about
The interaction between Myc and Miz1 is required to antagonize TGFbeta-dependent autocrine signaling during lymphoma formation and maintenanceDisturbance of tumor necrosis factor alpha-mediated beta interferon signaling in cervical carcinoma cells.Sustained regression of tumors upon MYC inactivation requires p53 or thrombospondin-1 to reverse the angiogenic switch.Lymphomas that recur after MYC suppression continue to exhibit oncogene addiction.Cellular senescence is an important mechanism of tumor regression upon c-Myc inactivationMYC as a regulator of ribosome biogenesis and protein synthesis.MYC-Master Regulator of the Cancer Epigenome and Transcriptome.p19ARF is a critical mediator of both cellular senescence and an innate immune response associated with MYC inactivation in mouse model of acute leukemia.High throughput automated chromatin immunoprecipitation as a platform for drug screening and antibody validation.TGFβ-dependent gene expression shows that senescence correlates with abortive differentiation along several lineages in Myc-induced lymphomas.Ectopic expression of nonliganded retinoic acid receptor beta abrogates AP-1 activity by selective degradation of c-Jun in cervical carcinoma cells.DNMT3B overexpression contributes to aberrant DNA methylation and MYC-driven tumor maintenance in T-ALL and Burkitt's lymphoma.Loss of net as repressor leads to constitutive increased c-fos transcription in cervical cancer cells.Myc and a Cdk2 senescence switch.Targeting the MYC Oncogene in Burkitt Lymphoma through HSP90 InhibitionIndispensable role of the Ubiquitin-fold modifier 1-specific E3 ligase in maintaining intestinal homeostasis and controlling gut inflammation
P50
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P50
name
Jan van Riggelen
@en
type
label
Jan van Riggelen
@en
prefLabel
Jan van Riggelen
@en