Abstract
When a kinase inactive form of Protein Kinase D (PKD-K618N) was expressed in HeLa cells, it localized to the trans-Golgi network (TGN) and caused extensive tubulation. Cargo that was destined for the plasma membrane was found in PKD-K618N-containing tubes but the tubes did not detach from the TGN. As a result, the transfer of cargo from TGN to the plasma membrane was inhibited. We have also demonstrated the formation and subsequent detachment of cargo-containing tubes from the TGN in cells stably expressing low levels of PKD-K618N. Our results suggest that PKD regulates the fission from the TGN of transport carriers that are en route to the cell surface.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Biological Transport
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CD4 Antigens / metabolism
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Cell Line
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Cell Membrane / enzymology*
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Cell Membrane / metabolism
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Clathrin / metabolism
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Coatomer Protein / metabolism
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Dose-Response Relationship, Drug
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Endoplasmic Reticulum / metabolism
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Endosomes / metabolism
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Fluorescent Antibody Technique
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Glutathione Transferase / metabolism
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Glycoproteins*
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HeLa Cells
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Humans
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Membrane Glycoproteins / metabolism
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Membrane Proteins*
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Phosphorylation
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Precipitin Tests
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Protein Kinase C / genetics
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Protein Kinase C / physiology*
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Protein Transport
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Recombinant Proteins / metabolism
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Temperature
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Time Factors
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Transfection
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Viral Envelope Proteins / metabolism
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trans-Golgi Network / metabolism*
Substances
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CD4 Antigens
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Clathrin
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Coatomer Protein
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G protein, vesicular stomatitis virus
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Glycoproteins
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Membrane Glycoproteins
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Membrane Proteins
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Recombinant Proteins
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TGOLN2 protein, human
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Viral Envelope Proteins
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Glutathione Transferase
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protein kinase D
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Protein Kinase C