| Mnt IRES | |
|---|---|
 Predicted secondary structure and sequence conservation of IRES_mnt | |
| Identifiers | |
| Symbol | IRES_mnt |
| Rfam | RF00457 |
| Other data | |
| RNA type | Cis-reg; IRES |
| Domain(s) | Eukaryota |
| GO | GO:0043022 |
| SO | SO:0000243 |
| PDB structures | PDBe |
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. [1]
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.
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 (CrPV IRES) is an RNA element required for the production of capsid proteins through ribosome recruitment to an intergenic region IRES (IGR IRES).
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 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].
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.
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 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.
MYC proto-oncogene, bHLH transcription factor is a protein that in humans is encoded by the MYC gene which is a member of the myc family of transcription factors. The protein contains basic helix-loop-helix (bHLH) structural motif.
MNT is a Max-binding protein that is encoded by the MNT gene
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.
Cripavirus is a genus of viruses in the order Picornavirales, in the family Dicistroviridae. Invertebrates serve as natural hosts. There are four species in this genus. Diseases associated with this genus include: DCV: increased reproductive potential; extremely pathogenic when injected with high associated mortality; CrPV: paralysis and death. These viruses can produce proteins directly from their RNA genome upon entering a cell; and therefore, does not require an RNA polymerase packaged in with it, as this may be produced from the genome after entering the cell. The name of the cripavirus family originates from its most famous member the Cricket Paralysis Virus. Which was made famous by its rather unusual IRES : the Cripavirus IRES. The Cripavirus IRES is an RNA element that allows the virus to bind the ribosome and translate without a need for any initiation factors – as initiation is the most regulated step of translation this allows the virus to avoid many mechanisms to inhibit viral activity.
In molecular biology, the Nrf2 internal ribosome entry site (IRES) is an RNA element present in the 5′ UTR of the mRNA encoding the transcription factor Nrf2. It contains a stem-loop structure upstream of a ribosome binding site. This stem loop inhibits ribosome binding and translation of Nrf2 under normal conditions, but allows translation under oxidative stress conditions.
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