High impact information on Chst3

• A nearly complete removal of N-glycans of the recombinant C6ST-1 by peptide N-glycosidase F increased the C6ST activity but decreased the KSST activity [1].
• Treatment with tunicamycin of COS-7 cells transfected with C6ST-1 cDNA totally abolished production of the active C6ST-1 [1].
• Wild-type recombinant C6ST-1 showed a typical Golgi localization, whereas M-4 recombinant C6ST-1, in which the fourth N-glycosylation site was deleted, colocalized with calnexin, an endoplasmic reticulum-resident protein [1].
• Chondroitin 6-sulfotransferase (C6ST) catalyzes the transfer of sulfate to position 6 of the N-acetylgalactosamine residue of chondroitin [2].
• Despite the disappearance of chondroitin sulfate D structure, brain development was normal in the C6st(-/-) mice [2].

Biological context of Chst3

• Transfection and expression of the mouse cDNA in COS-7 cells yielded C6ST activity [3].
• All genes except GST0 (chondroitin 6-O-sulfotransferase) contain intron-less ORFs [4].

Anatomical context of Chst3

• Further analysis revealed that the number of CD62L(+)CD44(low) T lymphocytes corresponding to naive T lymphocytes in the spleen of 5-6-week-old C6st(-/-) mice was significantly decreased, whereas those in other secondary lymphoid organs were unchanged [2].

References