This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.Gap Junction Channels (GJCs) are present in plasma membrane of contacting cells, have been associated with many cases of tumor suppression. Gap Junctions are composed by connexons, GJC precursors, require hexameric proteins named connexins and abnormal GJC may be consequence of failures in assembling or connexin degradation. Similar to other plasma membrane proteins, gap junction proteins are delivered to the cell surface through the secretory pathway. So, the goal of this study is to identify if the degradation routes of connexin 43 has influenced the GJC maintenance. Both proteasomal and lysosomal pathways are involved in degradation of connexins but the degradation of gap junction plaques is commonly presented as proteasome-dependent. The treatment with proteasomal inhibitor generally increased the connexin 43 abundance at appositional membranes So, the correlation of fluorescent and electron microscopy will be fundamental to understand the protein assembly in GJCs and its association with degradation patways in hepatocarcinoma cells as even the regulation of connexin half-life.
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