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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 EMBO journal | Dec 15, 1998

http://www.ncbi.nlm.nih.gov/pubmed/9857183

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.

Pubmed ID: 9857183 RIS Download

Mesh terms: ADAM Proteins | Catalytic Domain | Disintegrins | Epidermal Growth Factor | Heparin-binding EGF-like 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

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