Results suggest that it is the presence of rare syntenic SEC16A and MAMDC4 deletions that increases susceptibility to axial spondyloarthritis in family members who carry the HLA-B*27 allele.
growth factors modulate Sec16 protein levels and dynamics. Sec16 acts as part of a coherent feed-forward loop which integrates secretion and growth factor signaling.
Data show that knockdown of Sec16B but not Sec16A by RNAi affected the morphology of peroxisomes inhibited the transport of Pex16 from the ER to peroxisomes and suppressed expression of Pex3.
Results suggest that KIAA0310p a mammalian homologue of yeast Sec16 builds up endoplasmic reticulum (ER) exit sites in cooperation with p125 and plays a role in membrane traffic from the ER.
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