scholarly journals The site of HIV-1 integration in the human genome determines basal transcriptional activity and response to Tat transactivation

2001 ◽  
Vol 20 (7) ◽  
pp. 1726-1738 ◽  
Author(s):  
A. Jordan
Keyword(s):  
Human Genome ◽  
Transcriptional Activity ◽  
Basal Transcriptional Activity ◽  
Hiv 1

scholarly journals cis-acting sequences located downstream of the human immunodeficiency virus type 1 promoter affect its chromatin structure and transcriptional activity.

1996 ◽  
Vol 16 (6) ◽  
pp. 2958-2966 ◽  
Author(s):  
A el Kharroubi ◽  
M A Martin
Keyword(s):  
Human Immunodeficiency Virus ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Chromatin Structure ◽  
Transcriptional Activity ◽  
Regulatory Sequences ◽  
Immunodeficiency Virus ◽  
Basal Transcriptional Activity ◽  
Hiv 1

We have examined the roles of AP-1, AP-3-like, DBF1, and Sp1 binding sites, which are located downstream of the human immunodeficiency virus type 1 (HIV-1) promoter, in regulating basal transcriptional activity directed by the integrated viral long terminal repeat (LTR). Point mutations affecting all four of these elements functionally inactivated the HIV-1 LTR when it was constrained in a chromatin configuration. Analyses of the chromatin structures of the transcriptionally active wild-type and inactive mutated HIV-1 promoters revealed several differences. In the active promoter, the 3' half of the U3 region, including the basal promoter, the enhancer, and the putative upstream regulatory sequences are situated within a nuclease-hypersensitive region. However, the far upstream U3 region appears to be packaged into a nuclease-resistant nucleosomal structure, whereas the R, U5, and gag leader sequences are associated with a region of altered chromatin that is sensitive to restriction endonucleases. In the inactive template, only the basal promoter and enhancer element remain sensitive to nucleases, and the adjacent upstream and downstream regions are incorporated into nuclease-resistant nucleosomal structures. Taken together, these results indicate that the chromatin structure of the integrated HIV-1 LTR plays a critical role in modulating basal transcriptional activity.

scholarly journals NK-cell activation is associated with increased HIV transcriptional activity following allogeneic hematopoietic cell transplantation

2018 ◽  
Vol 2 (12) ◽  
pp. 1412-1416
Author(s):  
Louise E. Hogan ◽  
Christian Körner ◽  
Kristen Hobbs ◽  
Camille R. Simoneau ◽  
Cassandra Thanh ◽  
...  
Keyword(s):  
Cell Death ◽  
Transcriptional Activity ◽  
Cell Activation ◽  
Hematopoietic Cell Transplantation ◽  
Nk Cell ◽  
Killer Cell ◽  
Graft Versus Host ◽  
Key Points ◽  
Hiv 1

Key Points Graft-versus-host effects may lead to HIV-1 reactivation and cell death of infected pre-HCT CD4+ T cells. Natural killer cell activation correlates with in vitro HIV-1 transcriptional activity in the setting of HCT.

scholarly journals Regulation of the Mechanism ofTWIST1Transcription by BHLHE40 and BHLHE41 in Cancer Cells

2015 ◽  
Vol 35 (24) ◽  
pp. 4096-4109 ◽  
Author(s):  
Kazuo Asanoma ◽  
Ge Liu ◽  
Takako Yamane ◽  
Yoko Miyanari ◽  
Tomoka Takao ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Invasion ◽  
Transcriptional Activity ◽  
Epithelial To Mesenchymal Transition ◽  
Tumor Cell Invasion ◽  
Dependent Manner ◽  
Promoter Regions ◽  
Mesenchymal Transition ◽  
Basal Transcriptional Activity

BHLHE40 and BHLHE41 (BHLHE40/41) are basic helix-loop-helix type transcription factors that play key roles in multiple cell behaviors. BHLHE40/41 were recently shown to be involved in an epithelial-to-mesenchymal transition (EMT). However, the precise mechanism of EMT control by BHLHE40/41 remains unclear. In the present study, we demonstrated that BHLHE40/41 expression was controlled in a pathological stage-dependent manner in human endometrial cancer (HEC). Ourin vitroassays showed that BHLHE40/41 suppressed tumor cell invasion. BHLHE40/41 also suppressed the transcription of the EMT effectorsSNAI1,SNAI2, andTWIST1. We identified the critical promoter regions ofTWIST1for its basal transcriptional activity. We elucidated that the transcription factor SP1 was involved in the basal transcriptional activity ofTWIST1and that BHLHE40/41 competed with SP1 for DNA binding to regulate gene transcription. This study is the first to report the detailed functions of BHLHE40 and BHLHE41 in the suppression of EMT effectorsin vitro. Our results suggest that BHLHE40/41 suppress tumor cell invasion by inhibiting EMT in tumor cells. We propose that BHLHE40/41 are promising markers to predict the aggressiveness of each HEC case and that molecular targeting strategies involving BHLHE40/41 and SP1 may effectively regulate HEC progression.

scholarly journals The G1 Cyclin Cln3 Promotes Cell Cycle Entry via the Transcription Factor Swi6

2002 ◽  
Vol 22 (12) ◽  
pp. 4402-4418 ◽  
Author(s):  
Herman Wijnen ◽  
Allison Landman ◽  
Bruce Futcher
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Transcriptional Activity ◽  
Leucine Zipper ◽  
Stable Complex ◽  
Amino Terminus ◽  
Cyclin Dependent Kinase ◽  
Cell Cycle Entry ◽  
Basal Transcriptional Activity ◽  
Commitment To Cell Division

ABSTRACT In Saccharomyces cerevisiae (budding yeast), commitment to cell division in late G1 is promoted by the G1 cyclin Cln3 and its associated cyclin-dependent kinase, Cdc28. We show here that all known aspects of the function of Cln3 in G1 phase, including control of cell size, pheromone sensitivity, cell cycle progress, and transcription, require the protein Swi6. Swi6 is a component of two related transcription factors, SBF and MBF, which are known to regulate many genes at the G1-S transition. The Cln3-Cdc28 complex somehow activates SBF and MBF, but there was no evidence for direct phosphorylation of SBF/MBF by Cln3-Cdc28 or for a stable complex between SBF/MBF and Cln3-Cdc28. The activation also does not depend on the ability of Cln3 to activate transcription when artificially recruited directly to a promoter. The amino terminus and the leucine zipper of Swi6 are important for the ability of Swi6 to respond to Cln3 but are not essential for the basal transcriptional activity of Swi6. Cln3-Cdc28 may activate SBF and MBF indirectly, perhaps by phosphorylating some intermediary protein.

scholarly journals Nucleolin stabilizes G-quadruplex structures folded by the LTR promoter and silences HIV-1 viral transcription

2015 ◽  
Vol 43 (18) ◽  
pp. 8884-8897 ◽  
Author(s):  
Elena Tosoni ◽  
Ilaria Frasson ◽  
Matteo Scalabrin ◽  
Rosalba Perrone ◽  
Elena Butovskaya ◽  
...  
Keyword(s):  
Transcriptional Activity ◽  
Cellular Protein ◽  
Spectrometric Analysis ◽  
Viral Transcription ◽  
Mobility Shift ◽  
Binding Preference ◽  
G Quadruplex ◽  
Mobility Shift Assay ◽  
Ltr Promoter ◽  
Hiv 1

Abstract Folding of the LTR promoter into dynamic G-quadruplex conformations has been shown to suppress its transcriptional activity in HIV-1. Here we sought to identify the proteins that control the folding of this region of proviral genome by inducing/stabilizing G-quadruplex structures. The implementation of electrophorethic mobility shift assay and pull-down experiments coupled with mass spectrometric analysis revealed that the cellular protein nucleolin is able to specifically recognize G-quadruplex structures present in the LTR promoter. Nucleolin recognized with high affinity and specificity the majority, but not all the possible G-quadruplexes folded by this sequence. In addition, it displayed greater binding preference towards DNA than RNA G-quadruplexes, thus indicating two levels of selectivity based on the sequence and nature of the target. The interaction translated into stabilization of the LTR G-quadruplexes and increased promoter silencing activity; in contrast, disruption of nucleolin binding in cells by both siRNAs and a nucleolin binding aptamer greatly increased LTR promoter activity. These data indicate that nucleolin possesses a specific and regulated activity toward the HIV-1 LTR promoter, which is mediated by G-quadruplexes. These observations provide new essential insights into viral transcription and a possible low mutagenic target for antiretroviral therapy.

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