Blood vessel epicardial substance (BVES), also known as protein 1 (POPDC1), is encoded by the humans BVES gene. BVES is a highly conserved transmembrane protein involved in cell adhesion, cell movement, and has recently been shown to play a role in vesicle transport. It present in various organisms (from flies to humans), and is a member of the evolutionarily conserved protein family Popdc.
Basic Information of BVES | |
Protein Name | Blood vessel epicardial substance |
Gene Name | BVES |
Aliases | HPOP1, POPDC1, LGMD2X |
Organism | Homo sapiens (Human) |
UniProt ID | Q8NE79 |
Transmembrane Times | 3 |
Length (aa) | 360 |
Sequence | MNYTESSPLRESTAIGFTPELESIIPVPSNKTTCENWREIHHLVFHVANICFAVGLVIPTTLHLHMIFLRGMLTLGCTLYIVWATLYRCALDIMIWNSVFLGVNILHLSYLLYKKRPVKIEKELSGMYRRLFEPLRVPPDLFRRLTGQFCMIQTLKKGQTYAAEDKTSVDDRLSILLKGKMKVSYRGHFLHNIYPCAFIDSPEFRSTQMHKGEKFQVTIIADDNCRFLCWSRERLTYFLESEPFLYEIFRYLIGKDITNKLYSLNDPTLNDKKAKKLEHQLSLCTQISMLEMRNSIASSSDSDDGLHQFLRGTSSMSSLHVSSPHQRASAKMKPIEEGAEDDDDVFEPASPNTLKVHQLP |
BVES acts as a cell adhesion molecule involved in the establishment and/or maintenance of cellular integrity. It is involved in the formation and regulation of a tight junction (TJ) paracellular permeability barrier in epithelial cells. Through its interaction with VAMP3, BVES plays a role in VAMP3-mediated vesicle trafficking and recycling of different receptor molecules. Besides, BVES is also a caveolae-associated protein, which is important for protecting the cavernous structure and functional integrity of the cell membrane and protecting the heart from ischemic damage.
Fig .1 Structure of BVES membrane protein.
This article reports that BVES is highly conserved among all three species at the amino acid level with 75% identity and 92% similarity.
This article reveals a function for BVES in epithelia and supports the hypothesis that BVES contributes to the establishment and/or maintenance of epithelial cell integrity.
Authors in this group knocked down POPDC3 expression with short hairpin RNAs and examined the consequences on cell migration and invasion. Knockdown of POPDC3 in SNU-216 cells caused increased cell migration and invasion.
This article concluded that POPDC gene expression is modified in end-stage heart failure in humans in a manner suggesting regulatory and/or functional differences between the three family members.
This article evaluates BVES prevents EMT, and its epigenetic silencing may be an important step in promoting EMT programs during colon carcinogenesis.
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