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How does the loss of aldolase b gene expression impact cell growth or productivity in mammalian cells?? 


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The loss of aldolase B (ALDOB) gene expression in mammalian cells has significant implications on cell growth and productivity. Studies have shown that ALDOB downregulation is associated with aggressive characteristics in hepatocellular carcinoma (HCC), while high ALDOB expression in human islets is linked to lower insulin secretion. Furthermore, ALDOB overexpression in colon adenocarcinoma cells induces the functional loss of DNA mismatch repair (MMR) proteins, leading to irreversible DNA damage and apoptosis. In HCC, the suppression of ALDOB promotes tumorigenesis by enhancing glucose-6-phosphate dehydrogenase (G6PD) activity and pentose phosphate pathway metabolism. Therefore, the loss of ALDOB gene expression can impair DNA repair mechanisms, alter metabolic pathways, and impact insulin secretion, ultimately influencing cell growth and productivity in mammalian cells.

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Loss of Aldolase B (ALDOB) gene expression in hepatocellular carcinoma cells leads to increased aggressiveness, reduced cell migration, and inhibition of metastasis through upregulation of Ten-Eleven Translocation 1 (TET1).
Loss of aldolase B gene expression prevents high glucose-induced methylglyoxal overproduction, AGE formation, oxidative stress, and cellular dysfunction in endothelial cells, indicating a crucial role in maintaining cellular function.
High aldolase B expression in colon adenocarcinoma induces DNA mismatch repair impairment and apoptosis, rather than affecting proliferation, by disrupting EZH2-Rad51 expression and causing ERK inactivation.

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