The BL6 subline was derived from the @entity48401 line, which was derived from the B16 @entity19 @entity320 cell line. BL6 cells are more invasive than @entity48401 cells and differ genetically from @entity48401 cells by an alteration of the gene encoding the B56gamma regulatory subunit of protein phosphatase 2A ( @entity20433 ). This alteration results in the transcription of mRNA encoding a truncated variant of the B56gamma1 isoform (Delta-gamma-1). Delta-gamma-1 is capable of targeting @entity20433 to the specific subcellular sites but incapable of promoting the dephosphorylation of specific substrates that is normally mediated by the B56gamma subunit-containing @entity20433 holoenzyme. It thus appears that activities of this type of holoenzymes decrease in cells expressing Delta-gamma-1. Recently, we found two possible ways how Delta-gamma-1 contributes to the enhanced metastatic potential of BL6 cells. The two ways seemed far away from each other: Delta-gamma-1 influenced both the nuclear and cytoplasmic functions of the cell. In the cytoplasm, Delta-gamma-1 localized at the Golgi complex and accelerated Golgi-mediated vesicle transport. On the other hand, Delta-gamma-1 disturbed the cell-cycle regulation. In response to gamma-irradiation, protein levels of Delta-gamma-1 were markedly increased in BL6 cells. Subsequently the integrity of cell-cycle checkpoint became more aberrant in BL6 cells than that in @entity48401 cells. These two actions of Delta-gamma-1 could results in the enhancement of the malignant phenotypes of @entity320 cells, as discussed in this review.

A mutation in protein phosphatase type 2A as a cause of XXXX progression.

@entity19 :: ('10090', 'Species') :: ['mouse'] @entity48401 :: ('14058(Tax:10090)', 'Gene') :: ['F10'] @entity320 :: ('MESH:D008545', 'Disease') :: ['melanoma'] @entity20433 :: ('51792(Tax:10090)', 'Gene') :: ['PP2A']
@entity320 :: (MESH:D008545,Disease) :: ['melanoma']
