Brian Kraemer
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brianckraemer.bsky.social
Brian Kraemer
@brianckraemer.bsky.social
Father
Husband
Dementia Neuroscientist, Classical Geneticist
Outdoor Enthusiast
Opinions are my own.
https://kraemerlab.uw.edu/
Pinned
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/
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 ...
pubmed.ncbi.nlm.nih.gov
Reposted by Brian Kraemer
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!
March 1, 2025 at 5:39 PM
Reposted by Brian Kraemer
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...
February 8, 2025 at 5:55 PM
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/
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...
pubmed.ncbi.nlm.nih.gov
January 18, 2025 at 6:26 AM
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/
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 ...
pubmed.ncbi.nlm.nih.gov
January 2, 2025 at 8:58 PM
Reposted by Brian Kraemer
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
October 3, 2024 at 2:47 AM