نتایج جستجو برای: basal core promoter double mutations
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background as most hbv-related acute-on-chronic liver failure (aclf) have concurrent cirrhosis, it is important to clarify the association of viral factors with aclf with or without cirrhosis. objectives the aim of this study was to analyze the association of hbv genotypes and mutations with aclf development underlying different chronic liver diseases. patients and methods eighty-seven aclf pat...
The core promoter of eukaryotic coding and non-coding genes that are transcribed by RNA polymerase II (RNAP II) is composed of DNA elements surrounding the transcription start site. These elements serve as the docking site of the basal transcription machinery and have an important role in determining the position and directing the rate of transcription initiation. This review summarizes the cur...
TFIID binds promoter DNA to recruit RNA polymerase II and other basal factors for transcription. Although the TATA-binding protein (TBP) subunit of TFIID is necessary and sufficient for in vitro transcription, the TBP-associated factor (TAF) subunits recognize downstream promoter elements, act as coactivators, and interact with nucleosomes. In yeast nuclear extracts, transcription induces stabl...
The basal core promoter (BCP) of hepatitis B virus (HBV) directs the transcription of both precore RNA and core RNA which code for e antigen (HBeAg) and core antigen, respectively. A double mutation in the BCP which converts nucleotide (nt) 1762 from A to T and nt 1764 from G to A is frequently observed in patients with chronic hepatitis B. We recently demonstrated that this double mutation pre...
While the minute virus of mice (MVM) P4 promoter, which drives the viral nonstructural genes, is highly active in the absence of viral proteins, P38, the capsid gene promoter, is strictly dependent on the viral nonstructural protein NS1. Once fully transactivated, however, P38 mediates twice the steady-state level of expression achieved by P4. In this report, we address the discrepancy between ...
To identify molecular factors regulating apo A-I production in vivo, we induced in transgenic mice the experimental nephrotic syndrome, which results in elevated levels of HDL cholesterol (HDL-C), plasma apo A-I, and hepatic apo A-I mRNA. Human (h) apo A-I transgenic mice with different length 5' flanking sequences (5.5 or 0.256 kb, the core promoter for hepatic-specific basal expression) were ...
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