David Teis

🥳 congrats hesso and team - targeting the folded protein response kills multiple myeloma

Targeting proteostasis in multiple myeloma through inhibition of LTK Leukemia - Targeting proteostasis in multiple myeloma through inhibition of LTK

Our new paper is out in Leukemia on Targeting proteostasis in multiple myeloma through inhibition of LTK. Thanks to Ludvig and Thea for this great collaborative work
rdcu.be/evyfX

excellent PhD opportunity if you are interested in studying the cell biology of CART cell and AML interaction!! apply now ! also we work in a nice location in the heart of the alps

Our lab is hiring 1 PhD and 1 Postdoc to study the mechanism of lipid transport using computational methods (Molecular Dynamics, AI). Fully funded by @snsf-ch.bsky.social for 4 years, with amazing collaborators and excellent life and working conditions. Apply by email. Please share and repost!

Bryce Brownfield's review on the structural biology of Golgi trafficking has been published!
authors.elsevier.com/a/1kqrY3PA3s...

Bryce is now a postdoc in the @buzbarstow.bsky.social lab, we miss him dearly!

thank you - it’s an important paper!!

Any1 is a phospholipid scramblase involved in #endosome biogenesis, say Jieqiong Gao, Christian Ungermann and colleagues (Osnabrück University): rupress.org/jcb/article/...

#Membrane #lipid #Organelles #Biochemistry

An in vitro platform for the enzymatic characterization of the rhomboid protease RHBDL4 Rhomboid proteases are ubiquitous intramembrane serine proteases that can cleave transmembrane substrates within lipid bilayers. They exhibit many and…

Our work is finally published! We developed a robust in vitro platform to study a disease relevant membrane protease, notoriously difficult to isolate.This protease has linked to cancer & neurodegen,and our platform opens new doors for structural & drug discovery.
sciencedirect.com/science/arti...

Excited to see work led by @autophazeke.bsky.social, @minghaochen.bsky.social, Thanh Nguyen, and Ainara Claveras out in @science.org today, the culmination of a 15-year project to understand structurally how the synthesis of the critical lipid of autophagy, PI3P, is regulated. tinyurl.com/ywvjh8u4

the disciples of ERES

I am looking for a #PhD working on this exciting project! In case you are interested in how #immunometabolism and #macrophages affect #adipose tissue function, check the link below and apply! www.immunometabolism.at/job-openings/

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A unique postdoc position in academic drug discovery is open in the Hurley lab. We have a biochemistry-driven Parkinson’s disease drug discovery project funded and supported by SPARK-NS, which has an innovative model that turbocharges drug discovery in academic labs.
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PhDs in biochemistry, structural biology, pharmacology, or similar, located in the US and with strong publication track records and a high motivation to solve Parkinson's, please send CV directly to me at jimhurley@berkeley.edu.
Repost appreciated.

👍🥳👌

Excited to share our latest findings on how the phosphoinositide PI4P pool at the trans-Golgi network (TGN) is regulated through a SYS1-ARFRP1-ARL5-ARMH3-PI4KB pathway, in which ARMH3 (also known as C10orf76) acts as an ARL5 effector to activate PI4KB. rdcu.be/d1dZ2

TXNIP mediates LAT1/SLC7A5 endocytosis to reduce amino acid uptake in cells entering quiescence Entry and exit from quiescence require changes in cellular nutrient acquisition. How quiescent cells reduce nutrient uptake was unclear. Here, we demonstrate that cells entering quiescence select plas...

How do quiescent cells stop to eat? TXNIP mediates LAT1/SLC7A5 endocytosis to curb amino acid uptake and to meet low metabolic needs of cells entering quiescence. Defects can result in metabolic disease. biorxiv.org/content/10.1... by @Jenny12119
with @Hesso_F_Sci
@ThedieckLab

Welcome @teislab.bsky.social ;(