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T., Bertelsen, M
We propose a model wherein SYK upregulation serves as a compensatory mechanism that bolsters SC metabolic capacity, fulfilling a dual role: (1) it promotes SC survival by maintaining bioenergetic homeostasis and mitigating mitochondrial damage under stress, thereby preventing glial apoptosis
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1,2 It is coabsorbed with intrinsic factor, a product of the stomach's parietal cells, in the terminal ileum after being extracted by gastric acid 1,2 (Figure 1 3 )
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