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MetabolomicsMyeloid PFKFB3-mediated glycolysis promotes kidney fibrosis
Excessive renal fibrosis is a common pathology in progressive chronic kidney diseases. Inflammatory injury and aberrant repair processes contribute to the development of kidney fibrosis. Myeloid cells, particularly monocytes/macrophages, play a crucial role in kidney fibrosis by releasing their proi...
2024-03-12 | MTBLS8278 | MetaboLights
UnknownImpacts of climate change on future air quality and human health in China.
Not available
S-EPMC6717307 | biostudies-literature
UnknownA new cytoplasmic interaction between junctin and ryanodine receptor Ca2+ release channels.
Not available
S-EPMC4342579 | biostudies-literature
UnknownMACF1 links Rapsyn to microtubule- and actin-binding proteins to maintain neuromuscular synapses.
Not available
S-EPMC6504910 | biostudies-literature
UnknownAn early HIV mutation within an HLA-B*57-restricted T cell epitope abrogates binding to the killer inhibitory receptor 3DL1.
Not available
S-EPMC3094954 | biostudies-literature
MetabolomicsPFKFB3-mediated glycolysis boosts fibroblast activation and subsequent kidney fibrosis

Renal fibrosis, a hallmark of chronic kidney diseases, is driven by the activation of renal fibroblasts. Recent studies have highlighted the role of glycolysis in this process. Nevertheless, one critical glycolytic activator, 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3), remain...

2024-03-12 | MTBLS8281 | MetaboLights
TranscriptomicsTranscription profiling of heart left ventricles from 15 week old inbred COP, DA, and F1(COP x DA) offspring with respect to aerobic running capacity (low, high, and intermediate performers respectively)
We used high density oligonucleotide arrays to measure the relative expression levels of ~27,000 probe sets in the left ventricles of inbred rat strains; DA (high performing), Copenhagen (COP, low performing), as well as F1(COPxDA) rats bred from these tw
ORGANISM(S): Rattus norvegicus 
2007-09-13 | E-GEOD-1795 | biostudies-arrayexpress
ProteomicsSirt2 inhibition reprograms T cell metabolism for optimal anti-tumor immunity: Sirt2 Interacting Proteins
Growing evidence indicates that metabolism is a key driver of T cell functions. A switch from oxidative phosphorylation to aerobic glycolysis is a hallmark of T cell activation and is required to meet metabolic demands of proliferation and effector functions. However, the mechanisms underlying the m...
ORGANISM(S): Mus musculus (Mouse) 
2020-06-15 | PXD012811 | Pride
T cell Sirtuin 2 Metabolism Interacting proteins Glycolysis 
ProteomicsSirt2 inhibition reprograms T cell metabolism for optimal anti-tumor immunity: Lysine Acetylation
Growing evidence indicates that metabolism is a key driver of T cell functions. A switch from oxidative phosphorylation to aerobic glycolysis is a hallmark of T cell activation and is required to meet metabolic demands of proliferation and effector functions. However, the mechanisms underlying the m...
ORGANISM(S): Mus musculus (Mouse) 
2020-06-15 | PXD012796 | Pride
T cell Sirtuin 2 Metabolism Acetylation Glycolysis 
ProteomicsSirt2 inhibition reprograms T cell metabolism for optimal anti-tumor immunity: Sirt2 Interacting Proteins 2
Growing evidence indicates that metabolism is a key driver of T cell functions. A switch from oxidative phosphorylation to aerobic glycolysis is a hallmark of T cell activation and is required to meet metabolic demands of proliferation and effector functions. However, the mechanisms underlying the m...
ORGANISM(S): Mus musculus (Mouse) 
2020-07-03 | PXD020150 | Pride
T cell Sirtuin 2 Metabolism Interacting proteins Glycolysis 
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