@barakrotblat
You're twisting my melon man Opinions will change over time PI Ben-Gurion University of the Negev barakrotblat.wixsite.com/rotblatlab Conferences can be like this https://youtu.be/n8S13FQ8g0o?si=6wzd0DvkaMUQMAdp
cute as hell
yesturday i learned that you can get a structure of a SAMLL protein, eg lysosime, using cryo EM
if only there were a reparsitory for validated ABs
Some use LLM to craft a better grant, this does not necessarily mean they write faster but rather better.
for sure there will be those who use it to write faster and submit more. the system will have to learn to adjust.
i hope it wont lead to giving even more money to big labs/institutes
Shiran and Linor helped with the RNAseq experiments.
Tal and Shatha, and Moshe helped with the in vivo experiments.
Funding by ISF and WWC
This is a collaborative work, Hila Ben-David and Shani Gabbay run most of the experiments.
Our friends at the lab of Anat Ben-Zvi, Sufa and Evalina did the worm experiments.
Albert, Ifat, Nili, Loron and Yariv did the metabolomics analysis.
Shimon and Noga helped with the in vitro folding assays.
If HSP60 and 10 mainly function together to fold the same set of proteins, we expect the pattern to be similar between the KO worms. This is not the case, supporting that HSP60 and 10 evolved divergent functions
We used C elegans engineered in a way that cells experiencing unfolded protein stress in the mitochondria express GFP. We crossed HSP10 KO and HSP60 KO worms with the UPRmito worms.
The gut light up in the HSP60 KO worms and the mussels in the HSP10 KO worms
When we knock down HSPD1 or HSPE1 and measure how cells respond to this using RNAseq and metabolomics, we found little overlap between the conditions. This agrees well with the two having divergent functions.
But what about a whole organism you ask?
We wondered, perhaps our model was right and HSPD1 and HSPE1 have divergent functions.
We tested whether HSPD1/E1 folds MTHFD2 directly using recombinant proteins. One of our controls surprised us, HSPD1 could fold MTHFD2 without HSPE1! This was also true in cells.
We found that HSPD1 (human HSP60) is essential for the folding of MTHFD2, an important cancer protein that plays an essential role in the one-carbon pathway.
Previously, we used ecological network analysis and cancer data to construct a mito chaperone-client network that predicts the clients of mito chaperones.
One surprising prediction was that HSP60 and HSP10 cluster with different clients.
Here we challenged our model using wet-lab experiments.
During and following import, these proteins interact with chaperones, pulling them in and helping them fold.
There are 15 chaperones (including co-chaperones and proteases) in the mitochondria that fold >1,000 proteins, and it is not well known which chaperones fold which proteins
The problem is that most mitochondrial proteins are encoded in the nuclear genome, synthesized in the cytosol, and imported into the mitochondria in a linear manner through small channels. Fun fact, mito can’t have big holes because it needs to maintain a gradient potential.
For example, transcription factors known to drive metabolic changes, eg, HIF1A, MYC, p53, and NRF2, do so by changing the expression of metabolic enzymes.
Cell state is determined by its metabolic profile.
Eukaryotic cells change state by changing the expression of metabolic enzymes in the cytosol and mitochondria.
Just published is BioRxiv!!🔥
Is protein folding a limiting factor in metabolic reprogramming? And do HSP60-HSP10 (mitochondrial GroEL-Gro-ES) always work together?
www.biorxiv.org/content/10.6...
"I much rather read your broken English than your ai slop"
open.spotify.com/episode/0aM6...
What is the appropriate age to open a LinkedIn account for my kids?*
* im running for Father of the year award
when we were in our undergrad studies, my friend, Ari Robinson, and I had an idea, the origin of life must have started in temp where you get higher order in water but not freezing. 30 years later the experiments show this could be true 👇
spotted near our department
MYC 3' utr is essential for myc-dependent tumor cells
how cool is that!👇
fun fact: protein biosynthesis is by far the largest consumer of energy during cellular proliferation
Good Sunday, all! Here is the curated weekly collection of papers in #cancermetabolism and #mitochondrialbiology. Don't miss it; find it here: biomed.news/bims-camemi/... Biomed News #keepreading
"It's very simple to be happy. But it's very difficult to be simple." - Rabindranath Tagore
Job alert! Assistant professor position in the Department of Molecular Genetics (University of Toronto). Amazing department and city. jobs.utoronto.ca/job/Toronto-... Please share.
Polyamine-dependent metabolic shielding regulates alternative splicing
www.nature.com/articles/s41...
yeh well most of the data is pre 2023 so whatever that means🤷♂️
ai pre 2022 = road accidents pre cars
