Drosophila DBT Autophosphorylation of Its C-Terminal Domain Antagonized by SPAG and Involved in UV-Induced Apoptosis

No abstract is available for this paper.

• Publication year

  2015

• Venue

  Molecular and Cellular Biology

• Publication date

  2015-05-04

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1128/MCB.00390-15PMID 25939385PMCID PMC4475922
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Drosophila Spaghetti and Doubletime Link the Circadian Clock and Light to Caspases, Apoptosis and Tauopathy

  2015cited by this paper
• The role of casein kinase I in the Drosophila circadian clock.

  2015cited by this paper
• Drosophila Spag Is the Homolog of RNA Polymerase II-associated Protein 3 (RPAP3) and Recruits the Heat Shock Proteins 70 and 90 (Hsp70 and Hsp90) during the Assembly of Cellular Machineries* ♦

  2014cited by this paper
• Noncanonical FK506-binding protein BDBT binds DBT to enhance its circadian function and forms foci at night.

  2013cited by this paper
• Molecular genetic analysis of circadian timekeeping in Drosophila.

  2011influential reference
• IC261 induces cell cycle arrest and apoptosis of human cancer cells via CK1δ/ɛ and Wnt/β-catenin independent inhibition of mitotic spindle formation

  2011cited by this paper
• The Pih1-Tah1 Cochaperone Complex Inhibits Hsp90 Molecular Chaperone ATPase Activity*

  2010cited by this paper
• DOUBLETIME Plays a Noncatalytic Role To Mediate CLOCK Phosphorylation and Repress CLOCK-Dependent Transcription within the Drosophila Circadian Clock

  2009cited by this paper
• Drosophila and Vertebrate Casein Kinase Iδ Exhibits Evolutionary Conservation of Circadian Function

  2009cited by this paper
• Interactions between Casein Kinase Iε (CKIε) and Two Substrates from Disparate Signaling Pathways Reveal Mechanisms for Substrate-Kinase Specificity

  2009cited by this paper
• The genetics of mammalian circadian order and disorder: implications for physiology and disease

  2008cited by this paper
• The Hsp90 chaperone controls the biogenesis of L7Ae RNPs through conserved machinery

  2008cited by this paper
• Phosphoproteome analysis of Drosophila melanogaster embryos.

  2008cited by this paper
• PhosphoPep—a phosphoproteome resource for systems biology research in Drosophila Kc167 cells

  2007cited by this paper
• Drosophila DBT Lacking Protein Kinase Activity Produces Long-Period and Arrhythmic Circadian Behavioral and Molecular Rhythms

  2007cited by this paper
• The Drosophila Casein kinase Iε/δ Discs overgrown promotes cell survival via activation of DIAP1 expression

  2007cited by this paper
• The Drosophila casein kinase Iepsilon/delta Discs overgrown promotes cell survival via activation of DIAP1 expression.

  2007cited by this paper
• Balance between DBT/CKIepsilon kinase and protein phosphatase activities regulate phosphorylation and stability of Drosophila CLOCK protein.

  2006cited by this paper
• The circadian clock-containing photoreceptor cells in Xenopus laevis express several isoforms of casein kinase I.

  2005cited by this paper
• Functional consequences of a CKIδ mutation causing familial advanced sleep phase syndrome

  2005cited by this paper
• Proteomic Analysis of Oxidative Stress-resistant Cells

  2004cited by this paper
• Regulation of Casein Kinase Iϵ Activity by Wnt Signaling*

  2004cited by this paper
• Drosophila doubletime Mutations Which either Shorten or Lengthen the Period of Circadian Rhythms Decrease the Protein Kinase Activity of Casein Kinase I

  2004cited by this paper
• Mechanism of Regulation of Casein Kinase I Activity by Group I Metabotropic Glutamate Receptors*

  2002cited by this paper
• Time zones: a comparative genetics of circadian clocks

  2001cited by this paper
• Phosphorylation of period is influenced by cycling physical associations of double-time, period, and timeless in the Drosophila clock.

  2001cited by this paper
• The Drosophila double-timeS Mutation Delays the Nuclear Accumulation of period Protein and Affects the Feedback Regulation of period mRNA

  2001cited by this paper
• A TIMELESS-independent function for PERIOD proteins in the Drosophila clock.

  2000cited by this paper
• Positional syntenic cloning and functional characterization of the mammalian circadian mutation tau.

  2000cited by this paper
• Two Novel doubletime Mutants Alter Circadian Properties and Eliminate the Delay between RNA and Protein inDrosophila

  2000cited by this paper
• Identification of Inhibitory Autophosphorylation Sites in Casein Kinase I ε*

  1999cited by this paper
• The Drosophila clock gene double-time encodes a protein closely related to human casein kinase Iepsilon.

  1998cited by this paper
• double-time is a novel Drosophila clock gene that regulates PERIOD protein accumulation.

  1998cited by this paper
• The Drosophila Clock Gene double-time Encodes a Protein Closely Related to Human Casein Kinase Iε

  1998cited by this paper
• Regulation of the Drosophila protein timeless suggests a mechanism for resetting the circadian clock by light.

  1996cited by this paper
• Light-Induced Degradation of TIMELESS and Entrainment of the Drosophila Circadian Clock

  1996cited by this paper
• A light-entrainment mechanism for the Drosophila circadian clock

  1996cited by this paper
• Role of COOH-terminal Phosphorylation in the Regulation of Casein Kinase Iδ (*)

  1995cited by this paper
• Suppression of PERIOD protein abundance and circadian cycling by the Drosophila clock mutation timeless.

  1995cited by this paper
• Temporal phosphorylation of the Drosophila period protein.

  1994cited by this paper

• Evolution of casein kinase 1 and functional analysis of new doubletime mutants in Drosophila

  2022cites this paper
• Stability of selected reference genes in Sf9 cells treated with extrinsic apoptotic agents

  2019cites this paper
• Circadian Rhythm Neuropeptides in Drosophila: Signals for Normal Circadian Function and Circadian Neurodegenerative Disease

  2017cites this paper