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Each element of the blood transport mechanism to the heart, when failing, sequentially causes blood stasis in the veins, the development of inflammation, damage to the endothelial layer lining the vessel, subsequently forming a thrombus that prevents blood transport to the heart

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This functional diversity is further exemplified by alternative splicing of SHMT2 gene, which generates two distinct isoforms: the canonical mitochondrial SHMT2 and a shorter variant, SHMT2, lacking the mitochondrial targeting sequence due to exon 1 exclusion

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[Abstract] J Exp Clin Cancer Res