Our #phosphoproteomics analysis of insulin signaling in bone uncovered a new mechanism of transcriptional activation via S6K phosphorylation of AFF4. It appears to play a role in regulating the expression of genes in ageing and insulin resistance. https://t.co/CRp54OJniL
Congrats to the CMR's @duttmri, @Ben_Leo_Parker and Team for their new Nature Comms paper "Phosphoproteomics of aged insulin-resistant bone identifies P70S6K phosphorylation of AFF4 as a gene-specific transcriptional regulator"
@UniMelbMDHS @UniMelb
https://t.co/8GZAtsEikL
Protein:protein interactions are dynamic so how do we quantify and discover changes in native tissues? Our new study uses qXL-MS and PCP-MS to study dynamic remodeling of interactions following skeletal muscle insulin resistance. https://t.co/jz7Vr5Ep6S #myotwitter#proteomics
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https://t.co/LEMjq38lLx
@funtoshs@ItsBiniR@UCDProteomics @ProteomicsNews Ah, I see. Maybe you could simply dimethylate a lysate and use this to preclear? Simple protocol here (obviously just using ‘light’ for your application) https://t.co/ejkiIh7S2z
@brettcollins100@igordownunder@arc_gov_au More than crazy. A complete disregard of academics in general. Grant outcomes on Xmas eve, shifting dates, changing rules, modifying eligibility, cutting sections or adding new ones to make the most complicated applications in the world, the list goes on….It’s an absolute mess!
UFMylation is a ubiquitin like modification of UFM1 applied to substrate lysine residues. <15 substrates have been identified (a nice summary: https://t.co/DNQ9nSLP7f). RPL26 has been most extensively characterised and suggested to be the major substrate: https://t.co/DppOMtRP4f
Why do we care? Because we have previously shown that UFC1 levels are negatively correlated with lean mass in various mouse strains, and knockdown of UFC1/UFMylation can increase muscle function. Maybe myosin UFMylation is a key link?
https://t.co/ufhku18mk7