explore | Grilled Cheese

@febsj.bsky.social Oct 15, 2026, 12:00 PM

🚀 Our Issue 20 is now online, packed with fascinating research from across the life sciences! From the effects of GLP-1 agonists and LRH-1 to the roles of Bip1 and Erd2 in ER stress, and new key players in the fungal bioluminescence pathway. Discover the full issue here ➡️ buff.ly/w2vS2ZJ
#GLP1 #AMPK

@lagaylife.bsky.social Oct 12, 2026, 4:43 PM

ICYMI: La caféine contenue dans le café active une enzyme clé, l’AMPK, responsable de réguler le stress cellulaire et le métabolisme, ce qui pourrait contribuer à ralentir le vieillissement et améliorer la santé globale. #Gaylife #Quoideneuf #ADN #AMPK #café

@virusesmdpi.bsky.social Oct 9, 2026, 1:58 AM

🦟 AMPK-Orchestrated Metabolic Reprogramming in Some #Flavivirus Infections

How #AMPK balances lipid metabolism, autophagy, mitochondrial dynamics, and innate immunity during #dengue, #Zika, WNV, JEV, and YFV infection — and its therapeutic potential.

🔗 www.mdpi.com/1999-4915/18...

@robertlufkinmd.bsky.social Oct 9, 2026, 1:45 AM

Full breakdown coming on the Health Longevity Secrets podcast www.youtube.com/@RobertLufkinMD

#MetabolicHealth #HealthLongevitySecrets #AgingResearch #AMPK (4/4)

@lagaylife.bsky.social Oct 2, 2026, 4:42 PM

La caféine contenue dans le café active une enzyme clé, l’AMPK, responsable de réguler le stress cellulaire et le métabolisme, ce qui pourrait contribuer à ralentir le vieillissement et améliorer la santé globale. #Gaylife #Quoideneuf #ADN #AMPK #café

@cochemelab.bsky.social Oct 2, 2026, 8:09 AM

Thanks #UKRI for featuring our research on #Ageing! We show that direct activation of the energy sensor #AMPK extends #Lifespan in multiple pre-clinical models. This strong evolutionary conservation highlights potential for future #Translation.

www.ukri.org/news/experts...

doi.org/10.1111/acel...

@donporque.bsky.social Oct 1, 2026, 9:49 AM

¿Cómo puede la enzima AMPK alargar un 25% la vida de varios animales? #Ciencia #Longevidad #Envejecimiento #AMPK #Salud #Investigación #Biotecnología #Genética #Medicina #Antienvejecimiento #VidaSaludable #felizjueves #1deoctubre

@alicefrolov.bsky.social Sep 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.

@sigtrans-sttt.bsky.social Sep 17, 2026, 12:45 PM

Age-related regenerative loss can compromise repair after liver injury.
Hepassocin activates #AMPK via ANXA2–ERK–p90RSK–LKB1 signaling, countering hepatic #Senescence and impaired #Autophagy while supporting regeneration in the aging liver.

#STTT #OpenAccess: doi.org/10.1038/s413...
#Inflammation