An internal ribosome entry site, abbreviated IRES, is an RNA element that allows for translation initiation in a cap-independent manner, as part of the greater process of protein synthesis. In eukaryotic translation, initiation typically occurs at the 5' end of mRNA molecules, since 5' cap recognition is required for the assembly of the initiation complex. The location for IRES elements is often in the 5'UTR, but can also occur elsewhere in mRNAs.
Eukaryotic translation is the biological process by which messenger RNA is translated into proteins in eukaryotes. It consists of four phases: initiation, elongation, termination, and recycling.
The bag-1 internal ribosome entry site (IRES) is a cis-acting element located in the 5 ' untranslated region of the BAG-1 protein mRNA. Its effects apoptosis through IRES mediated translation of the BAG-1 protein.
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-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. It is thought that the three IRES elements are somehow responsive to cellular changes and act to regulate the level of translation.
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 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 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.
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.
Red clover necrotic mosaic virus (RCNMV) contains several structural elements present within the 3' and 5' untranslated regions (UTR) of the genome that enhance translation. In eukaryotes transcription is a prerequisite for translation. During transcription the pre-mRNA transcript is processes where a 5' cap is attached onto mRNA and this 5' cap allows for ribosome assembly onto the mRNA as it acts as a binding site for the eukaryotic initiation factor eIF4F. Once eIF4F is bound to the mRNA this protein complex interacts with the poly(A) binding protein which is present within the 3' UTR and results in mRNA circularization. This multiprotein-mRNA complex then recruits the ribosome subunits and scans the mRNA until it reaches the start codon. Transcription of viral genomes differs from eukaryotes as viral genomes produce mRNA transcripts that lack a 5’ cap site. Despite lacking a cap site viral genes contain a structural element within the 5’ UTR known as an internal ribosome entry site (IRES). IRES is a structural element that recruits the 40s ribosome subunit to the mRNA within close proximity of the start codon.
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.
