Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Drug
Enzyme
Compound
Query: EC:2.7.11.22 (
cdc2
)
8,319
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Budding yeast strains have three CLN genes, which have limited cyclin homology. At least one of the three is required for cell cycle START. Four B cyclins are known in yeast; two have been shown to function in mitosis. We have discovered a fifth B-cyclin gene, called CLB5, which when cloned on a CEN plasmid can rescue strains deleted for all three CLN genes. CLB5 transcript abundance peaks in G1, coincident with the CLN2 transcript but earlier than the CLB2 transcript. CLB5 deletion does not cause lethality, either alone or in combination with other CLN or
CLB
deletions. However, strains deleted for CLB5 require more time to complete S phase, suggesting that CLB5 promotes some step in DNA synthesis. CLB5 is the only yeast cyclin whose deletion lengthens S phase. CLB5 may also have some role in promoting the G1/S transition, because cln1 cln2 strains require both CLN3 and CLB5 for viability on glycerol media and cln1,2,3- strains require CLB5 for rescue by the Drosophila melanogaster
cdc2
gene. In conjunction with cln1,2,3- rescue by CLB5 overexpression and the coincident transcriptional regulation of CLB5 and CLN2, these observations are suggestive of partial functional redundancy between CLB5 and CLN genes.
...
PMID:CLB5: a novel B cyclin from budding yeast with a role in S phase. 138 26
The budding yeast cell cycle oscillates between states of low and high cyclin B/cyclin-dependent kinase (
CLB
/
CDK
) activity. Remarkably, the two transitions that link these states are governed by ubiquitin-mediated proteolysis. The transition from low to high
CLB
activity is triggered by degradation of the
CLB
/
CDK
inhibitor SIC1, and the complementary excursion is propelled by the proteolytic destruction of CLBs. The extracellular environment controls this two-state circuit by regulating G1 cyclin/
CDK
activity, which is directly required for SIC1 proteolysis. Thus, stable oscillations of chromosome replication and segregation in budding yeast are propagated by the interplay between protein phosphorylation and protein degradation.
...
PMID:Phosphorylation and proteolysis: partners in the regulation of cell division in budding yeast. 902 29
In Saccharomyces cerevisiae, entry into S phase requires the activation of the protein kinase
Cdc28p
through binding with cyclin Clb5p or Clb6p, as well as the destruction of the cyclin-dependent kinase inhibitor Sic1p. Mutants that are defective in this activation event arrest after START, with unreplicated DNA and multiple, elongated buds. These mutants include cells defective in CDC4, CDC34 or CDC53, as well as cells that have lost all
CLB
function. Here we describe mutations in another gene, CAK1, that lead to a similar arrest. Cells that are defective in CAK1 are inviable and arrest with a single nucleus and multiple, elongated buds. CAK1 encodes a protein kinase most closely related to the Cdc2p family of protein kinases. Mutations that lead to the production of an inactive kinase that can neither autophosphorylate, nor phosphorylate
Cdc28p
in vitro are also incapable of rescuing a cell with a deletion of CAK1. These results underscore the importance of the
Cak1p
protein kinase activity in cell cycle progression.
...
PMID:Mutational analysis of Cak1p, an essential protein kinase that regulates cell cycle progression. 939 34