Annotation inferences using phylogenetic trees
Electronic Gene Ontology annotations created by ARBA machine learning models
Distinct subcellular localization patterns contribute to functional specificity of the Cln2 and Cln3 cyclins of Saccharomyces cerevisiae.
A comprehensive analysis of protein-protein interactions in Saccharomyces cerevisiae.
Cks1 is required for G(1) cyclin-cyclin-dependent kinase activity in budding yeast.
Mechanisms controlling subcellular localization of the G(1) cyclins Cln2p and Cln3p in budding yeast.
Relationship between the function and the location of G1 cyclins in S. cerevisiae.
The Cln3-Cdc28 kinase complex of S. cerevisiae is regulated by proteolysis and phosphorylation.
The G1 cyclin Cln3p controls vacuolar biogenesis in Saccharomyces cerevisiae.
Assigning function to yeast proteins by integration of technologies.
Dual regulation by pairs of cyclin-dependent protein kinases and histone deacetylases controls G1 transcription in budding yeast.
Recruitment of Cln3 cyclin to promoters controls cell cycle entry via histone deacetylase and other targets.
A global protein kinase and phosphatase interaction network in yeast.
Cell cycle arrest caused by CLN gene deficiency in Saccharomyces cerevisiae resembles START-I arrest and is independent of the mating-pheromone signalling pathway.
CDK-dependent Hsp70 Phosphorylation controls G1 cyclin abundance and cell-cycle progression.
A family of cyclin homologs that control the G1 phase in yeast.
An essential G1 function for cyclin-like proteins in yeast.
The WHI1+ gene of Saccharomyces cerevisiae tethers cell division to cell size and is a cyclin homolog.
DAF1, a mutant gene affecting size control, pheromone arrest, and cell cycle kinetics of Saccharomyces cerevisiae.
Comparison of the Saccharomyces cerevisiae G1 cyclins: Cln3 may be an upstream activator of Cln1, Cln2 and other cyclins.
Cln3 activates G1-specific transcription via phosphorylation of the SBF bound repressor Whi5.
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Whi5 is an SBF-bound repressor; Cln3 promotes Whi5 dissociation in vivo and Cln/CDK phosphorylation dissociates Whi5 from SBF in vitro; whi5 inactivation bypasses the requirement for Cln3.
"Dissociation of Whi5 is promoted by Cln3 in vivo. Cln/CDK phosphorylation of Whi5 in vitro promotes its dissociation from SBF complexes"
CDK activity antagonizes Whi5, an inhibitor of G1/S transcription in yeast.
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Deletion of WHI5 bypasses upstream activators (Cln3, Bck2) of SBF/MBF and accelerates G1/S; CDK phosphorylation dissociates Whi5 from SBF and exports it from the nucleus.
"Deletion of WHI5 bypasses the requirement for upstream activators of the G1/S transcription factors SBF/MBF and thereby accelerates the G1/S transition"
Cyclin Cln3 is retained at the ER and released by the J chaperone Ydj1 in late G1 to trigger cell cycle entry.
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Cln3 is retained at the ER in early G1 in a Cdc28-dependent manner and released for nuclear accumulation in late G1 by the J chaperone Ydj1, which is limiting for cell cycle entry.
"We show here that Cln3 is retained bound to the ER in early G1 cells. ER retention requires binding of Cln3 to the cyclin-dependent kinase Cdc28, a fraction of which also associates to the ER"
Dilution of the cell cycle inhibitor Whi5 controls budding-yeast cell size.
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Cln3 synthesis scales with cell size so that its concentration is nearly constant in pre-Start G1; size control arises from dilution of Whi5 rather than rising Cln3 concentration, although Cln3 concentration still modulates the rate of Start.
"although Cln3 concentration does modulate the rate at which cells pass Start, its synthesis increases in proportion to cell size so that its total concentration is nearly constant during pre-Start G1"
Falcon deep research report for CLN3