| First Author | Yamazaki S | Year | 2003 |
| Journal | J Cell Biol | Volume | 163 |
| Issue | 3 | Pages | 469-75 |
| PubMed ID | 14597776 | Mgi Jnum | J:86547 |
| Mgi Id | MGI:2680746 | Doi | 10.1083/jcb.200307035 |
| Citation | Yamazaki S, et al. (2003) Mice with defects in HB-EGF ectodomain shedding show severe developmental abnormalities. J Cell Biol 163(3):469-75 |
| abstractText | Heparin-binding EGF-like growth factor (HB-EGF) is first synthesized as a membrane-anchored form (proHB-EGF), and its soluble form (sHB-EGF) is released by ectodomain shedding from proHB-EGF. To examine the significance of proHB-EGF processing in vivo, we generated mutant mice by targeted gene replacement, expressing either an uncleavable form (HBuc) or a transmembrane domain-truncated form (HBdeltatm) of the molecule. HB(uc/uc) mice developed severe heart failure and enlarged heart valves, phenotypes similar to those in proHB-EGF null mice. On the other hand, mice carrying HBdeltatm exhibited severe hyperplasia in both skin and heart. These results indicate that ectodomain shedding of proHB-EGF is essential for HB-EGF function in vivo, and that this process requires strict control. |
