The ARF tumor suppressor inhibits BCL6-mediated transcriptional repression

ARF antagonizes the ability of Miz-1 to inhibit p53-mediated transactivation

“…Over-expressed 3 Â Flag-labeled Miz-1 and ARF in H1299 and purified them first with anti-Flag M2 agarose affinity gel (Sigma), and followed by addition of excess of free 3 Â Flag peptide (Sigma) to release 3 Â Flag-ARF or 3 Â Flag-Miz-1 into supernatant. Role of Miz-1 in ARF-p53 pathway L Miao et al interaction with other proteins (Suzuki et al, 2005;Wanzel et al, 2005). It is well known that p14ARF is able to activate p53-regulated transcription, and in this study, we show that Miz-1 represses the transcriptional activity of p53, indicating that Miz-1 may antagonize the function of p14ARF in activating p53-mediated transcription.…”

p14ARFis capable of promoting HIV-1 Tat degradation

“…Examples include E2F, Myc, as well as other transcription factors, including the forkhead FOXM1B, BCL6, p63, HIF-1a. [9][10][11][12][13][14][15][16][17][18][19] However, the molecular mechanism underlying the repressor activity of ARF remains largely unknown. It has been shown that ARF-induced sumoylation observed for some ARF-interacting proteins as WRN helicase, Hdm2, E2F-1, HIF-1a TBP-1, p120E4F, 24,25 might be a mechanism for ARF action through a common modification of different binding proteins.…”

“…Similarly, ARF antagonizes the activities of other transcription factors, including the forkhead box (Fox) family member FOXM1B, 16 B-cell lymphoma 6 (BCL6), p63 and HIF-1a. [17][18][19] In this report, we have analyzed the role of ARF in controlling transactivation ability of the HIV-1 Tat protein. Tat functions through binding to a short leader RNA sequences (TAR) whereby regulates transcription from the HIV-1 long terminal repeat (LTR) by recruiting coactivator complexes, such as P-TEFb, to mediate hyperphosphorylation of RNAPII CTD and stimulates transcription elongation.…”

Mutational profile and prognostic significance of TP53 in diffuse large B-cell lymphoma patients treated with R-CHOP: report from an International DLBCL Rituximab-CHOP Consortium Program Study

“…p16 INK4A can cause cell-cycle arrest by inhibiting CDK4; p14 ARF sequesters the p53-negative regulator MDM2, thereby enhancing p53 level and activity, or induces cell-cycle arrest and apoptosis by p53-independent pathways. p14 ARF also inhibits the function of BCL-6, 46 which is expressed in B-cell germinal centers and activated in a subset of lymphomas. 44 The repression of CDKN2A by p53 has also been reported in a cell line study, 47 and might provide negative feedback to the TP53 pathway.…”