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To all annotated objects annotated to malate-aspartate shuttle. GOC:jl Comment None History See term history for GO:0043490 at QuickGO Subset None Related Link Metabolic pathways to adapt to nutrient and antigen availability.Accession GO:0043490 Name malate-aspartate shuttle Ontology biological_process Synonyms malate aspartate shuttle, malate/aspartate shuttle, malate:aspartate shuttle Alternate IDs None Definition The process of transferring reducing equivalents from the cytosol into the mitochondria NADH is used to synthesise malate in the cytosol this compound is then transported into the mitochondria where it is converted to oxaloacetate using NADH, the oxaloacetate reacts with gluamate to form aspartate, and the aspartate then returns to the cytosol to complete the cycle. These results present an example of how immune cells alter their GOT1 was shown to desensitize CD8+ TĬells to environmental nutrient limitation and persistent antigenic stimulation-induced loss of Summarized, the presented work revealed that persistent stimulation with tumor and viralĪntigens induced GOT1 expression on CD8+ T cells. Supports effector CD8+ T cells that are nutrient restricted and chronically stimulated. Oxygen species (ROS) production and decreased ΔΨm. Got1 deficiency reduced the NAD+/NADH ratio, increased reactive Instead, Got1 deficiency became onlyĬatastrophic for CD8+ T cells when extracellular nutrients were restricted, and antigenic ΔΨm when cells were cultured in complete medium. Responses required GOT1 in the presence of persistent, but not transient antigenic stimulation.įurther analysis revealed that Got1 deficiency alone did not affect CD8+ T cell metabolism or Responses, but not the memory T cell formation after viral clearance, suggesting that CD8+ Lymphocytic choriomeningitis virus (LCMV) Armstrong acute infection and the LCMV clone 13Ĭhronic infection model, we found that Got1 deficiency affected the ongoing antiviral effector Potential to sustain long term immune responses in a mouse melanoma model. Impaired tumor-specific effector CD8+ T cell accumulation, effector cytokine production and Tumor-infiltrating lymphocytes (TILs) from human colon cancer. Induced by persistent antigenic stimulation in mouse CD8+ T cells and upregulated in CD8+ GOT1 because it is a key enzyme of the MAS, and we observed that GOT1 expression was Glutamic oxaloacetic transaminase 1 (Got1, encoding the MAS enzyme GOT1). To test this hypothesis, we have generated a mouse model with T cell-specific deficiency of We, therefore, hypothesize that MAS may regulate ΔΨm Produces and transports electron carriers into the mitochondrial matrix and donates electrons Pump protons to establish a membrane potential. Mitochondrial complexes acceptĮlectrons from tricarboxylic acid (TCA) cycle-derived electron carriers, transfer electrons, and Regulates T cell exhaustion in chronic infection and cancer. Immunotherapies revive exhausted T cells, enhance effector cytokine production, and haveĪchieved clinical success in several types of cancers. Molecules, reduction in effector cytokine secretion, and alterations in cellular metabolism, suchĪs loss of mitochondrial membrane potential (ΔΨm). Exhausted T cells are characterized by the expression of immune checkpoint Observed that CD8+ T cells are functionally compromised or “exhausted” in chronic infectionsĪnd solid tumors. Citation of documents: Please do not cite the URL that is displayed in your browser location input, instead use the DOI, URN or the persistent URL below, as we can guarantee their long-time accessibility.ĬD8+ T cells play a crucial role in fighting infectious diseases and cancers, but it is frequently