Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Electronic Gene Ontology annotations created by ARBA machine learning models
Regulation of transcription at the Saccharomyces cerevisiae start transition by Stb1, a Swi6-binding protein.
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Cln2-Cdc28 kinase immunoprecipitated from yeast phosphorylates Stb1 in vitro, and in vivo Stb1 phosphoforms depend on the CLN genes, with Cln1/Cln2-Cdc28 as the physiological kinases.
"Stb1 was an excellent substrate for both the Cln1-Cdc28 and Cln2-Cdc28 kinases in vitro and was a better in vitro substrate than histone H1"
Distinct subcellular localization patterns contribute to functional specificity of the Cln2 and Cln3 cyclins of Saccharomyces cerevisiae.
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Cln2 is predominantly cytoplasmic by immunofluorescence and fractionation, but an appended NES reduces its activity, so a nuclear pool is functionally important.
"Overall, it appears that Cln2p is required in both the cytoplasm and the nucleus of the cell for maximal function"
Cks1 is required for G(1) cyclin-cyclin-dependent kinase activity in budding yeast.
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Active Cln2-Cdc28 complexes require the Cks1 subunit, which stabilises and activates them.
"Cks1 can both stabilize Cln2-Cdc28 complexes and activate intact complexes in vitro"
Nuclear-specific degradation of Far1 is controlled by the localization of the F-box protein Cdc4.
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Purified Cdc28-Cln2 phosphorylates Far1 Ser87, which is required for Far1 ubiquitylation by SCF(Cdc4); Cln2-GFP is present in both nucleus and cytoplasm.
"ubiquitylation of Far1-nls1 or Far1-nls1/2 was dependent on phosphorylation of serine 87 by Cdc28–Cln2"
Mechanisms controlling subcellular localization of the G(1) cyclins Cln2p and Cln3p in budding yeast.
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Cln2 cytoplasmic localization depends on Cdc28 binding and Cdc28-dependent C-terminal phosphorylation; hypophosphorylated Cln2 is nuclear, consistent with regulated shuttling.
"These data are consistent with regulated shuttling of Cln2p in and out of the nucleus, where nonphosphorylated Cln2p is enriched in the nucleus and phosphorylated Cln2p is enriched in the cytoplasm"
Relationship between the function and the location of G1 cyclins in S. cerevisiae.
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Cln2 is in both nucleus and cytoplasm, concentrated at sites of polarized growth; forced localization shows distinct nuclear and cytoplasmic functions.
"Cln2 was found in both nucleus and cytoplasm"
Functional organization of the yeast proteome by systematic analysis of protein complexes.
Systematic identification of protein complexes in Saccharomyces cerevisiae by mass spectrometry.
Proteome survey reveals modularity of the yeast cell machinery.
A mechanism for cell-cycle regulation of MAP kinase signaling in a yeast differentiation pathway.
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G1 CDK (Cln/Cdc28) phosphorylates multiple sites flanking the membrane-binding motif of the MAPK scaffold Ste5, blocking its membrane recruitment and shutting off pheromone signalling after Start.
"In this study, we report that G1 CDK activity inhibits pheromone signaling by inhibiting Ste5 membrane recruitment"
A global protein kinase and phosphatase interaction network in yeast.
G1-specific cyclins of S. cerevisiae: cell cycle periodicity, regulation by mating pheromone, and association with the p34CDC28 protein kinase.
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Cln2 protein and CLN1/CLN2 transcripts peak in G1 and fall in S phase or on pheromone exposure; Cln2 associates with p34CDC28 in an active protein kinase complex.
"we demonstrate that the Cln2 polypeptide interacts with p34CDC28 to form an active protein kinase complex"
Cell cycle arrest caused by CLN gene deficiency in Saccharomyces cerevisiae resembles START-I arrest and is independent of the mating-pheromone signalling pathway.
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cln1 cln2 cln3 cells arrest as unbudded G1 cells at START, independently of the pheromone pathway.
"These results are consistent with a specific CLN requirement for START transit"
A family of cyclin homologs that control the G1 phase in yeast.
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CLN1 and CLN2 were cloned as dosage suppressors of cdc28-ts; the dominant CLN2-1 allele advances G1/S and prevents G1 arrest in response to external signals.
"A dominant mutation in the CLN2 gene, CLN2-1, advances the G1- to S-phase transition in cycling cells and impairs the ability of cells to arrest in G1 phase in response to external signals"
An essential G1 function for cyclin-like proteins in yeast.
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Cln1, Cln2 and Cln3 share an essential, redundant G1 function consistent with activation of Cdc28 for the G1-to-S transition.
"Mutational elimination of the CLN1, CLN2, and DAF1/WHI1 products leads to cell cycle arrest independent of cell type, while expression of any one of the genes allows cell proliferation"
G1 cyclin-dependent activation of p34CDC28 (Cdc28p) in vitro.
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GST-Cln2 binds and activates Cdc28 as a histone H1 kinase in a cyclin-depleted G1 extract, dependent on ATP, cytosol and Cdc28 Thr169.
"A glutathione S-transferase-G1 cyclin chimera (GST-Cln2p) efficiently binds to and activates Cdc28p as a histone H1 kinase"
Comparison of the Saccharomyces cerevisiae G1 cyclins: Cln3 may be an upstream activator of Cln1, Cln2 and other cyclins.
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Cln1 and Cln2 are abundant, cell-cycle-regulated cyclins with strong associated H1 kinase activity and are proposed to directly catalyse Start downstream of Cln3.
"the G1 cyclins Cln1, Cln2 and Cln3 regulate entry into the cell cycle (Start) by activating the Cdc28 protein kinase"
POG1, a novel yeast gene, promotes recovery from pheromone arrest via the G1 cyclin CLN2.
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POG1 promotes recovery from pheromone arrest through CLN2, and Cln2 protein acts primarily through Ste20.
"Genetic tests strongly argue that POG1 promotes recovery through upregulation of the CLN2 gene and that the resulting Cln2 protein promotes recovery primarily through an effect on Ste20, an activator of the mating MAPK cascade"
Dual regulation by pairs of cyclin-dependent protein kinases and histone deacetylases controls G1 transcription in budding yeast.
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Whi5 phosphorylation in vivo depends on Cln-Cdc28 (absent in cln1 cln2 cells), and recombinant Cln2-Cdc28 phosphorylates Whi5 and releases it from SBF in vitro.
"As expected, Cln2-Cdc28 phosphorylation caused most of the SBF-bound Whi5 to be released into the soluble fraction"
Cascades of multisite phosphorylation control Sic1 destruction at the onset of S phase.
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Purified Cln2-Cdk1 initiates the processive multisite phosphorylation of Sic1 (priming at T5 via a Cln2-specific docking motif), creating the platform that Clb5-Cdk1 completes to build the SCF(Cdc4) phosphodegrons.
"We propose that in late G1, Clb5-Cdk1 is inhibited by Sic1, and the cascade of phosphorylation events begins with T5 phosphorylation by Cln2-Cdk1"
Cln3 activates G1-specific transcription via phosphorylation of the SBF bound repressor Whi5.
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Cln/CDK phosphorylation of Whi5 in vitro dissociates it from SBF; Whi5 is an Rb-like G1 transcriptional repressor antagonised by CDK.
"Cln/CDK phosphorylation of Whi5 in vitro promotes its dissociation from SBF complexes"
Falcon deep research report for CLN2