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https://www.readbyqxmd.com/read/25121932/conditional-inactivation-of-upstream-binding-factor-reveals-its-epigenetic-functions-and-the-existence-of-a-somatic-nucleolar-precursor-body
#1
Nourdine Hamdane, Victor Y Stefanovsky, Michel G Tremblay, Attila Németh, Eric Paquet, Frédéric Lessard, Elaine Sanij, Ross Hannan, Tom Moss
Upstream Binding Factor (UBF) is a unique multi-HMGB-box protein first identified as a co-factor in RNA polymerase I (RPI/PolI) transcription. However, its poor DNA sequence selectivity and its ability to generate nucleosome-like nucleoprotein complexes suggest a more generalized role in chromatin structure. We previously showed that extensive depletion of UBF reduced the number of actively transcribed ribosomal RNA (rRNA) genes, but had little effect on rRNA synthesis rates or cell proliferation, leaving open the question of its requirement for RPI transcription...
August 2014: PLoS Genetics
https://www.readbyqxmd.com/read/21098478/rna-polymerase-1-driven-transcription-as-a-mediator-of-bdnf-induced-neurite-outgrowth
#2
Cynthia Gomes, Scott C Smith, Mark N Youssef, Jing-Juan Zheng, Theo Hagg, Michal Hetman
Neurite outgrowth is essential for development of the nervous system. Neurotrophins including BDNF are among extracellular signals that regulate neurite outgrowth. The ERK1/2 pathway contributes to intracellular signaling networks transducing the pro-neuritic effects of BDNF. In the nucleolus, RNA polymerase-1 (Pol1)-mediated transcription regulates ribosomal biogenesis, enabling cellular protein synthesis and growth. Hence, we tested the possibility that Pol1 is an effector for pro-neuritic signals such as BDNF...
February 11, 2011: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/10610177/a-ra-dependent-tumour-growth-suppressive-transcription-complex-is-the-target-of-the-pml-raralpha-and-t18-oncoproteins
#3
S Zhong, L Delva, C Rachez, C Cenciarelli, D Gandini, H Zhang, S Kalantry, L P Freedman, P P Pandolfi
PML and Tif1a are fused to RARA and Braf, respectively, resulting in the production of PML-RARalpha and Tif1alpha-B-Raf (T18) oncoproteins. Here we show that PML, Tif1alpha and RXRalpha/RARalpha function together in a transcription complex that is dependent on retinoic acid (RA). We found that PML acts as a ligand-dependent coactivator of RXRalpha/RARalpha. PML interacts with Tif1alpha and CBP. In Pml-/- cells, the RA-dependent induction of genes such as RARB2 and the ability of Tif1alpha and CBP to act as transcriptional coactivators on RA are impaired...
November 1999: Nature Genetics
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