Recruitment of TBP or TFIIB to a Promoter Proximal Position Leads to Stimulation of RNA Polymerase II Transcription without Activator Proteins bothin Vivoandin Vitro

Huh, Jun R.; Park, Jin Mo; Kim, Mijin; Carlson, Bradley A.; Hatfield, Dolph L.; Lee, Byeong Jae

doi:10.1006/bbrc.1999.0280

Cited by 13 publications

(6 citation statements)

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“…Although there is evidence for the regulation of reinitiation by some activators, many studies report that the addition of classical transcriptional activator proteins to an in vitro transcription assay causes transcriptional activation only if they are added before assembly of the preinitiation complex; that is, they modify the probability of the successful formation of such complexes. 3,14,15,[31][32][33][34][35][36][37][38][39][40][41] The cis-acting elements recognized by transcription factors are commonly grouped in the vicinity of proximal promoters or enhancers. As predicted from the in vitro actions of transcription factors, compound elements such as enhancers act to increase the probability of transcription in intact cells.…”

Section: Regulation Of Transcription: Probabilities Multiply!mentioning

confidence: 99%

Probability in transcriptional regulation and its implications for leukocyte differentiation and inducible gene expression

Hume

2000

Blood

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The phenotype of individual hematopoietic cells, like all other differentiated mammalian cells, is determined by selective transcription of a subset of the genes encoded within the genome. This overview summarizes the recent evidence that transcriptional regulation at the level of individual cells is best described in terms of the regulation of the probability of transcription rather than the rate. In this model, heterogeneous gene expression among populations of cells arises by chance, and the degree of heterogeneity is a function of the stability of the mRNA and protein products of individual genes. The probabilistic nature of transcriptional regulation provides one explanation for stochastic phenomena, such as stem cell lineage commitment, and monoallelic expression of inducible genes, such as lymphokines and cytokines.

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Section: Regulation Of Transcription: Probabilities Multiply!mentioning

confidence: 99%

Probability in transcriptional regulation and its implications for leukocyte differentiation and inducible gene expression

Hume

2000

Blood

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“…At the molecular level, gene expression is regulated by many core transcriptional complexes, such as TFIID, along with different cofactors [ 35 ]. Previous studies revealed TFIID as an integral component of the core transcriptional machinery for RNA polymerase II in mRNA-encoding genes [ 35 , 36 ], and demonstrated that it is assembled with TBP and multiple TAFs [ 37 ]. To date, many TAFs and several tissue-specific variants have been characterized [ 38 ].…”

Section: Discussionmentioning

confidence: 99%

Transcriptomic Analysis Reveals That Granulocyte Colony-Stimulating Factor Trigger a Novel Signaling Pathway (TAF9-P53-TRIAP1-CASP3) to Protect Retinal Ganglion Cells after Ischemic Optic Neuropathy

Tsai

Lin

Huang

et al. 2022

IJMS

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Optic nerve head (ONH) infarct can result in progressive retinal ganglion cell (RGC) death. The granulocyte colony-stimulating factor (GCSF) protects the RGC after ON infarct. However, protective mechanisms of the GCSF after ONH infarct are complex and remain unclear. To investigate the complex mechanisms involved, the transcriptome profiles of the GCSF-treated retinas were examined using microarray technology. The retinal mRNA samples on days 3 and 7 post rat anterior ischemic optic neuropathy (rAION) were analyzed by microarray and bioinformatics analyses. GCSF treatment influenced 3101 genes and 3332 genes on days 3 and 7 post rAION, respectively. ONH infarct led to changes in 702 and 179 genes on days 3 and 7 post rAION, respectively. After cluster analysis, the levels of TATA box-binding protein (TBP)-associated factor were significantly reduced after ONH infarct, but these significantly increased after GCSF treatment. The network analysis revealed that TBP associated factor 9 (TAF9) can bind to P53 to induce TP53-regulated inhibitor of apoptosis 1 (TRIAP1) expression. To evaluate the function of TAF9 in RGC apoptosis, GCSF plus TAF9 siRNA-treated rats were evaluated using retrograde labeling with FluoroGold assay, TUNEL assay, and Western blotting in an rAION model. The RGC densities in the GCSF plus TAF9 siRNA-treated rAION group were 1.95-fold (central retina) and 1.75-fold (midperipheral retina) lower than that in the GCSF-treated rAION group (p < 0.05). The number of apoptotic RGC in the GCSF plus TAF9 siRNA-treated group was threefold higher than that in the GCSF-treated group (p < 0.05). Treatment with TAF9 siRNA significantly reduced GCSF-induced TP53 and TRIAP1 expression by 2.4-fold and 4.7-fold, respectively, in the rAION model. Overexpression of TAF9 significantly reduced apoptotic RGC and CASP3 levels, and induced TP53 and TRIAP1 expression in the rAION model. Therefore, we have demonstrated that GCSF modulated a new pathway, TAF9-P53-TRIAP1-CASP3, to control RGC death and survival after ON infarct.

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“…At the molecular level, gene expression is regulated by many core transcriptional complexes, such as TFIID, along with different cofactors [36]. Previous studies revealed TFIID as an integral component of the core transcriptional machinery for RNA polymerase II at mRNA encoding genes [36,37] and demonstrated that it is assembled with TBP and multiple TAFs [38]. To date, many TAFs and several tissue-speci c variants are characterized [39].…”

Section: Discussionmentioning

confidence: 99%

Granulocyte Colony-Stimulating Factor-Induced TAF9 Modulates P53-TRIAP1-CASP3 Axis to Prevent Retinal Ganglion Cell Death after Optic Nerve Ischemia

Wen

Lin

Huang

et al. 2021

Preprint

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BackgroundOptic nerve head (ONH) infarct can result in progressive retinal ganglion cell (RGC) death. Some evidences indicated that the granulocyte colony-stimulating factor (GCSF) provides positive effects against ischemic damage on RGCs. However, protective mechanisms of the GCSF after ONH infarct are complex and remain unclear. MethodsTo investigate the complex mechanisms, the transcriptome profiles of the GCSF-treated retinas were examined using microarray technology. The retinal mRNA samples on days 3 and 7 post rat anterior ischemic optic neuropathy model (rAION) were analyzed by microarray and bioinformatics analyses. To evaluate the TAF9 function in RGC apoptosis, GCSF plus TAF9 siRNA-treated rats were evaluated using retrograde labeling with FluoroGold assay, TUNEL assay, and Western blotting in a rAION.ResultsGCSF treatment influenced 3101 genes and 3332 genes on days 3 and 7 post rAION, respectively. ONH infarct led to changes in 702 and 179 genes on days 3 and 7 post rAION, respectively. After cluster analysis, the TATA box-binding protein (TBP)-associated factor levels were significantly reduced after ONH infarct but significantly increased after GCSF treatment. The network analysis revealed that TBP associated factor 9 (TAF9) can bind to TP53 to induce TP53 regulated inhibitor of apoptosis 1 (TRIAP1) expression. The RGC density in the GCSF plus TAF9 siRNA-treated group was 1.95-fold (central retina) and 1.75-fold (midperipheral retina) lower than that in the GCSF-treated group (p < 0.05). The number of apoptotic RGC in the GCSF plus TAF9 siRNA-treated group is threefold higher than that in the GCSF-treated group (p < 0.05). Treatment with TAF9 siRNA significantly reduced GCSF-induced TP53 and TRIAP1 expression by 2.4-fold and 4.7-fold, respectively, in the rAION model. Overexpression of TAF9 significantly reduced apoptotic RGC and CASP3 levels and induced TP53 and TRIAP1 expression in the rAION model. ConclusionOur in vivo study is the first to report that GCSF is able to induce TAF9 expression to control RGC death and survival after ON infarct. Besides, the binding of TAF9 and TP53 is crucial to inhibit TP53 degradation and to modulate TRIAP1-CASP3 axis. Thus, we considered that TAF9 is a potential drug for patient with NAION.

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Recruitment of TBP or TFIIB to a Promoter Proximal Position Leads to Stimulation of RNA Polymerase II Transcription without Activator Proteins bothin Vivoandin Vitro

Cited by 13 publications

References 40 publications

Probability in transcriptional regulation and its implications for leukocyte differentiation and inducible gene expression

Probability in transcriptional regulation and its implications for leukocyte differentiation and inducible gene expression

Transcriptomic Analysis Reveals That Granulocyte Colony-Stimulating Factor Trigger a Novel Signaling Pathway (TAF9-P53-TRIAP1-CASP3) to Protect Retinal Ganglion Cells after Ischemic Optic Neuropathy

Granulocyte Colony-Stimulating Factor-Induced TAF9 Modulates P53-TRIAP1-CASP3 Axis to Prevent Retinal Ganglion Cell Death after Optic Nerve Ischemia

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