Cyclin-dependent kinase (CDK) catalytic subunit; master regulator of mitotic and meiotic cell cycles; alternately associates with G1, S, G2/M phase cyclins, which provide substrate specificity; regulates metabolism, basal transcription, chromosome dynamics, growth and morphogenesis; transcript induction in osmostress involves antisense RNA; human homologs CDK1, CDK2, CDK3 can complement yeast conditional cdc28 mutants; human CDK1, CDK2 can complement yeast cdc28 null mutant.

G1/S-specific cyclin CLN1; G1 cyclin involved in regulation of the cell cycle; activates Cdc28p kinase to promote the G1 to S phase transition; late G1 specific expression depends on transcription factor complexes, MBF (Swi6p-Mbp1p) and SBF (Swi6p-Swi4p); CLN1 has a paralog, CLN2, that arose from the whole genome duplication; cell cycle arrest phenotype of the cln1 cln2 cln3 triple null mutant is complemented by any of human cyclins CCNA2, CCNB1, CCNC, CCND1, or CCNE1.

Cyclin-dependent kinase (CDK) catalytic subunit; master regulator of mitotic and meiotic cell cycles; alternately associates with G1, S, G2/M phase cyclins, which provide substrate specificity; regulates metabolism, basal transcription, chromosome dynamics, growth and morphogenesis; transcript induction in osmostress involves antisense RNA; human homologs CDK1, CDK2, CDK3 can complement yeast conditional cdc28 mutants; human CDK1, CDK2 can complement yeast cdc28 null mutant.

G1/S-specific cyclin CLN2; G1 cyclin involved in regulation of the cell cycle; activates Cdc28p kinase to promote the G1 to S phase transition; late G1 specific expression depends on transcription factor complexes, MBF (Swi6p-Mbp1p) and SBF (Swi6p-Swi4p); CLN2 has a paralog, CLN1, that arose from the whole genome duplication; cell cycle arrest phenotype of the cln1 cln2 cln3 triple null mutant is complemented by any of human cyclins CCNA2, CCNB1, CCNC, CCND1, or CCNE1.

Cyclin-dependent kinase (CDK) catalytic subunit; master regulator of mitotic and meiotic cell cycles; alternately associates with G1, S, G2/M phase cyclins, which provide substrate specificity; regulates metabolism, basal transcription, chromosome dynamics, growth and morphogenesis; transcript induction in osmostress involves antisense RNA; human homologs CDK1, CDK2, CDK3 can complement yeast conditional cdc28 mutants; human CDK1, CDK2 can complement yeast cdc28 null mutant.

G1/S-specific cyclin CLN3; G1 cyclin involved in cell cycle progression; activates Cdc28p kinase to promote G1 to S phase transition; plays a role in regulating transcription of other G1 cyclins, CLN1 and CLN2; regulated by phosphorylation and proteolysis; acetyl-CoA induces CLN3 transcription in response to nutrient repletion to promote cell-cycle entry; cell cycle arrest phenotype of the cln1 cln2 cln3 triple null mutant is complemented by any of human cyclins CCNA2, CCNB1, CCNC, CCND1, or CCNE1.

Cyclin-dependent kinase (CDK) catalytic subunit; master regulator of mitotic and meiotic cell cycles; alternately associates with G1, S, G2/M phase cyclins, which provide substrate specificity; regulates metabolism, basal transcription, chromosome dynamics, growth and morphogenesis; transcript induction in osmostress involves antisense RNA; human homologs CDK1, CDK2, CDK3 can complement yeast conditional cdc28 mutants; human CDK1, CDK2 can complement yeast cdc28 null mutant.

CDK inhibitor and nuclear anchor; during the cell cycle Far1p sequesters the GEF Cdc24p in the nucleus; phosphorylation by Cdc28p-Cln results in SCFCdc4 complex-mediated ubiquitin-dependent degradation, releasing Cdc24p for export and activation of GTPase Cdc42p; in response to pheromone, phosphorylation of Far1p by MAPK Fus3p results in association with, and inhibition of Cdc28p-Cln, as well as Msn5p mediated nuclear export of Far1p-Cdc24p, targeting Cdc24p to polarity sites.

Cyclin-dependent kinase (CDK) catalytic subunit; master regulator of mitotic and meiotic cell cycles; alternately associates with G1, S, G2/M phase cyclins, which provide substrate specificity; regulates metabolism, basal transcription, chromosome dynamics, growth and morphogenesis; transcript induction in osmostress involves antisense RNA; human homologs CDK1, CDK2, CDK3 can complement yeast conditional cdc28 mutants; human CDK1, CDK2 can complement yeast cdc28 null mutant.

Mitogen-activated serine/threonine protein kinase involved in mating; phosphoactivated by Ste7p; substrates include Ste12p, Far1p, Bni1p, Sst2p; inhibits invasive growth during mating by phosphorylating Tec1p, promoting its; inhibits recruitment of Ste5p, Cdc42p-mediated asymmetry and mating morphogenesis.

G1/S-specific cyclin CLN1; G1 cyclin involved in regulation of the cell cycle; activates Cdc28p kinase to promote the G1 to S phase transition; late G1 specific expression depends on transcription factor complexes, MBF (Swi6p-Mbp1p) and SBF (Swi6p-Swi4p); CLN1 has a paralog, CLN2, that arose from the whole genome duplication; cell cycle arrest phenotype of the cln1 cln2 cln3 triple null mutant is complemented by any of human cyclins CCNA2, CCNB1, CCNC, CCND1, or CCNE1.

Cyclin-dependent kinase (CDK) catalytic subunit; master regulator of mitotic and meiotic cell cycles; alternately associates with G1, S, G2/M phase cyclins, which provide substrate specificity; regulates metabolism, basal transcription, chromosome dynamics, growth and morphogenesis; transcript induction in osmostress involves antisense RNA; human homologs CDK1, CDK2, CDK3 can complement yeast conditional cdc28 mutants; human CDK1, CDK2 can complement yeast cdc28 null mutant.

G1/S-specific cyclin CLN1; G1 cyclin involved in regulation of the cell cycle; activates Cdc28p kinase to promote the G1 to S phase transition; late G1 specific expression depends on transcription factor complexes, MBF (Swi6p-Mbp1p) and SBF (Swi6p-Swi4p); CLN1 has a paralog, CLN2, that arose from the whole genome duplication; cell cycle arrest phenotype of the cln1 cln2 cln3 triple null mutant is complemented by any of human cyclins CCNA2, CCNB1, CCNC, CCND1, or CCNE1.

G1/S-specific cyclin CLN2; G1 cyclin involved in regulation of the cell cycle; activates Cdc28p kinase to promote the G1 to S phase transition; late G1 specific expression depends on transcription factor complexes, MBF (Swi6p-Mbp1p) and SBF (Swi6p-Swi4p); CLN2 has a paralog, CLN1, that arose from the whole genome duplication; cell cycle arrest phenotype of the cln1 cln2 cln3 triple null mutant is complemented by any of human cyclins CCNA2, CCNB1, CCNC, CCND1, or CCNE1.

G1/S-specific cyclin CLN1; G1 cyclin involved in regulation of the cell cycle; activates Cdc28p kinase to promote the G1 to S phase transition; late G1 specific expression depends on transcription factor complexes, MBF (Swi6p-Mbp1p) and SBF (Swi6p-Swi4p); CLN1 has a paralog, CLN2, that arose from the whole genome duplication; cell cycle arrest phenotype of the cln1 cln2 cln3 triple null mutant is complemented by any of human cyclins CCNA2, CCNB1, CCNC, CCND1, or CCNE1.

G1/S-specific cyclin CLN3; G1 cyclin involved in cell cycle progression; activates Cdc28p kinase to promote G1 to S phase transition; plays a role in regulating transcription of other G1 cyclins, CLN1 and CLN2; regulated by phosphorylation and proteolysis; acetyl-CoA induces CLN3 transcription in response to nutrient repletion to promote cell-cycle entry; cell cycle arrest phenotype of the cln1 cln2 cln3 triple null mutant is complemented by any of human cyclins CCNA2, CCNB1, CCNC, CCND1, or CCNE1.

G1/S-specific cyclin CLN1; G1 cyclin involved in regulation of the cell cycle; activates Cdc28p kinase to promote the G1 to S phase transition; late G1 specific expression depends on transcription factor complexes, MBF (Swi6p-Mbp1p) and SBF (Swi6p-Swi4p); CLN1 has a paralog, CLN2, that arose from the whole genome duplication; cell cycle arrest phenotype of the cln1 cln2 cln3 triple null mutant is complemented by any of human cyclins CCNA2, CCNB1, CCNC, CCND1, or CCNE1.

CDK inhibitor and nuclear anchor; during the cell cycle Far1p sequesters the GEF Cdc24p in the nucleus; phosphorylation by Cdc28p-Cln results in SCFCdc4 complex-mediated ubiquitin-dependent degradation, releasing Cdc24p for export and activation of GTPase Cdc42p; in response to pheromone, phosphorylation of Far1p by MAPK Fus3p results in association with, and inhibition of Cdc28p-Cln, as well as Msn5p mediated nuclear export of Far1p-Cdc24p, targeting Cdc24p to polarity sites.

G1/S-specific cyclin CLN1; G1 cyclin involved in regulation of the cell cycle; activates Cdc28p kinase to promote the G1 to S phase transition; late G1 specific expression depends on transcription factor complexes, MBF (Swi6p-Mbp1p) and SBF (Swi6p-Swi4p); CLN1 has a paralog, CLN2, that arose from the whole genome duplication; cell cycle arrest phenotype of the cln1 cln2 cln3 triple null mutant is complemented by any of human cyclins CCNA2, CCNB1, CCNC, CCND1, or CCNE1.

Mitogen-activated serine/threonine protein kinase involved in mating; phosphoactivated by Ste7p; substrates include Ste12p, Far1p, Bni1p, Sst2p; inhibits invasive growth during mating by phosphorylating Tec1p, promoting its; inhibits recruitment of Ste5p, Cdc42p-mediated asymmetry and mating morphogenesis.

G1/S-specific cyclin CLN2; G1 cyclin involved in regulation of the cell cycle; activates Cdc28p kinase to promote the G1 to S phase transition; late G1 specific expression depends on transcription factor complexes, MBF (Swi6p-Mbp1p) and SBF (Swi6p-Swi4p); CLN2 has a paralog, CLN1, that arose from the whole genome duplication; cell cycle arrest phenotype of the cln1 cln2 cln3 triple null mutant is complemented by any of human cyclins CCNA2, CCNB1, CCNC, CCND1, or CCNE1.

Cyclin-dependent kinase (CDK) catalytic subunit; master regulator of mitotic and meiotic cell cycles; alternately associates with G1, S, G2/M phase cyclins, which provide substrate specificity; regulates metabolism, basal transcription, chromosome dynamics, growth and morphogenesis; transcript induction in osmostress involves antisense RNA; human homologs CDK1, CDK2, CDK3 can complement yeast conditional cdc28 mutants; human CDK1, CDK2 can complement yeast cdc28 null mutant.

G1/S-specific cyclin CLN2; G1 cyclin involved in regulation of the cell cycle; activates Cdc28p kinase to promote the G1 to S phase transition; late G1 specific expression depends on transcription factor complexes, MBF (Swi6p-Mbp1p) and SBF (Swi6p-Swi4p); CLN2 has a paralog, CLN1, that arose from the whole genome duplication; cell cycle arrest phenotype of the cln1 cln2 cln3 triple null mutant is complemented by any of human cyclins CCNA2, CCNB1, CCNC, CCND1, or CCNE1.

G1/S-specific cyclin CLN1; G1 cyclin involved in regulation of the cell cycle; activates Cdc28p kinase to promote the G1 to S phase transition; late G1 specific expression depends on transcription factor complexes, MBF (Swi6p-Mbp1p) and SBF (Swi6p-Swi4p); CLN1 has a paralog, CLN2, that arose from the whole genome duplication; cell cycle arrest phenotype of the cln1 cln2 cln3 triple null mutant is complemented by any of human cyclins CCNA2, CCNB1, CCNC, CCND1, or CCNE1.

G1/S-specific cyclin CLN2; G1 cyclin involved in regulation of the cell cycle; activates Cdc28p kinase to promote the G1 to S phase transition; late G1 specific expression depends on transcription factor complexes, MBF (Swi6p-Mbp1p) and SBF (Swi6p-Swi4p); CLN2 has a paralog, CLN1, that arose from the whole genome duplication; cell cycle arrest phenotype of the cln1 cln2 cln3 triple null mutant is complemented by any of human cyclins CCNA2, CCNB1, CCNC, CCND1, or CCNE1.

G1/S-specific cyclin CLN3; G1 cyclin involved in cell cycle progression; activates Cdc28p kinase to promote G1 to S phase transition; plays a role in regulating transcription of other G1 cyclins, CLN1 and CLN2; regulated by phosphorylation and proteolysis; acetyl-CoA induces CLN3 transcription in response to nutrient repletion to promote cell-cycle entry; cell cycle arrest phenotype of the cln1 cln2 cln3 triple null mutant is complemented by any of human cyclins CCNA2, CCNB1, CCNC, CCND1, or CCNE1.

G1/S-specific cyclin CLN2; G1 cyclin involved in regulation of the cell cycle; activates Cdc28p kinase to promote the G1 to S phase transition; late G1 specific expression depends on transcription factor complexes, MBF (Swi6p-Mbp1p) and SBF (Swi6p-Swi4p); CLN2 has a paralog, CLN1, that arose from the whole genome duplication; cell cycle arrest phenotype of the cln1 cln2 cln3 triple null mutant is complemented by any of human cyclins CCNA2, CCNB1, CCNC, CCND1, or CCNE1.

CDK inhibitor and nuclear anchor; during the cell cycle Far1p sequesters the GEF Cdc24p in the nucleus; phosphorylation by Cdc28p-Cln results in SCFCdc4 complex-mediated ubiquitin-dependent degradation, releasing Cdc24p for export and activation of GTPase Cdc42p; in response to pheromone, phosphorylation of Far1p by MAPK Fus3p results in association with, and inhibition of Cdc28p-Cln, as well as Msn5p mediated nuclear export of Far1p-Cdc24p, targeting Cdc24p to polarity sites.

G1/S-specific cyclin CLN2; G1 cyclin involved in regulation of the cell cycle; activates Cdc28p kinase to promote the G1 to S phase transition; late G1 specific expression depends on transcription factor complexes, MBF (Swi6p-Mbp1p) and SBF (Swi6p-Swi4p); CLN2 has a paralog, CLN1, that arose from the whole genome duplication; cell cycle arrest phenotype of the cln1 cln2 cln3 triple null mutant is complemented by any of human cyclins CCNA2, CCNB1, CCNC, CCND1, or CCNE1.

Mitogen-activated serine/threonine protein kinase involved in mating; phosphoactivated by Ste7p; substrates include Ste12p, Far1p, Bni1p, Sst2p; inhibits invasive growth during mating by phosphorylating Tec1p, promoting its; inhibits recruitment of Ste5p, Cdc42p-mediated asymmetry and mating morphogenesis.

G1/S-specific cyclin CLN3; G1 cyclin involved in cell cycle progression; activates Cdc28p kinase to promote G1 to S phase transition; plays a role in regulating transcription of other G1 cyclins, CLN1 and CLN2; regulated by phosphorylation and proteolysis; acetyl-CoA induces CLN3 transcription in response to nutrient repletion to promote cell-cycle entry; cell cycle arrest phenotype of the cln1 cln2 cln3 triple null mutant is complemented by any of human cyclins CCNA2, CCNB1, CCNC, CCND1, or CCNE1.

Cyclin-dependent kinase (CDK) catalytic subunit; master regulator of mitotic and meiotic cell cycles; alternately associates with G1, S, G2/M phase cyclins, which provide substrate specificity; regulates metabolism, basal transcription, chromosome dynamics, growth and morphogenesis; transcript induction in osmostress involves antisense RNA; human homologs CDK1, CDK2, CDK3 can complement yeast conditional cdc28 mutants; human CDK1, CDK2 can complement yeast cdc28 null mutant.

G1/S-specific cyclin CLN3; G1 cyclin involved in cell cycle progression; activates Cdc28p kinase to promote G1 to S phase transition; plays a role in regulating transcription of other G1 cyclins, CLN1 and CLN2; regulated by phosphorylation and proteolysis; acetyl-CoA induces CLN3 transcription in response to nutrient repletion to promote cell-cycle entry; cell cycle arrest phenotype of the cln1 cln2 cln3 triple null mutant is complemented by any of human cyclins CCNA2, CCNB1, CCNC, CCND1, or CCNE1.

G1/S-specific cyclin CLN1; G1 cyclin involved in regulation of the cell cycle; activates Cdc28p kinase to promote the G1 to S phase transition; late G1 specific expression depends on transcription factor complexes, MBF (Swi6p-Mbp1p) and SBF (Swi6p-Swi4p); CLN1 has a paralog, CLN2, that arose from the whole genome duplication; cell cycle arrest phenotype of the cln1 cln2 cln3 triple null mutant is complemented by any of human cyclins CCNA2, CCNB1, CCNC, CCND1, or CCNE1.

G1/S-specific cyclin CLN3; G1 cyclin involved in cell cycle progression; activates Cdc28p kinase to promote G1 to S phase transition; plays a role in regulating transcription of other G1 cyclins, CLN1 and CLN2; regulated by phosphorylation and proteolysis; acetyl-CoA induces CLN3 transcription in response to nutrient repletion to promote cell-cycle entry; cell cycle arrest phenotype of the cln1 cln2 cln3 triple null mutant is complemented by any of human cyclins CCNA2, CCNB1, CCNC, CCND1, or CCNE1.

G1/S-specific cyclin CLN2; G1 cyclin involved in regulation of the cell cycle; activates Cdc28p kinase to promote the G1 to S phase transition; late G1 specific expression depends on transcription factor complexes, MBF (Swi6p-Mbp1p) and SBF (Swi6p-Swi4p); CLN2 has a paralog, CLN1, that arose from the whole genome duplication; cell cycle arrest phenotype of the cln1 cln2 cln3 triple null mutant is complemented by any of human cyclins CCNA2, CCNB1, CCNC, CCND1, or CCNE1.

G1/S-specific cyclin CLN3; G1 cyclin involved in cell cycle progression; activates Cdc28p kinase to promote G1 to S phase transition; plays a role in regulating transcription of other G1 cyclins, CLN1 and CLN2; regulated by phosphorylation and proteolysis; acetyl-CoA induces CLN3 transcription in response to nutrient repletion to promote cell-cycle entry; cell cycle arrest phenotype of the cln1 cln2 cln3 triple null mutant is complemented by any of human cyclins CCNA2, CCNB1, CCNC, CCND1, or CCNE1.

CDK inhibitor and nuclear anchor; during the cell cycle Far1p sequesters the GEF Cdc24p in the nucleus; phosphorylation by Cdc28p-Cln results in SCFCdc4 complex-mediated ubiquitin-dependent degradation, releasing Cdc24p for export and activation of GTPase Cdc42p; in response to pheromone, phosphorylation of Far1p by MAPK Fus3p results in association with, and inhibition of Cdc28p-Cln, as well as Msn5p mediated nuclear export of Far1p-Cdc24p, targeting Cdc24p to polarity sites.

G1/S-specific cyclin CLN3; G1 cyclin involved in cell cycle progression; activates Cdc28p kinase to promote G1 to S phase transition; plays a role in regulating transcription of other G1 cyclins, CLN1 and CLN2; regulated by phosphorylation and proteolysis; acetyl-CoA induces CLN3 transcription in response to nutrient repletion to promote cell-cycle entry; cell cycle arrest phenotype of the cln1 cln2 cln3 triple null mutant is complemented by any of human cyclins CCNA2, CCNB1, CCNC, CCND1, or CCNE1.

Mitogen-activated serine/threonine protein kinase involved in mating; phosphoactivated by Ste7p; substrates include Ste12p, Far1p, Bni1p, Sst2p; inhibits invasive growth during mating by phosphorylating Tec1p, promoting its; inhibits recruitment of Ste5p, Cdc42p-mediated asymmetry and mating morphogenesis.