LCD1/YDR499W Literature Guide Help

Other names published for LCD1: DDC2, PIE1, YDR499W

LCD1 - Genetic Interactions (13)

ReferenceOther Genes Addressed
Douglas AC, et al.  (2012) Functional analysis with a barcoder yeast gene overexpression system. G3 (Bethesda) 2(10):1279-89
Manfrini N, et al.  (2012) G(1)/S and G(2)/M cyclin-dependent kinase activities commit cells to death in the absence of the S-phase checkpoint. Mol Cell Biol 32(24):4971-85
Refolio E, et al.  (2011) The Ddc2/ATRIP checkpoint protein monitors meiotic recombination intermediates. J Cell Sci 124(Pt 14):2488-500
Baldo V, et al.  (2008) Dominant TEL1-hy mutations compensate for Mec1 lack of functions in the DNA damage response. Mol Cell Biol 28(1):358-75
Bonilla CY, et al.  (2008) Colocalization of sensors is sufficient to activate the DNA damage checkpoint in the absence of damage. Mol Cell 30(3):267-76
Choi DH, et al.  (2008) The Mutation of a Novel Saccharomyces cerevisiae SRL4 Gene Rescues the Lethality of rad53 and lcd1 Mutations by Modulating dNTP Levels. J Microbiol 46(1):75-80
Mordes DA, et al.  (2008) Dpb11 activates the Mec1-Ddc2 complex. Proc Natl Acad Sci U S A 105(48):18730-4
Grandin N and Charbonneau M  (2007) Control of the yeast telomeric senescence survival pathways of recombination by the Mec1 and Mec3 DNA damage sensors and RPA. Nucleic Acids Res 35(3):822-38
Nakada D, et al.  (2005) Role of the C terminus of Mec1 checkpoint kinase in its localization to sites of DNA damage. Mol Biol Cell 16(11):5227-35
Wysocki R, et al.  (2005) Role of Dot1-dependent histone H3 methylation in G1 and S phase DNA damage checkpoint functions of Rad9. Mol Cell Biol 25(19):8430-43
Lee SJ, et al.  (2004) A Ddc2-Rad53 fusion protein can bypass the requirements for RAD9 and MRC1 in Rad53 activation. Mol Biol Cell 15(12):5443-55
Pan X, et al.  (2004) A robust toolkit for functional profiling of the yeast genome. Mol Cell 16(3):487-96
Clerici M, et al.  (2001) Hyperactivation of the yeast DNA damage checkpoint by TEL1 and DDC2 overexpression. EMBO J 20(22):6485-98