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Gut pathogen Clostridium symbiosum rewires macrophage succinylation to drive enteric neuron loss in inflammatory bowel disease Zhao et al. identify an IBD-enriched gut pathogen, Clostridium symbiosum, that promotes enteric neuron loss and colitis. C. symbiosum-derived succinate rewires macrophage glycolytic metabolism to sustain IL-1β signaling, thereby activating neuronal NLRP3 inflammasomes and driving neuron loss. Targeting C. symbiosum with a phage-derived endolysin preserves enteric neurons and alleviates intestinal inflammation.

#WeekendRead! #EveryCellIsAnImmuneCell! #InflammasomePower! #ImmunometabolismPower! Zhao &co show @cp-cellhostmicrobe.bsky.social that a clostridium enriched in #IBD exacerbates colitis via boosting #glycolysis & IL1b by macrophages & activating NLRP3 in enteric #neurons, causing their loss!

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U01.01.097 Regulation by fructose-2,6- bisphosphate A comprehensive review of U01.01.097 Fructose-2,6-bisphosphate regulation. Understand the "Fed vs. Fasted" hormonal signaling, the phosphorylation state of the bifunctional enzyme, and why F-2,6-BP is the most potent stimulator of PFK-1.

🔄 The Master Toggle: Mastering Fructose-2,6-bisphosphate! 🔄
#USMLEStep1 #MedEd #Biochemistry #Metabolism #Glycolysis #Gluconeogenesis #PFK2 #Insulin #Glucagon #Step1Prep #HighYield #MedSchool #Endocrinology #Physiology #FutureDoctor #StudyGram #MedTwitter

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U01.01.096 Glycolysis regulation A deep dive into U01.01.096 Glycolysis Regulation. Learn how ATP, Citrate, and AMP modulate metabolic flux, the importance of the PFK-2/FBPase-2 complex, and the feed-forward activation of Pyruvate Kinase.

🚦 The Metabolic Gas Pedal: Mastering Glycolysis Regulation! 🚦
#USMLEStep1 #MedEd #Biochemistry #Metabolism #Glycolysis #PFK1 #Insulin #Glucagon #Step1Prep #HighYield #MedSchool #Endocrinology #Physiology #FutureDoctor #StudyGram #MedTwitter

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U01.01.095 Hexokinase vs glucokinase A definitive comparison of U01.01.095 Hexokinase vs. Glucokinase. Learn how these isoenzymes differ in their affinity for glucose, their response to Insulin, and their role in maintaining blood glucose homeostasis.

🧪 The First Step of Glycolysis: Hexokinase vs. Glucokinase! 🧪
#USMLEStep1 #MedEd #Biochemistry #Metabolism #Glycolysis #Hexokinase #Glucokinase #Step1Prep #HighYield #MedSchool #Endocrinology #Diabetes #FutureDoctor #StudyGram #MedTwitter

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U01.01.090 Rate-determining enzymes of metabolic processes A comprehensive review of U01.01.090 Metabolic Pathways. Identify the "bottleneck" enzymes of carbohydrate, lipid, and nucleotide metabolism and the allosteric effectors that control fuel storage versus mobilization.

🚦 The Metabolic Traffic Lights: Master the Rate-Limiting Steps! 🚦
#USMLEStep1 #MedEd #Biochemistry #Metabolism #Enzymes #Step1Prep #HighYield #MedSchool #Endocrinology #Glycolysis #LipidMetabolism #Statins #FutureDoctor #StudyGram

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TREM2-mediated Macrophage Glycolysis Promotes Skin Wound Angiogenesis via the Akt/mTOR/HIF-1α Signaling Axis

TREM2-mediated Macrophage Glycolysis Promotes Skin Wound Angiogenesis via the Akt/mTOR/HIF-1α Signaling Axis

This study finds that #TREM2#Macrophages drive # WoundRepair by linking #Glycolysis to #Angiogenesis via Akt/#mTOR/#HIF1α pathway, revealing #therapeutic targets for #TissueRegeneration. #medsky

Full article here: doi.org/10.1007/s115...
#WoundHealing #TherapeuticTargets #DrugDiscovery

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USP7-mediated deubiquitination and nuclear translocation of PFKM promotes brain tumor development by sensing fructose-2,6-bisphosphate. USP7 interacts with PFKM regulated by F-2,6-BP, resulting in the ubiquitination of PFKM K615 after GD treatment. Deubiquitinated PFKM translocates into nucleus and interacts with c-Myc. PFKM facilitates c-MYC binding to CPT1B promoter and promotes transcription of CPT1B, thereby enhancing FAO and cell survival.

USP7-mediated deubiquitination and nuclear translocation of PFKM promotes brain tumor development by sensing fructose-2,6-bisphosphate. USP7 interacts with PFKM regulated by F-2,6-BP, resulting in the ubiquitination of PFKM K615 after GD treatment. Deubiquitinated PFKM translocates into nucleus and interacts with c-Myc. PFKM facilitates c-MYC binding to CPT1B promoter and promotes transcription of CPT1B, thereby enhancing FAO and cell survival.

How does nutrient deficiency in the #tumor #microenvironment lead to metabolic reprogramming? This study reveals a mechanism for glioblastoma survival via switching from #glycolysis to #FattyAcid oxidation in mice, with implications for cancer medicine @plosbiology.org 🧪 plos.io/3P6pSg4

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A sugar-processing enzyme studied for 70 years has a hidden second function: the yeast Pfk2 subunit unwinds RNA and promotes translation of cell cycle mRNAs, independently of its catalytic glycolytic activity. www.surrey.ac.uk/news/sugar-p... #CellBiology #Glycolysis

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USP7-mediated deubiquitination and nuclear translocation of PFKM promotes brain tumor development by sensing fructose-2,6-bisphosphate. USP7 interacts with PFKM regulated by F-2,6-BP, resulting in the ubiquitination of PFKM K615 after GD treatment. Deubiquitinated PFKM translocates into nucleus and interacts with c-Myc. PFKM facilitates c-MYC binding to CPT1B promoter and promotes transcription of CPT1B, thereby enhancing FAO and cell survival.

USP7-mediated deubiquitination and nuclear translocation of PFKM promotes brain tumor development by sensing fructose-2,6-bisphosphate. USP7 interacts with PFKM regulated by F-2,6-BP, resulting in the ubiquitination of PFKM K615 after GD treatment. Deubiquitinated PFKM translocates into nucleus and interacts with c-Myc. PFKM facilitates c-MYC binding to CPT1B promoter and promotes transcription of CPT1B, thereby enhancing FAO and cell survival.

How does nutrient deficiency in the #tumor #microenvironment lead to metabolic reprogramming? This study reveals a mechanism for glioblastoma survival via switching from #glycolysis to #FattyAcid oxidation in mice, with implications for cancer medicine @plosbiology.org 🧪 plos.io/3P6pSg4

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USP7-mediated deubiquitination and nuclear translocation of PFKM promotes brain tumor development by sensing fructose-2,6-bisphosphate. USP7 interacts with PFKM regulated by F-2,6-BP, resulting in the ubiquitination of PFKM K615 after GD treatment. Deubiquitinated PFKM translocates into nucleus and interacts with c-Myc. PFKM facilitates c-MYC binding to CPT1B promoter and promotes transcription of CPT1B, thereby enhancing FAO and cell survival.

USP7-mediated deubiquitination and nuclear translocation of PFKM promotes brain tumor development by sensing fructose-2,6-bisphosphate. USP7 interacts with PFKM regulated by F-2,6-BP, resulting in the ubiquitination of PFKM K615 after GD treatment. Deubiquitinated PFKM translocates into nucleus and interacts with c-Myc. PFKM facilitates c-MYC binding to CPT1B promoter and promotes transcription of CPT1B, thereby enhancing FAO and cell survival.

How does nutrient deficiency in the #tumor #microenvironment lead to metabolic reprogramming? This study reveals a mechanism for glioblastoma survival via switching from #glycolysis to #FattyAcid oxidation in mice, with implications for cancer medicine @plosbiology.org 🧪 plos.io/3P6pSg4

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This review shows #glycometabolic reprogramming fuels #Osteosarcoma progression via #glycolysis, mitochondrial dysfunction & immune suppression, highlighting metabolic targeting as a promising strategy to overcome therapy resistance.

#OpenAccess: doi.org/10.1016/j.ge...

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Good Old Friends Stick Together

Good Old Friends Stick Together

Good Old Friends Stick Together

#Biology #Metabolism #Glycolysis #Krebscycle #Cellularrespiration

sciencehumor.io/biology-memes/good-old-f...

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Global Prevalence of Long COVID, Its Subtypes, and Risk Factors: An Updated Systematic Review and Meta-analysis Quantitative evidence shows a persistent prevalence of long COVID globally, with a significant burden of symptoms that last 1–2 years postinfection, unders

resulting in decreased mitochondrial function & an increased reliance on less efficient anaerobic metabolism ( #glycolysis) for energy, leading to extreme fatigue, weakness & pain.

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Dual SHP2/MEK inhibition remodels mitochondria and rewires #PDAC metabolism—reducing #glycolysis, altering #ROS and lipid peroxidase pathways, and creating a #ferroptosis vulnerability that could reinforce RAS-pathway inhibition.

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

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N6‐Methyladenosine Modification of circIST1 Promotes Hypoxia‐Inducible Factor α–mediated Glycolysis and Progression in Hepatocellular Carcinoma We identified first time a critical m6A modification of circIST1 on miR-140-3p/miR-182-HIF1α regulatory network involved in the HCC progression and tumor glycolysis, gaining mechanistic insights into...

#Article in #MedComm
This article identified first time a critical #m6A modification of #circIST1 on miR-140-3p/miR-182-HIF1α regulatory network involved in the #HCC progression and #tumor #glycolysis. doi.org/10.1002/mco2...

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ENO1 stimulates lactate & ATP production by regulating #Glycolysis, affecting #LactateHomeostasis & intracellular ATP pools, which modulate the AMPK/#mTOR & PI3K/AKT signaling, driving #GastricCancer stemness & progression.

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

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📰New & Featured | #Cell: #GPX4 released during #ferroptosis binds to dendritic #ZP3, activating cAMP-PPKA signaling
🔸Inhibits #glycolysis
🔸Impairs DC maturation and activation
🔸Eventually results in T cell priming defect
🧐Blocking GPX4-ZP3 interaction potentially drives #antitumor activity

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🧨 Role of #Glycolysis in #SARSCoV2 Induced Microglia Senescence
- ⏫️ in glycolysis in immune cells, incl monocytes & potentially microglia ➡️ induces mitochondrial dysfunction & ROS production, which stabilizes hypoxia-inducible factor-1α (HIF-1α) 🔑 regulator of #glycolysis

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#Medsky🧪 #IDsky #Neurosky #publichealth
#SARSCoV2 #nucleocapsid (N) protein induces microglia senescence
& associated cognitive impairment by causing mitochondrial dysfunction which forces a metabolic shift ➡️ #glycolysis. The glycolytic reprogramming triggers the activation of cellular senescence.

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In restrictive #cardiomyopathy mice with cTnI R193H mutation, early #DiastolicDysfunction features prolonged relaxation, enhanced #glycolysis, and PI3K/AKT‑driven #glucoseuptake, linking altered energy metabolism to #fibrosis and #HeartFailure.

#OpenAccess: doi.org/10.1016/j.ge...

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The latest and most detailed review on a fundamental biochemical pathway: #glycolysis
#microbiology #biochemistry
onlinelibrary.wiley.com/doi/full/10....

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Intracellular C. neoformans infection stimulates increased glycolytic activity in fetal liver-derived alveolar-like macrophages
Callison, E. N. et al.
Paper
Details
#Cryptococcus #Glycolysis #MacrophageImmunity

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New study shows agrimoniin may treat #HepatopulmonarySyndrome by activating #PGC1α to inhibit #Glycolysis and #Angiogenesis, pointing to a promising therapeutic strategy. #medsky

#OpenAccess: www.sciencedirect.com/science/arti...

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This review highlights recent advances in #EnergyMetabolism, detailing key pathways like #glycolysis, #OXPHOS, and #FAO, their dysregulation in diseases, and emerging strategies for precision treatment. #multiomics #CRISPR #medsky

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

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✨ In this week's DB unit seminar @embl.org, Hidenobu Miyazawa, a postdoc in the Aulehla group, shared insights on the role of glycolysis in mouse embryo axis segmentation #DevelopmentalBiology #Glycolysis #MouseEmbryos

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Presenting my poster at the 15th #Markesbery symposium organized by the Sanders-Brown Center on Aging and Alzheimer's Disease Research Center, UKy.

I decided to wearing my own poster themed on #glycolysis, one of the most prolific #metabolic pathways in the #brain.

@bauerhartzlab.bsky.social

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The early evolution of the glycolytic pathway from autotrophic origins to glycogen and back The evolution of enzymes involved in carbohydrate metabolism of bacteria and archaea reflect an origin of glycolysis from glycogen reserves accumulated thr

The early evolution of the glycolytic pathway from autotrophic origins to glycogen and back
#microbiology #biochemistry #evolution #Glycolysis
@femsmicro.org @femsjournals.bsky.social
academic.oup.com/femsre/artic...

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Seen on the white board in the fellows room. And I didn’t draw it. 🤗

#krebs #glycolysis @sgreenberggc.bsky.social

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AlphaFold model of the complex formed between HK2 and the SOX10 5′UTR (189–204 nts). The predicted RNA structure is shown in cyan, and HK2 protein is shown in green. HK2 residues and SOX10 mRNA nucleotides at the interaction interface are highlighted in red. Inset: schematic representation of the secondary structure of the SOX10 5′UTR (189–204 nts) predicted by Mfold, with the putative HK2-binding region (194–198 nts) marked in red.

AlphaFold model of the complex formed between HK2 and the SOX10 5′UTR (189–204 nts). The predicted RNA structure is shown in cyan, and HK2 protein is shown in green. HK2 residues and SOX10 mRNA nucleotides at the interaction interface are highlighted in red. Inset: schematic representation of the secondary structure of the SOX10 5′UTR (189–204 nts) predicted by Mfold, with the putative HK2-binding region (194–198 nts) marked in red.

‬‬Hexokinase 2 (HK2) is known for its metabolic role in #glycolysis. This study shows that it also functions as an #RNAbindingProtein that regulates mRNA translation, particularly of SOX10, promoting #melanoma cell proliferation independently of glycolysis @plosbiology.org 🧪 plos.io/3ViI1qL

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AlphaFold model of the complex formed between HK2 and the SOX10 5′UTR (189–204 nts). The predicted RNA structure is shown in cyan, and HK2 protein is shown in green. HK2 residues and SOX10 mRNA nucleotides at the interaction interface are highlighted in red. Inset: schematic representation of the secondary structure of the SOX10 5′UTR (189–204 nts) predicted by Mfold, with the putative HK2-binding region (194–198 nts) marked in red.

AlphaFold model of the complex formed between HK2 and the SOX10 5′UTR (189–204 nts). The predicted RNA structure is shown in cyan, and HK2 protein is shown in green. HK2 residues and SOX10 mRNA nucleotides at the interaction interface are highlighted in red. Inset: schematic representation of the secondary structure of the SOX10 5′UTR (189–204 nts) predicted by Mfold, with the putative HK2-binding region (194–198 nts) marked in red.

‬‬Hexokinase 2 (HK2) is known for its metabolic role in #glycolysis. This study shows that it also functions as an #RNAbindingProtein that regulates mRNA translation, particularly of SOX10, promoting #melanoma cell proliferation independently of glycolysis @plosbiology.org 🧪 plos.io/3ViI1qL

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