Benjamin Parker

Research group of @Ben_Leo_Parker @UniMelb as we lost access to previous account. We love metabolic proteomics and signal transduction.

[Benjamin Parker @BenParkerLab]

Massive effort from @duttmri and thanks to @UniMelbCMR @MattWattUnimelb @garrondodd @GordonSLynch @WEHI_research and many others!

[Benjamin Parker @BenParkerLab]

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

[Benjamin Parker @BenParkerLab]

Thanks for all the support!

[Centre for Muscle Research @UniMelbCMR]

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

[Benjamin Parker @BenParkerLab]

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

[Benjamin Parker @BenParkerLab]

An amazing opportunity with such a cool team!

[A/Prof Garron Dodd @garrondodd]

🚨 Join Our Team! 🚨
We’re on the hunt for a brilliant postdoctoral researcher with a passion for neuroscience or metabolic disease. This is your chance to work at the intersection of academia & industry, driving innovation in obesity & T2D research. 🌟
https://t.co/LEMjq38lLx

[Benjamin Parker @BenParkerLab]

Thanks for the leadership @MattWattUnimelb! Couldn’t have done it without you.

[Matthew Watt @MattWattUnimelb]

Thrilled that the metabolism theme in Dept of Anatomy & Physiology were awarded NHMRC and ARC grants in #obesity #MASLD, #fibrosis and #aging. Go ⁦@garrondodd⁩ ⁦@Ben_Leo_Parker⁩ ⁦@MagdaMontg64866⁩ ⁦⁦@MattWattUnimelb⁩ 🎉💯🙂 ⁦@UniMelbMDHS⁩

[Benjamin Parker @BenParkerLab]

@UniMelbCMR @JustinHardeePhD @UF @UFMyology @UniMelbMDHS @UniMelb You’ll be missed @JustinHardeePhD but good luck in the new position!

[Benjamin Parker @BenParkerLab]

@DrAJRose Beautiful work as always @DrAJRose and team.

[Benjamin Parker @BenParkerLab]

@MattWattUnimelb @UniMelbMDHS It was the best retreat I’ve ever attended!

[Benjamin Parker @BenParkerLab]

@ucdmrt Sorry, meant to say Cysteine not Lysine! That makes complete sense.

[PMV @PMV_Australia]

Abstract submissions are closing in a few weeks! Register now for the free WEHI Proteomics Symposium co-hosted by PMV.
https://t.co/pZocX2DaKn

[Benjamin Parker @BenParkerLab]

@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

[Benjamin Parker @BenParkerLab]

@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!

[Benjamin Parker @BenParkerLab]

@NgoShyuan @UQ_News @AIBNatUQ @UQMedicine Thanks Shu!

[Benjamin Parker @BenParkerLab]

A big thanks to @UniMelbMDHS and @CellSignal for supporting this research, and several collaborators @UniMelbCMR @JamesMc2327 @CraigAGoodman1 @OchDr @NgoShyuan and many others!

[Benjamin Parker @BenParkerLab]

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

[Benjamin Parker @BenParkerLab]

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