about
Phosphorylation at serine 331 is required for Aurora B activation.Viral mutations enhance the Max binding properties of the vMyc b-HLH-LZ domain.DNA damage control: regulation and functions of checkpoint kinase 1Interactions of the DNA mismatch repair proteins MLH1 and MSH2 with c-MYC and MAXThe ATM-Chk2 and ATR-Chk1 pathways in DNA damage signaling and cancerFascin 1 is transiently expressed in mouse melanoblasts during development and promotes migration and proliferation.Akt/PKB suppresses DNA damage processing and checkpoint activation in late G2.Cancer therapy. Targeting the poison within.Sab (SH3BP5), a novel mitochondria-localized JNK-interacting protein.Molecular mechanism and biological functions of c-Jun N-terminal kinase signalling via the c-Jun transcription factor.Loss of autophagy causes a synthetic lethal deficiency in DNA repair.Lethal errors in checkpoint control--life without Chk1.Invasion of normal human fibroblasts induced by v-Fos is independent of proliferation, immortalization, and the tumor suppressors p16INK4a and p53.Analysing the DNA damage and replication checkpoints in DT40 cells.PARP inhibitor olaparib increases the oncolytic activity of dl922-947 in in vitro and in vivo model of anaplastic thyroid carcinomaATR-Chk1 signaling pathway and homologous recombinational repair protect cells from 5-fluorouracil cytotoxicity.v-Jun overrides the mitogen dependence of S-phase entry by deregulating retinoblastoma protein phosphorylation and E2F-pocket protein interactions as a consequence of enhanced cyclin E-cdk2 catalytic activity.Mutant p53 drives invasion by promoting integrin recycling.Chk1 C-terminal regulatory phosphorylation mediates checkpoint activation by de-repression of Chk1 catalytic activity.c-Jun-deficient cells undergo premature senescence as a result of spontaneous DNA damage accumulation.Centrifugal elutriation as a means of cell cycle phase separation and synchronisation.Chk1-dependent slowing of S-phase progression protects DT40 B-lymphoma cells against killing by the nucleoside analogue 5-fluorouracil.Analysis of the variations in proviral cytosine methylation that accompany transformation and morphological reversion in a line of Rous sarcoma virus-infected Rat-1 cellsAutophagy is critically required for DNA repair by homologous recombination.KA1-targeted regulatory domain mutations activate Chk1 in the absence of DNA damageTranscription activation by Myc and Max: flanking sequences target activation to a subset of CACGTG motifs in vivo.Inhibition of adipocyte differentiation by cMyc is not accompanied by alterations in cell cycle control.v-Jun represses c-jun proto-oncogene expression in vivo through a 12-O-tetradecanoylphorbol-13-acetate-responsive element in the proximal gene promoter.Mitogenesis by v-Src: fluctuations throughout G1 of classical immediate early AP-1 and mitogen-activated protein kinase responses that parallel the need for the oncoprotein.Stress-activated protein kinases bind directly to the delta domain of c-Jun in resting cells: implications for repression of c-Jun function.c-Myc inhibits myogenic differentiation and myoD expression by a mechanism which can be dissociated from cell transformation.Expression of integrated Rous sarcoma viruses: DNA rearrangements 5' to the provirus are common in transformed rat cells but not seen in infected but untransformed cellsChk1 regulates the density of active replication origins during the vertebrate S phase.Cell transformation by v-Jun deactivates ERK MAP kinase signalling.The v-Jun oncoprotein replaces p39 c-Jun as the predominant AP-1 constituent in ASV17-transformed fibroblasts: implications for SAPK/JNK-mediated signal transduction.Insulin-stimulated expression of c-fos, fra1 and c-jun accompanies the activation of the activator protein-1 (AP-1) transcriptional complex.Short-circuiting the cell cycle for cancer therapy.Properties of middle-repeat sequences in nuclear deoxyribonucleic acid from baby-hamster kidney cells (BHK-21/C13) [proceedings]Estrogen receptor activation function 2 (AF-2) is essential for hormone-dependent transactivation and cell transformation induced by a v-Jun DNA binding domain-estrogen receptor chimera.Microarray analysis identifies Autotaxin, a tumour cell motility and angiogenic factor with lysophospholipase D activity, as a specific target of cell transformation by v-Jun.
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description
researcher ORCID ID = 0000-0002-6338-0544
@en
name
David A Gillespie
@ast
David A Gillespie
@en
David A Gillespie
@nl
type
label
David A Gillespie
@ast
David A Gillespie
@en
David A Gillespie
@nl
prefLabel
David A Gillespie
@ast
David A Gillespie
@en
David A Gillespie
@nl
P108
P108
P21
P31
P496
0000-0002-6338-0544