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VPS39 encodes a protein that may promote clustering and fusion of late endosomes and lysosomes. Additionally we are shipping VPS39 Antibodies (29) and and many more products for this protein.
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The present study provides the first phenotypic description of a lack of vam6 gene function in a multicellular organism.
our data indicate that TRAP1 and VPS39 are nonredundant and essentially required for early embryonic development
although only TBC1D15/Rab7-GAP altered Rab7-GTP levels, both Rab7-GAP and mVps39 regulate lysosomal morphology and play a role in maintaining growth factor dependence
Antibodies to VAMP and SNAP inhibited sperm-zona pellucida interaction, suggesting their possible involvement in sperm membrane vesiculation.
TLP expression contributes to hypertrophic scar formation and contraction.
TLP likely acts as a molecular modulator capable of altering the balance of Smad3- and Smad2-dependent signaling through regulation of phosphorylation, thus facilitating collagen synthesis in fibroblasts.
Vps39 knockdown impairs late endosome fusion and fusion between late endosomes and lysosomes.
Merkel cell polyomavirus large T antigen disrupts lysosome clustering by translocating human Vam6p from the cytoplasm to the nucleus
propose that TLP might regulate the balance of Smad2 and Smad3 signaling by localizing Smad4 intracellularly, thus contributing to cellular specificity of TGF-beta transcriptional responses in both normal and pathophysiology
This gene encodes a protein that may promote clustering and fusion of late endosomes and lysosomes. The protein may also act as an adaptor protein that modulates the transforming growth factor-beta response by coupling the transforming growth factor-beta receptor complex to the Smad pathway.
, vacuolar protein sorting 39 homolog (S. cerevisiae)
, vesicle fusion protein
, vacuolar protein sorting 39
, TRAP1-like protein