CAS/CSE protein, C-terminus; Mammalian cellular apoptosis susceptibility (CAS) proteins are homologous to the yeast chromosome-segregation protein, CSE1. This family aligns the C-terminal halves (approximately). CAS is involved in both cellular apoptosis and proliferation. Apoptosis is inhibited in CAS-depleted cells, while the expression of CAS correlates 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 intracellular localization (predominantly nuclear vs. predominantly cytosolic) of CAS. In the nucleus, CAS acts as a nuclear transport factor in the importin pathway. The importin 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 and transcription factors), it has been suggested that CAS also enables apoptosis by facilitating the nuclear import of at least a subset of these essential proteins.

                          10        20        30        40        50        60        70        80
                  ....*....|....*....|....*....|....*....|....*....|....*....|....*....|....*....|
gi 808354725    4 VLNTMFRRVQSSKTPKFMKLFIVFLCRFTIARSAQDLVQSCENIQTGMFGMLIEKVVcidLPGLKQTTTGPEKRIIAIGM 83
Cdd:pfam03378 243 IFSLLFQRLQNSKTEKFVKRFVIFYHLYSAKHGADFLIQLIDAIQPGVFGMIYLNVI---LPETQKLAGPLDRKLAAVSY 319

                  ....*.
gi 808354725   84 GNLLAD 89
Cdd:pfam03378 320 TKLLCE 325

CAS/CSE protein, C-terminus; Mammalian cellular apoptosis susceptibility (CAS) proteins are homologous to the yeast chromosome-segregation protein, CSE1. This family aligns the C-terminal halves (approximately). CAS is involved in both cellular apoptosis and proliferation. Apoptosis is inhibited in CAS-depleted cells, while the expression of CAS correlates 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 intracellular localization (predominantly nuclear vs. predominantly cytosolic) of CAS. In the nucleus, CAS acts as a nuclear transport factor in the importin pathway. The importin 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 and transcription factors), it has been suggested that CAS also enables apoptosis by facilitating the nuclear import of at least a subset of these essential proteins.

                          10        20        30        40        50        60        70        80
                  ....*....|....*....|....*....|....*....|....*....|....*....|....*....|....*....|
gi 808354725    4 VLNTMFRRVQSSKTPKFMKLFIVFLCRFTIARSAQDLVQSCENIQTGMFGMLIEKVVcidLPGLKQTTTGPEKRIIAIGM 83
Cdd:pfam03378 243 IFSLLFQRLQNSKTEKFVKRFVIFYHLYSAKHGADFLIQLIDAIQPGVFGMIYLNVI---LPETQKLAGPLDRKLAAVSY 319

                  ....*.
gi 808354725   84 GNLLAD 89
Cdd:pfam03378 320 TKLLCE 325

CAS/CSE protein, C-terminus; Mammalian cellular apoptosis susceptibility (CAS) proteins are homologous to the yeast chromosome-segregation protein, CSE1. This family aligns the C-terminal halves (approximately). CAS is involved in both cellular apoptosis and proliferation. Apoptosis is inhibited in CAS-depleted cells, while the expression of CAS correlates 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 intracellular localization (predominantly nuclear vs. predominantly cytosolic) of CAS. In the nucleus, CAS acts as a nuclear transport factor in the importin pathway. The importin 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 and transcription factors), it has been suggested that CAS also enables apoptosis by facilitating the nuclear import of at least a subset of these essential proteins.

                          10        20        30        40        50        60        70        80
                  ....*....|....*....|....*....|....*....|....*....|....*....|....*....|....*....|
gi 808354725    4 VLNTMFRRVQSSKTPKFMKLFIVFLCRFTIARSAQDLVQSCENIQTGMFGMLIEKVVcidLPGLKQTTTGPEKRIIAIGM 83
Cdd:pfam03378 243 IFSLLFQRLQNSKTEKFVKRFVIFYHLYSAKHGADFLIQLIDAIQPGVFGMIYLNVI---LPETQKLAGPLDRKLAAVSY 319

                  ....*.
gi 808354725   84 GNLLAD 89
Cdd:pfam03378 320 TKLLCE 325