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Transcription factor

About: Transcription factor is a research topic. Over the lifetime, 82881 publications have been published within this topic receiving 5400448 citations. The topic is also known as: transcription factors.


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Journal ArticleDOI
TL;DR: It is suggested that Sp3 is an inhibitory member of the Sp family, and neither the glutamine‐rich domains A and B nor the D domain of Sp1 can be replaced by the homologous regions of Sp3.
Abstract: Sp1, Sp3 (SPR-2) and Sp4 (SPR-1) are human sequence-specific DNA binding proteins with very similar structural features In this report, we have analyzed Sp3 in direct comparison with Sp1 We have raised antibodies against both Sp1 and Sp3, and show that Sp3 protein, like Sp1, is expressed in various cell lines Co-transfection experiments in different mammalian cell lines reveal that in contrast to Sp1 and Sp4, Sp3 is not able to activate several Sp1 responsive promoters In addition, Sp3 also fails to activate reporter constructs in Drosophila SL2 cells lacking endogenous Sp factors Instead, we find that Sp3 represses Sp1-mediated activation in a linear dose-dependent manner A mutant of Sp3 lacking the DNA binding domain does not affect activation by Sp1, suggesting that the inhibition is most likely due to the competition with Sp1 for their common binding sites To determine if any structurally similar domain of Sp3 is able to replace partially homologous domains of Sp1, we have generated chimeric proteins and tested their activation characteristics in gene transfer experiments It appears that neither the glutamine-rich domains A and B nor the D domain of Sp1 can be replaced by the homologous regions of Sp3 Our results suggest that Sp3 is an inhibitory member of the Sp family

690 citations

Journal ArticleDOI
20 Feb 2009-Science
TL;DR: It is shown that human HSF1 is inducibly acetylated at a critical residue that negatively regulates DNA binding activity and establishes a role for SIRT1 in protein homeostasis and the HSR.
Abstract: Heat shock factor 1 (HSF1) is essential for protecting cells from protein-damaging stress associated with misfolded proteins and regulates the insulin-signaling pathway and aging. Here, we show that human HSF1 is inducibly acetylated at a critical residue that negatively regulates DNA binding activity. Activation of the deacetylase and longevity factor SIRT1 prolonged HSF1 binding to the heat shock promoter Hsp70 by maintaining HSF1 in a deacetylated, DNA–binding competent state. Conversely, down-regulation of SIRT1 accelerated the attenuation of the heat shock response (HSR) and release of HSF1 from its cognate promoter elements. These results provide a mechanistic basis for the requirement of HSF1 in the regulation of life span and establish a role for SIRT1 in protein homeostasis and the HSR.

690 citations

Journal ArticleDOI
03 Jul 2013-Cell
TL;DR: It is demonstrated that non-CSCs of human basal breast cancers are plastic cell populations that readily switch from a non- CSC to CSC state, and this findings support a dynamic model in which interconversions between low and high tumorigenic states occur frequently, thereby increasing tumorigenics and malignant potential.

690 citations

Journal ArticleDOI
TL;DR: This work not only discovered new transcription regulatory components in the signaling network of SAR but also demonstrated that functional studies of large gene families have to take into consideration sequence similarity as well as the expression patterns of the candidates.
Abstract: Many biological processes are controlled by intricate networks of transcriptional regulators. With the development of microarray technology, transcriptional changes can be examined at the whole-genome level. However, such analysis often lacks information on the hierarchical relationship between components of a given system. Systemic acquired resistance (SAR) is an inducible plant defense response involving a cascade of transcriptional events induced by salicylic acid through the transcription cofactor NPR1. To identify additional regulatory nodes in the SAR network, we performed microarray analysis on Arabidopsis plants expressing the NPR1-GR (glucocorticoid receptor) fusion protein. Since nuclear translocation of NPR1-GR requires dexamethasone, we were able to control NPR1-dependent transcription and identify direct transcriptional targets of NPR1. We show that NPR1 directly upregulates the expression of eight WRKY transcription factor genes. This large family of 74 transcription factors has been implicated in various defense responses, but no specific WRKY factor has been placed in the SAR network. Identification of NPR1-regulated WRKY factors allowed us to perform in-depth genetic analysis on a small number of WRKY factors and test well-defined phenotypes of single and double mutants associated with NPR1. Among these WRKY factors we found both positive and negative regulators of SAR. This genomics-directed approach unambiguously positioned five WRKY factors in the complex transcriptional regulatory network of SAR. Our work not only discovered new transcription regulatory components in the signaling network of SAR but also demonstrated that functional studies of large gene families have to take into consideration sequence similarity as well as the expression patterns of the candidates.

690 citations

Journal ArticleDOI
28 Jun 1996-Cell
TL;DR: The proto-oncogene c-maf, a basic region/leucine zipper transcription factor, controls tissue-specific expression of IL-4 in Th1 cells, B cells, and nonlymphoid cells and acts in synergy with the nuclear factor of activated T cells (NF-ATp) to initiate endogeneous IL- 4 production by B cells.

689 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20234,678
20226,545
20213,663
20203,530
20193,362
20183,288