procollagen lysyl hydroxylase 2 is essential for hypoxia-induced breast cancer metastasis. The enzyme is critical for fibrillary collagen formation by breast cancer cells, increases tumor stiffness, and is required for metastasis to lymph nodes and lungs
knockdown of GLT25D1 HEK cells modified for the stable expression of adiponectin (Adipo-HEK cell) as well as in Simpson Golabi-Behmel-Syndrome adipocytes (SGBS) causes a significant decrease in high-molecular-weight adiponectin in Adipo-HEK cells with no change in total adiponectin. Knockdown in the SGBS cells caused an increase in lipid accumulation yet inhibits adipogenesis. Adiponectin forms a protein complex with lysyl hydroxylase 3 and GLT25D1. The intracellular retention of lysyl hydroxylase 3 is dependent on GLT25D1
loss of GLT25D1 leads to increased expression and intracellular accumulation of collagen type I. Inactivation of the GLT25D1 gene results in a compensatory induction of isoform GLT25D2 expression. Loss of GLT25D1 decreases collagen glycosylation by up to 60% but does not alter collagen folding and thermal stability. Cells harboring individually inactivated GLT25D1 and GLT25D2 genes can be recovered and maintained in culture, cell clones with simultaneously inactive GLT25D1 and GLT25D2 genes cannot be grown
loss of GLT25D2 has no effect on collagen secretion. Inactivation of the GLT25D1 gene results in a compensatory induction of isoform GLT25D2 expression. Cells harboring individually inactivated GLT25D1 and GLT25D2 genes can be recovered and maintained in culture, cell clones with simultaneously inactive GLT25D1 and GLT25D2 genes cannot be grown
mice fed a standard chow or high-fat diet for 5 weeks show significantly decreased level of GLT25D1 which coincides with a decrease in high-molecular-weight adiponectin