These data suggest that decreased B3GALT4 and GM1 expression can increase cell vulnerability to potentially toxic stressors and that such mechanisms may contribute to dopaminergic neurodegeneration in PD.
These data show that residual neuromelanin-containing neurons in the PD SN have decreased expression of the ganglioside biosynthetic genes B3GALT4 and ST3GAL2, consistent with previous reports of decreased levels of gangliosides GM1, GD1a, GD1b and GT1b in the PD SN.
Reduced levels of brain gangliosides GD1a, GD1b, GT1b and to a lesser extent GM1 have been found in substantia nigra (SN) from Parkinson's disease (PD) patients, along with decreased gene expression for key enzymes (B3Galt4, St3gal2) involved in synthesis of these gangliosides.
The present study revealed that the transcription level of β3GalT4 in patients with breast cancer was decreased compared with healthy control subjects.
The present study revealed that the transcription level of β3GalT4 in patients with breast cancer was decreased compared with healthy control subjects.
Inactivating mutations in the GALT-II gene (B3GALT6) associated with Ehlers-Danlos syndrome cause proteoglycan maturation defects similar to FAM20B deletion.
Inactivating mutations in the GALT-II gene (B3GALT6) associated with Ehlers-Danlos syndrome cause proteoglycan maturation defects similar to FAM20B deletion.