File:Model of L-proline-mediated differentiation of mESCs to EPL cells mouse embryo.png

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Description FIGURE 9. Model of L-proline-mediated differentiation of mESCs to EPL cells. L-Pro enters the cell via the SNAT2 transporter (Tan et al., 2011) where it (A) acts on various signaling pathways including the amino acidsensing signaling mTOR pathway, ERK and P38 pathways to induce differentiation (Lonic, 2007; Washington et al., 2010; Tan et al., 2016). (B) L-Pro is metabolized to pyrroline-5-carboxylate (P5C) by proline oxidase (POX) via the proline cycle in the mitochondria. P5C can then be converted to glutamate (Glu) by P5C dehydrogenase (P5CD). Glu is further converted to alpha-ketoglutarate, which enters the TCA cycle with subsequent production of ATP via oxidative phosphorylation (OxPhos). Glu can also be converted to L-Pro via the sequential actions of P5C synthase (P5CS) and P5C reductase (P5CR). This conversion produces NADP+, which is required to stimulate the pentose phosphate pathway (PPP) in the cytoplasm of the cell (Pandhare et al., 2009; Phang et al., 2010). The PPP is required to generate the ribose components needed for DNA and RNA synthesis and is coupled with aerobic glycolysis to generate ATP in highly proliferative cells such as ESCs and cancer cells (Liu et al., 2015). Stimulation of the PPP and glycolysis in the presence of L-Pro (Liu et al., 2015) may stimulate the differentiation of mESCs to EPL cells and support the increased proliferation rates observed in EPL cells. (C) When mESCs are starved of L-Pro, the amino acid response (AAR) pathway is activated to control L-Pro production and uptake into the cell. Free prolyl-tRNA (i.e., not loaded with L-Pro) binds to General Control Non-Depressible-2 (Gcn2) kinase which phosphorylates Eukaryotic Initiation Factor-2 (eIF2), resulting in Activating Transcription Factor-4 (Atf4) regulating the expression of genes involved in L-Pro transport and metabolism. The net result of this autoregulatory loop is self-limiting concentrations of L-Pro resulting in mESC self-renewal (D’Aniello et al., 2015). When L-Pro is added exogenously, this pathway is overwhelmed triggering differentiation.
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Source https://www.researchgate.net/publication/334407321_Modeling_Mammalian_Commitment_to_the_Neural_Lineage_Using_Embryos_and_Embryonic_Stem_CellsModeling_Mammalian_Commitment_to_the_Neural_Lineage_Using_Embryos_and_Embryonic_Stem_Cells Modeling Mammalian Commitment to the Neural Lineage Using Embryos and Embryonic Stem Cells. July 2019. Frontiers in Physiology 10 DOI:10.3389/fphys.2019.00705
Author Rachel A. Shparberg, Hannah J. Glover, Michael B. Morris
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current20:57, 30 April 2024Thumbnail for version as of 20:57, 30 April 2024988 × 1,040 (263 KB)Rasbak (talk | contribs){{Information |description=FIGURE 9. Model of L-proline-mediated differentiation of mESCs to EPL cells. L-Pro enters the cell via the SNAT2 transporter (Tan et al., 2011) where it (A) acts on various signaling pathways including the amino acidsensing signaling mTOR pathway, ERK and P38 pathways to induce differentiation (Lonic, 2007; Washington et al., 2010; Tan et al., 2016). (B) L-Pro is metabolized to pyrroline-5-carboxylate (P5C) by proline oxidase (POX) via the proline cycle in the mitoc...

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