The APC internal ribosome entry site (IRES) is an RNA element which is located in the coding sequence of the APC gene. APC is a tumour suppressor gene which is associated with the inherited disease adenomatous polyposis coli (APC). It is thought that IRES-mediated translation of APC is important for an apoptotic cascade.
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 Cripavirus internal ribosome entry site is an RNA element required for the production of capsid proteins through ribosome recruitment to an intergenic region IRES.
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 FGF-2 internal ribosome entry site is an RNA element present in the 5' UTR of the mRNA of fibroblast growth factor-2. It has been found that the FGF-2 internal ribosome entry site (IRES) activity is strictly controlled and highly tissue specific. It is thought that translational IRES dependent activation of FGF-2 plays a vital role in embryogenesis and in the adult brain [1]. When expressed the fibroblast growth factor 2 FGF-2 protein plays a pivotal role in cell proliferation, differentiation and survival as well as being involved in wound-healing [1,2].
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 L-myc internal ribosome entry site (IRES) is an RNA element present in the 5' UTR of the mRNA of L-myc that allows cap-independent translation. L-myc undergoes translation via the internal ribosome entry site and bypasses the typical eukaryotic cap-dependent translation pathway [1]. The myc family of genes when expressed are known to be involved in the control of cell growth, differentiation and apoptosis.
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 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 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.
This family represents the vascular endothelial growth factor (VEGF) internal ribosome entry site (IRES) A. VEGF is an endothelial cell mitogen with many crucial functions such as embryogenic development and wound healing. The 5' UTR of VEGF mRNA contains two IRES elements which are able to promote efficient translation at the AUG start codon, this family represents IRES A.
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 Ure2 internal ribosome entry site (IRES) is an RNA element present in the 5' UTR of the mRNA of Ure2. It allows 5' cap- and eIF4E-independent translation of an N-terminally truncated form of Ure2. This truncated form lacks the prion-forming domain. It is a 104 nucleotide region, smaller than most viral IRES elements, which forms a stem-loop structure. EIF2A represses this IRES resulting in an inhibition of translation of the N-terminally truncated Ure2.
