Implementation issues of diffusion-based molecular communications receivers based on transcriptional elements

2021 ◽  
pp. 103160
Author(s):  
Mauro Femminella ◽  
Gianluca Reali
Keyword(s):  
Transcriptional Elements

Cloning of the Rat Tissue Factor cDNA and Promoter: Identification of a Serum-response Region

1996 ◽  
Vol 76 (05) ◽  
pp. 697-702 ◽  
Author(s):  
Olivier Taby ◽  
Claire-Lise Rosenfield ◽  
Vladimir Bogdanov ◽  
Yale Nemerson ◽  
Mark B Taubman
Keyword(s):  
Tissue Factor ◽  
General Structure ◽  
Amino Acid Sequences ◽  
Proximal Promoter ◽  
Striking Similarity ◽  
Upstream Sequence ◽  
Tf Gene ◽  
Rat Tissue ◽  
High Degree ◽  
Transcriptional Elements

SummaryTissue factor (TF) initiates coagulation and its expression in vascular smooth muscle cells (VSMC) likely plays a role in the propagation of arterial thrombosis. We report cloning the cDNA and proximal promoter region of the rat TF gene. While maintaining the general structure and organization of the TF molecule, there is a surprising divergence (≈ 18%) between the derived amino acid sequences of the rat and mouse TF. In contrast, there is striking similarity (90%) in the 5’ untranslated regions. High levels of basal promoter activity were seen in rat VSMC with constructs containing 106 bp of sequence downstream from the putative transcription start site and 426 to 103 bp of upstream sequence. Deletion of the sequence from −103 to −79, containing a single SP1 site, removed virtually all of the basal and serum-induced activity. Removal of the NFkB site or two additional upstream SP1 sites had little effect on serum responsiveness. Removal of the 5’ untranslated region abolished most of the basal activity of the TF promoter, suggesting that its high degree of conservation may be due to the presence of transcriptional elements critical for TF expression in rodent VSMC.

Positive and negative transcriptional elements of the human type IV collagenase gene

1990 ◽  
Vol 10 (12) ◽  
pp. 6524-6532
Author(s):  
S M Frisch ◽  
J H Morisaki
Keyword(s):  
Core Promoter ◽  
Type Iv Collagenase ◽  
Mobility Shift ◽  
Specific Expression ◽  
Enhancer Element ◽  
Type Iv ◽  
Dnase I Footprinting ◽  
Gel Mobility Shift ◽  
Transcriptional Elements ◽  
Mcf 7

Proteolysis by type IV collagenase (T4) has been implicated in the process of tumor metastasis. The T4 gene is expressed in fibroblasts, but not in normal epithelial cells, and its expression is specifically repressed by the E1A oncogene of adenovirus. We present an investigation of the transcriptional elements responsible for basal, E1A-repressible, and tissue-specific expression. 5'-Deletion analysis, DNase I footprinting, and gel mobility shift assays revealed a strong, E1A-repressible enhancer element, r2, located about 1,650 bp upstream of the start site. This enhancer bound a protein with binding specificity very similar to that of the transcription factor AP-2. A potent silencer sequence was found 2 to 5 bp downstream of this enhancer. The silencer repressed transcription from either r2 or AP-1 enhancer elements and in the context of either type IV collagenase or thymidine kinase (tk) gene core promoters; enhancerless transcription from the latter core promoter was also repressed. Comprising the silencer were two contiguous, autonomously functioning silencer elements. Negative regulation of T4 transcription by at least two factors was demonstrated. mcf-7 proteins specifically binding both elements were detected by gel mobility shift assays; a protein of approximately 185 kDa that bound to one of these elements was detected by DNA-protein cross-linking. The silencer repressed transcription, in an r2 enhancer-tk promoter context, much more efficiently in T4-nonproducing cells (mcf-7 or HeLa) than in T4-producing cells (HT1080), suggesting that cell type-specific silencing may contribute to the regulation of this gene.

scholarly journals p300/CBP-associated factor (P/CAF) interacts with nuclear respiratory factor-1 to regulate the UDP-N-acetyl-alpha-d-galactosamine: polypeptide N-acetylgalactosaminyltransferase-3 gene

2003 ◽  
Vol 373 (3) ◽  
pp. 713-722 ◽  
Author(s):  
Hiroto IZUMI ◽  
Ryo OHTA ◽  
Gunji NAGATANI ◽  
Tomoko ISE ◽  
Yoshifumi NAKAYAMA ◽  
...  
Keyword(s):  
Sodium Butyrate ◽  
Nuclear Extract ◽  
Binding Motif ◽  
Induced Expression ◽  
Associated Factor ◽  
Nuclear Respiratory Factor ◽  
Nuclear Respiratory Factor 1 ◽  
Butyrate Treatment ◽  
Transcriptional Elements ◽  
Mcf 7

We demonstrated recently that expression of the UDP-N-acetyl-α-d-galactosamine: polypeptide N-acetylgalactosaminyltrans-ferase-3 (GalNAc-T3) gene is restricted to epithelial glands [Nomoto, Izumi, Ise, Kato, Takano, Nagatani, Shibao, Ohta, Imamura, Kuwano, Matsuo, Yamada, Itoh and Kohno (1999) Cancer Res. 59, 6214–6222]. In the present study, we show that sodium butyrate treatment of human breast cancer MCF-7 cells transcriptionally activates the GalNAc-T3 gene. Transient transfection of plasmids containing a reporter gene under the control of GalNAc-T3 indicated that several transcriptional elements are involved in response to sodium butyrate, with the nuclear respiratory factor-1 (NRF-1)-binding motif located between −88 and −77nt being the most important. Incubation of a labelled probe encompassing the NRF-1-binding motif with a nuclear extract of sodium butyrate-treated MCF-7 cells yielded a higher level of specific DNA–protein complex versus controls. Flag-tagged NRF-1 expressed in MCF-7 cells can bind to the NRF-1-binding motif of the GalNAc-T3 promoter. Nuclear content of NRF-1 remained constant in MCF-7 cells treated with or without sodium butyrate. Moreover, NRF-1 interacts with and is acetylated by p300/CBP-associated factor (P/CAF). Acetylation of NRF-1 enhances DNA binding. Co-transfection of the GalNAc-T3 reporter plasmid with either NRF-1 or P/CAF expression plasmid resulted in the activation of the GalNAc-T3 promoter. These results indicate a correlation between acetylation of NRF-1 by P/CAF and the butyrate-induced expression of the GalNAc-T3 gene. Additionally, induced expression of P/CAF may be a component of the adenocarcinoma differentiation process.

Role of Transcriptional Elements in Activating Origins of Replication

1992 ◽  
pp. 129-138
Author(s):  
Zong-Sheng Guo ◽  
Maria Wiekowski ◽  
Sadhan Majumder ◽  
Miriam Miranda ◽  
Melvin L. DePamphilis
Keyword(s):  
Origins Of Replication ◽  
Transcriptional Elements

scholarly journals Insulated transcriptional elements enable precise design of genetic circuits

2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Yeqing Zong ◽  
Haoqian M. Zhang ◽  
Cheng Lyu ◽  
Xiangyu Ji ◽  
Junran Hou ◽  
...  
Keyword(s):  
Genetic Circuits ◽  
Transcriptional Elements

scholarly journals S-S Synapsis during Class Switch Recombination Is Promoted by Distantly Located Transcriptional Elements and Activation-Induced Deaminase

Immunity ◽  
2007 ◽  
Vol 27 (5) ◽  
pp. 711-722 ◽  
Author(s):  
Robert Wuerffel ◽  
Lili Wang ◽  
Fernando Grigera ◽  
John Manis ◽  
Erik Selsing ◽  
...  
Keyword(s):  
Class Switch Recombination ◽  
Class Switch ◽  
Activation Induced Deaminase ◽  
Transcriptional Elements

scholarly journals Self-Inactivating Alpharetroviral Vectors with a Split-Packaging Design

2010 ◽  
Vol 84 (13) ◽  
pp. 6626-6635 ◽  
Author(s):  
Julia D. Suerth ◽  
Tobias Maetzig ◽  
Melanie Galla ◽  
Christopher Baum ◽  
Axel Schambach
Keyword(s):  
Mammalian Cells ◽  
High Titer ◽  
Viral Proteins ◽  
Retroviral Vectors ◽  
Long Terminal Repeats ◽  
Rous Sarcoma ◽  
Vector Systems ◽  
Cellular Genes ◽  
Integration Sites ◽  
Transcriptional Elements

ABSTRACT Accidental insertional activation of proto-oncogenes and potential vector mobilization pose serious challenges for human gene therapy using retroviral vectors. Comparative analyses of integration sites of different retroviral vectors have elucidated distinct target site preferences, highlighting vectors based on the alpharetrovirus Rous sarcoma virus (RSV) as those with the most neutral integration spectrum. To date, alpharetroviral vector systems are based mainly on single constructs containing viral coding sequences and intact long terminal repeats (LTR). Even though they are considered to be replication incompetent in mammalian cells, the transfer of intact viral genomes is unacceptable for clinical applications, due to the risk of vector mobilization and the potentially immunogenic expression of viral proteins, which we minimized by setting up a split-packaging system expressing the necessary viral proteins in trans. Moreover, intact LTRs containing transcriptional elements are capable of activating cellular genes. By removing most of these transcriptional elements, we were able to generate a self-inactivating (SIN) alpharetroviral vector, whose LTR transcriptional activity is strongly reduced and whose transgene expression can be driven by an internal promoter of choice. Codon optimization of the alpharetroviral Gag/Pol expression construct and further optimization steps allowed the production of high-titer self-inactivating vector particles in human cells. We demonstrate proof of principle for the versatility of alpharetroviral SIN vectors for the genetic modification of murine and human hematopoietic cells at a low multiplicity of infection.

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