylation in amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration with TDP-43 pathology (FTLD-TDP). H...

TDP-43 proteinopathy also provokes transcriptomic changes consistent with TDP-43 loss of function. The latest side project from Randall Eck in my group: pubmed.ncbi.nlm.nih.gov/39810199/

Identification of TMEM106B amyloid fibrils provides an updated view of TMEM106B biology in health and disease - PubMed Since the initial identification of TMEM106B as a risk factor for frontotemporal lobar degeneration (FTLD), multiple genetic studies have found TMEM106B variants to modulate disease risk in a variety ...

Here's a nice review from Rosa Rademakers & Co if you want to learn more about human TMEM106b proteinopathies. pubmed.ncbi.nlm.nih.gov/36056242/

For those of you that haven't heard about it, TMEM106b is an important risk factor for a variety of neurodegenerative diseases. It was first shown as a risk factor for FTLD-TDP by Viviana VanDeerlin & Co more than a decade ago. More recently, it has been show to form fibrils in these diseases.

Identification of TMEM106B amyloid fibrils provides an updated view of TMEM106B biology in health and disease - PubMed Since the initial identification of TMEM106B as a risk factor for frontotemporal lobar degeneration (FTLD), multiple genetic studies have found TMEM106B variants to modulate disease risk in a variety ...

Here's the latest work from my group! We built a C. elegans model of human TMEM106b proteinopathy by expressing the human gene in neurons. TMEM106b is a new kid on the block in terms of aggregating proteins. Long story short, it can driven neurodegeneration. pubmed.ncbi.nlm.nih.gov/36056242/

Seattle waterfront in the evening

Love science and Seattle? Come be my colleague! We are recruiting a physician scientist to join the Seattle VA GRECC with a joint appointment at University of Washington. Apply here: apply.interfolio.com/155179. Please share widely - this is an open rank search at Assistant/ Associate/ Full levels