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Version devBuilt at: 2026-10-10 01:38:52 EDT

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@aj-smith.bsky.socialSep 30, 2026, 2:48 PM

Huge thanks to Patrick, Sean, Merima, and @pagliarini-lab.bsky.social, and to NIDDK, NIGMS and HHMI. Questions and critiques very welcome!

#mitochondria #phosphoproteomics

@alicefrolov.bsky.socialSep 24, 2026, 5:02 PM

New visualization: Rewiring of nutrient-sensing phospho-signaling across the murine lifespan

I am sharing a figure summarizing how phosphorylation status across the insulin/IGF1–AKT–mTORC1.

#MTORC1 #AMPK #Phosphoproteomics #InsulinSignaling #IGF1 #NutrientSensing #HepaticMetabolism

New visualization: Rewiring of nutrient-sensing phospho-signaling across the murine lifespan I am sharing a figure summarizing how phosphorylation status across the insulin/IGF1–AKT–mTORC1 and AMPK axes remodels with hepatic aging. The subtitle reads: "Relative phosphorylation of key nodes in the insulin/IGF1-AKT-mTORC1 and AMPK axes in liver, young vs old." I want to emphasize at the outset that the underlying data are simulated; the visualization is constructed to illustrate a literature-grounded trend rather than to report primary measurements. The chart is a phospho-signaling connected dot matrix: nodes are arranged on a pathway lattice with node-link edges tracing canonical directional relationships (receptor engagement, PI3K–PDK1–AKT propagation, TSC1/2 regulation of RHEB, mTORC1 substrate phosphorylation, and the AMPK inhibitory arm). Each node is segmented into paired young-versus-old glyphs, encoding relative phosphostoichiometry at defined residues (e.g., AKT pT308/pS473, TSC2 pT1462, mTOR pS2448, S6K1 pT389, 4E-BP1, AMPKα pT172, ACC pS79, ULK1 pS757). The depicted trend reflects a recurrent motif in the literature: attenuated proximal insulin/IGF1 input coupled with paradoxical sustained or elevated distal mTORC1 substrate phosphorylation in aged liver, alongside blunted AMPK pT172 responsiveness. The connected-dot topology is intended to make the directionality of this dysregulation legible, foregrounding node-specific decoupling between receptor-proximal signaling and downstream effector output rather than uniform pathway suppression. Edge weighting and glyph saturation encode effect magnitude, so viewers can distinguish nodes exhibiting the strongest young-old divergence from those that remain comparatively stable. I would welcome methodological critique on residue selection, the choice of lattice layout, and whether the segmented-node encoding adequately conveys stoichiometric versus occupancy interpretations.