A metalloprotease-disintegrin, MDC9/meltrin-gamma/ADAM9 and PKCdelta are involved in TPA-induced ectodomain shedding of membrane-anchored heparin-binding EGF-like growth factor.

The ectodomains of many proteins located at the cell surface are shed upon cell stimulation. One such protein is the heparin-binding EGF-like growth factor (HB-EGF) that exists in a membrane-anchored form which is converted to a soluble form upon cell stimulation with TPA, an activator of protein kinase C (PKC). ...
We show that PKCdelta binds in vivo and in vitro to the cytoplasmic domain of MDC9/meltrin-gamma/ADAM9, a member of the metalloprotease-disintegrin family. Furthermore, the presence of constitutively active PKCdelta or MDC9 results in the shedding of the ectodomain of proHB-EGF, whereas MDC9 mutants lacking the metalloprotease domain, as well as kinase-negative PKCdelta, suppress the TPA-induced shedding of the ectodomain. These results suggest that MDC9 and PKCdelta are involved in the stimulus-coupled shedding of the proHB-EGF ectodomain.
Mesh Terms:
ADAM Proteins, Catalytic Domain, Disintegrins, Epidermal Growth Factor, Intercellular Signaling Peptides and Proteins, Isoenzymes, Membrane Proteins, Metalloendopeptidases, Muscle Proteins, Mutation, Protein Binding, Protein Kinase C, Protein Kinase C-delta, Protein Precursors, Protein Processing, Post-Translational, Recombinant Proteins, Solubility, Tetradecanoylphorbol Acetate
EMBO J.
Date: Dec. 15, 1998
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