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IRES sequences were first discovered in 1988 in the poliovirus (PV) and encephalomyocarditis virus (EMCV) RNA genomes in the laboratories of Nahum Sonenberg [1] and Eckard Wimmer, [2] respectively. They are described as distinct regions of RNA molecules that are able to recruit the eukaryotic ribosome to the mRNA.
HAV IRES, entero-/rhinovirus and cardio-/apthovirus IRES are all approximately 450 nt but differ greatly in their structures. A cardiovirus, EMCV, and an apthovirus, foot-and-mouth disease virus (FMDV) share about 50% identical IRES elements. HCV-like picornavirus IRES incorporates the most difference in IRES elements from the other three classes.
The c-sis internal ribosome entry site (IRES) is a RNA element found in the 5' UTR of the PDGF beta chain gene. The internal ribosome entry site contains three modules that can individually mediate internal ribosome entry. However, the full length sequence is required for maximal IRES activity.
This alternate mechanism relies on the direct binding of the 40S ribosomal subunit by the internal ribosome entry site (IRES) in the 5' UTR of HCV RNA. The HCV IRES adopts a complex structure, and may differ significantly from IRES elements identified in picornaviruses. A small number of eukaryotic mRNAs has been shown to be translated by ...
The RBS in prokaryotes is a region upstream of the start codon. This region of the mRNA has the consensus 5'-AGGAGG-3', also called the Shine-Dalgarno (SD) sequence. [1] The complementary sequence (CCUCCU), called the anti-Shine-Dalgarno (ASD) is contained in the 3’ end of the 16S region of the smaller (30S) ribosomal subunit.
The c-myc internal ribosome entry site (IRES) is an RNA element present in the 5' UTR of the mRNA of C-myc and allows cap-independent translation. The mammalian c-myc gene is a proto-oncogene which is required for cell proliferation, transformation and death. c-myc mRNA has an alternative method of translation via internal ribosome entry where ribosomes are recruited to the IRES located in the ...
Translation started by an internal ribosome entry site (IRES), which bypasses a number of regular eukaryotic initiation systems, can have a non-methinone start with GCU or CAA codons. [23] Mammalian cells can initiate translation with leucine using a specific leucyl-tRNA that decodes the codon CUG. This mechanism is independent of eIF2.
The 5′ UTR has a ribosome binding site [16] or internal ribosome entry site (IRES) that initiates the translation of a very long protein containing about 3,000 amino acids. The core domain of the HCV IRES contains a four-way helical Holliday junction that is integrated within a predicted pseudoknot. [17]