细胞周期遗传学-猫眼课题宝

细胞周期遗传学

批准号：

7382859

负责人：

STEPHEN J ELLEDGE

金额：

$35.0万

依托单位：

BRIGHAM AND WOMEN'S HOSPITAL

依托单位国家：

美国

项目类别：

财政年份：

1990

资助国家：

美国

项目状态：

已结题

起止时间：

1990-07-01 至 2013-06-30

来源：

https://reporter.nih.gov/project-details/7382859

关键词：

Affinity Affinity Chromatography Alleles Amino Acids Anaphase Antibodies Binding Biochemical Genetics C-terminal CCL26 gene CHEK2 gene Cations Cell Cycle Cell Cycle Arrest Cell Cycle Regulation Cells Characteristics Charge Chromatin Chromosome Segregation Chromosomes Complex Condition Consensus Cyclic AMP-Dependent Protein Kinases Cyclin-Dependent Kinases DNA Damage DNA Double Strand Break DNA Repair DNA Replication Damage DNA biosynthesis DNA damage checkpoint Databases Daughter Defect Ensure Essential Genes Eukaryota Eukaryotic Cell Event Failure Future Genetic Genetic Epistasis Genetic Screening Goals Grant Homologous Gene In Vitro Investigation Ionizing radiation Iron Kinetochores Lead Left Light Cell Link Localized MCM Protein Mammals Mass Spectrum Analysis Methods Microtubules Mitosis Mitotic Mitotic spindle Modeling Mutagenesis Mutagens Mutate Mutation N-terminal Nocodazole Nuclear Nuclear Protein Nuclear Proteins Numbers PDE2 phosphodiesterase Paint Paper Pathway interactions Peptide Fragments Peptides Phase Phenotype Phosphopeptides Phosphorylation Phosphorylation Site Phosphotransferases Play Process Protein Binding Protein Kinase Proteins Proteomics RNA Splicing Reagent Recruitment Activity Regulation Relative (related person)Resistance Role Saccharomyces cerevisiae Series Serine Set protein Signal Transduction Signal Transduction Pathway Sister Chromatid Site Stable Isotope Labeling Stress Structure Students Temperature Tern Trypsin Work Yeasts arginyllysine base cell cycle genetics crosslink daughter cell dosage helicase hydroxyurea imidazole-4-acetic acid in vivo inorganic phosphate interest mutant novel numb protein prevent protein function ras-Related G-Proteins repaired research study response sensor spindle pole body yeast protein

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Our lab has been focused on how cells sense and respond to DNA damage. We have been very active n elucidating the structures sensed by the DNA damage response sensors. Through work in both yeast and mammals we have established an outline of the signal transduction pathway that is activated in response to DNA damage. This pathway consists of a protein kinase cascade. We have been very interested in understanding how the DNA damage response controls various aspects of cell cycle regulation and have therefore studied the cell cycle as well. In order to understand how the DNA damage response accomplishes its goals, it is imperative we identify the substrates of the kinases activated in response to DNA damage and elucidate the function of these substrates.

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