This family represents the internal ribosome entry site (IRES) of the Picornaviruses. IRES elements allow cap and end-independent translation of mRNA in the host cell. The IRES achieves this by mediating the internal initiation of translation by recruiting a ribosomal 43S pre-initiation complex directly to the initiation codon and eliminates the requirement for the eukaryotic initiation factor eIF4F.
The BiP internal ribosome entry site (IRES) is an RNA element present in the 5' UTR of the mRNA of BiP protein and allows cap-independent translation. BiP protein expression has been found to be significantly enhanced by the heat shock response due to internal ribosome entry site (IRES)-dependent translation. It is thought that this translational mechanism is essential for the survival of cells under stress.
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 5' UTR thus bypassing the typical eukaryotic cap-dependent translation pathway.
The Epstein–Barr virus nuclear-antigen internal ribosome entry site is an internal ribosome entry site (IRES) that is found in an exon in the 5' untranslated region of the Epstein–Barr virus nuclear antigen 1 (EBNA1) gene. The EBNA IRES allows EBNA1 translation to occur under situations where initiation from the 5' cap structure and ribosome scanning is reduced. It is thought that the EBNA IRES is necessary for the regulation of latent-gene expression.
The FGF-1 internal ribosome entry site (IRES) is an RNA element present in the 5' UTR of the mRNA of fibroblast growth factor-1 and allows cap-independent translation. It is thought that FGF-1 internal ribosome entry site (IRES) activity is strictly controlled and highly tissue specific.
The heat shock protein 70 (Hsp70) internal ribosome entry site (IRES) is an RNA element that allows cap independent translation during conditions such as heat shock and stress. It has been shown that the 216 nucleotide long 5' UTR contains internal ribosome entry site activity.
This family represents the internal ribosome entry site (IRES) of the hepatitis A virus. HAV IRES is a 450 nucleotide long sequence located in the 735 nt long 5’ UTR of Hepatitis A viral RNA genome. IRES elements allow cap and end-independent translation of mRNA in the host cell. The IRES achieves this by mediating the internal initiation of translation by recruiting a ribosomal 40S pre-initiation complex directly to the initiation codon and eliminates the requirement for eukaryotic initiation factor, eIF4F.
The Hepatitis C virus internal ribosome entry site, or HCV IRES, is an RNA structure within the 5'UTR of the HCV genome that mediates cap-independent translation initiation.
The Mnt internal ribosome entry site (IRES) is an RNA element. Mnt is a transcriptional repressor related to the Myc/Mad family of transcription factors. It is thought that this IRES allows efficient Mnt synthesis when cap-dependent translation initiation is reduced.
The N-myc internal ribosome entry site (IRES) is an RNA element found in the n-myc gene. The myc family of genes when expressed are known to be involved in the control of cell growth, differentiation and apoptosis. n-myc mRNA has an alternative method of translation via an internal ribosome entry site where ribosomes are recruited to the IRES located in the 5' UTR thus bypassing the typical eukaryotic cap-dependent translation pathway.
This family represents the internal ribosome entry site (IRES) of the pestiviruses. The pestivirus IRES allows cap and end-independent translation of mRNA in the host cell. The IRES achieves this by mediating the internal initiation of translation by recruiting a ribosomal 43S pre-initiation complex directly to the initiation codon and eliminates the requirement for the eukaryotic initiation factor, eIF4F. The classical swine fever virus UTR described appears to be longer at the 5' end than other pestivirus UTRs. This family represents the conserved core.
This family represents the Picornavirus internal ribosome entry site (IRES). IRES elements allow cap and end-independent translation of mRNA in the host cell. It has been found that La autoantigen (La) is required for Coxsackievirus B3 (CVB3) IRES-mediated translation, and it has been suggested that La may be required for the efficient translation of the viral RNA in the pancreas.
The HIF-1α internal ribosome entry site (IRES) is an RNA element present in the 5' UTR of the mRNA of HIF-1α that allows cap-independent translation. The HIF-1α internal ribosome entry site (IRES) allows translation to be maintained under hypoxic cell conditions that inhibit cap-dependent translation [1]. The hypoxia-inducible factor-1α protein (HIF-1α) is a subunit of the HIF-1 transcription factor, which induces transcription of several genes involved in the cellular response to hypoxia.
The Tobamovirus internal ribosome entry site (IRES) is an element that allows cap and end-independent translation of mRNA in the host cell. The IRES achieves this by mediating the internal initiation of translation by recruiting a ribosomal 43S pre-initiation complex directly to the initiation codon and eliminates the requirement for the eukaryotic initiation factor, eIF4F.
The TrkB internal ribosome entry site (IRES) is an RNA element which is present in the 5' UTR sequence of the mRNA. TrkB is a neurotrophin receptor which is essential for the development and maintenance of the nervous system. The internal ribosome entry site IRES element allows cap-independent translation of TrkB which may be needed for efficient translation in neuronal dendrites.
A ribosome binding site, or ribosomal binding site (RBS), is a sequence of nucleotides upstream of the start codon of an mRNA transcript that is responsible for the recruitment of a ribosome during the initiation of protein translation. Mostly, RBS refers to bacterial sequences, although internal ribosome entry sites (IRES) have been described in mRNAs of eukaryotic cells or viruses that infect eukaryotes. Ribosome recruitment in eukaryotes is generally mediated by the 5' cap present on eukaryotic mRNAs.
Eukaryotic translation initiation factor 4 G (eIF4G) is a protein involved in eukaryotic translation initiation and is a component of the eIF4F cap-binding complex. Orthologs of eIF4G have been studied in multiple species, including humans, yeast, and wheat. However, eIF4G is exclusively found in domain Eukarya, and not in domains Bacteria or Archaea, which do not have capped mRNA. As such, eIF4G structure and function may vary between species, although the human eIF4G 1 has been the focus of extensive studies.
In molecular biology, the ODC internal ribosome entry site (IRES) is an RNA element present in the 5' UTR of the mRNA encoding ornithine decarboxylase. It has been suggested that this IRES allows cap-independent translation of ornithine decarboxylase at the G2/M phase of the cell cycle, however there is some doubt about this. Translation from this IRES is activated by the zinc finger protein ZNF9 and by Poly(rC)-binding protein 2 (PCBP2). It is also activated in Ras-transformed cells.
