癌症的基本特征包括细胞增殖、血管生成、迁移、凋亡逃避机制和细胞永生等。找到癌症发生过程中这些通路的关键标记物和对应的抗体用于检测至关重要。
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eRF1 Rabbit pAb
eRF1 Rabbit pAb
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Application 
| IHC-P, IHC-F, IF |
|---|---|
| Primary Accession | P62495 |
| Reactivity | Rat, Zebrafish, Dog, Horse |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 49031 Da |
| Physical State | Liquid |
| Immunogen | KLH conjugated synthetic peptide derived from human eRF1 |
| Epitope Specificity | 341-437/437 |
| Isotype | IgG |
| Purity | affinity purified by Protein A |
| Buffer | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| SUBCELLULAR LOCATION | Cytoplasm. |
| SIMILARITY | Belongs to the eukaryotic release factor 1 family. |
| SUBUNIT | Heterodimer of two subunits, one of which binds GTP. Component of the transient SURF (SMG1-UPF1-eRF1-eRF3) complex. |
| Post-translational modifications | Phosphorylated by multiple kinases including MAPK1/ERK2 at THR-526. Phosphorylation regulates the activity of ERF. |
| Important Note | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| Background Descriptions | This gene encodes a class-1 polypeptide chain release factor. The encoded protein plays an essential role in directing termination of mRNA translation from the termination codons UAA, UAG and UGA. This protein is a component of the SURF complex which promotes degradation of prematurely terminated mRNAs via the mechanism of nonsense-mediated mRNA decay (NMD). Alternate splicing results in coding and non-coding transcript variants. Pseudogenes of this gene are found on chromosomes 5, 7 and X. [provided by RefSeq, Jan 2012]. |
| Gene ID | 2107 |
|---|---|
| Other Names | Eukaryotic peptide chain release factor subunit 1, Eukaryotic release factor 1, eRF1, Protein Cl1, TB3-1, ETF1, ERF1, RF1, SUP45L1 |
| Target/Specificity | Highest levels in testis, ovary, pancreas, and heart. |
| Dilution | IHC-P=1:100-500,IHC-F=1:100-500,IF=1:100-500 |
| Storage | Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. |
| Name | ETF1 |
|---|---|
| Synonyms | ERF1, RF1, SUP45L1 |
| Function | Component of the eRF1-eRF3-GTP ternary complex, a ternary complex that mediates translation termination in response to the termination codons (PubMed:10676813, PubMed:16777602, PubMed:24486019, PubMed:26245381, PubMed:27863242, PubMed:36638793, PubMed:7990965). The eRF1-eRF3-GTP complex binds to a stop codon in the ribosomal A-site (PubMed:26245381, PubMed:27863242, PubMed:36638793). ETF1/ERF1 is responsible for stop codon recognition and inducing hydrolysis of peptidyl-tRNA (PubMed:26245381, PubMed:27863242, PubMed:36638793). Following GTP hydrolysis, eRF3 (GSPT1/ERF3A or GSPT2/ERF3B) dissociates, permitting ETF1/eRF1 to accommodate fully in the A-site and mediate hydrolysis of peptidyl-tRNA (PubMed:10676813, PubMed:16777602, PubMed:26245381, PubMed:27863242). Component of the transient SURF complex which recruits UPF1 to stalled ribosomes in the context of nonsense-mediated decay (NMD) of mRNAs containing premature stop codons (PubMed:19417104). Required for SHFL-mediated translation termination which inhibits programmed ribosomal frameshifting (-1PRF) of mRNA from viruses and cellular genes (PubMed:30682371). |
| Cellular Location | Cytoplasm. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
This gene encodes a class-1 polypeptide chain release factor. The encoded protein plays an essential role in directing termination of mRNA translation from the termination codons UAA, UAG and UGA. This protein is a component of the SURF complex which promotes degradation of prematurely terminated mRNAs via the mechanism of nonsense-mediated mRNA decay (NMD). Alternate splicing results in coding and non-coding transcript variants. Pseudogenes of this gene are found on chromosomes 5, 7 and X. [provided by RefSeq, Jan 2012].
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