作者: Meihui Wu , Mei Chung Moh , Herbert Schwarz
DOI: 10.1038/SREP36218
关键词: Cell growth 、 HEPACAM 、 Cell junction 、 Tumor progression 、 Gap junction 、 Cell biology 、 Suppressor 、 Transcription (biology) 、 Connexin 、 Biology
摘要: HepaCAM (GlialCAM) is frequently deleted in carcinomas, and reintroduction of hepaCAM into transformed cell lines reduces cellular growth induces senescence. Mutations HEPACAM give rise to the neurodegenerative disease megalencephalic leukoencephalopathy with subcortical cysts (MLC) since mutated prevents shuttling MLC1 protein astrocytic junctions plasma membrane. Here we identify that associates connexin 43, a main component gap junctions, enhances 43 localization membrane at junctions. also increases levels not by enhancing its transcription but stabilizing protein. In absence hepaCAM, undergoes faster degradation via lysosomal pathway while proteasomal seems be involved. cause MLC, or neutralization antibodies disrupt association By discovering requirement for localizing well-established tumor suppressor, it there, this study suggests mechanism which deletion may support progression.