| Type: | Domain | Name: | CAS/CSE, C-terminal |
| Description: | Mammalian cellular apoptosis susceptibility (CAS) proteins and the yeast chromosome-segregation protein, CSE1 are homologous []. CAS is involved in both cellular apoptosis and proliferation [, ]. Apoptosis is inhibited in CAS-depleted cells, while the expression of CAScorrelates to the degree of cellular proliferation. Like CSE1, it is essential for the mitotic checkpoint in the cell cycle (CAS depletion blocks the cell in the G2 phase), and has been shown to be associated with the microtubule network and the mitotic spindle [], as is the protein MEK, which is thought to regulate the intracellularlocalization (predominantly nuclear vs. predominantly cytosolic) of CAS. In the nucleus, CAS acts as a nuclear transport factor in the importin pathway []. Theimportin pathway mediates the nuclear transport of several proteins that are necessary for mitosis and further progression. CAS is therefore thought to affect the cell cycle through its effect on the nuclear transport of these proteins []. Since apoptosis also requires the nuclear import of several proteins (such as P53 andtranscription factors), it has been suggested that CAS also enables apoptosis by facilitating the nuclear import of at least a subset of these essential proteins [].This entry represents the C-terminal portion of these proteins. Structural studies of the yeast CSE1 protein indicate that this domain binds to both the transport-orchestrating protein RanGTP and the cargo molecule that is being exported []. | Short Name: | CAS_CSE1_C |
