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JMJD4 Blocking Peptide (N-term)
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Primary Accession | Q9H9V9 |
|---|---|
| Other Accession | Q32M74 |
| Gene ID | 65094 |
|---|---|
| Other Names | JmjC domain-containing protein 4, Jumonji domain-containing protein 4, JMJD4 |
| Target/Specificity | The synthetic peptide sequence is selected from aa 1-17 of HUMAN JMJD4 |
| Format | Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed. |
| Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C. |
| Precautions | This product is for research use only. Not for use in diagnostic or therapeutic procedures. |
| Name | JMJD4 |
|---|---|
| Function | Catalyzes the 2-oxoglutarate and iron-dependent C4-lysyl hydroxylation of ETF1 at 'Lys-63' thereby promoting the translational termination efficiency of ETF1. |
| Cellular Location | Cytoplasm. |
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abcepta to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
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Provided below are standard protocols that you may find useful for product applications.
Background
Covalent modification of histones plays critical role in regulating chromatin structure and transcription. While most covalent histone modifications are reversible, only recently has it been established that methyl groups are subject to enzymatic removal from histones. A family of novel JmjC domain-containing histone demethylation (JHDM) enzymes have been identified that perform this specific function. Histone demethylation by JHDM proteins requires cofactors Fe(II) and alpha-ketoglutarate. Family members include JHDM1 (demethylating histone 3 at lysine 36), and JHDM2A as well as JMJD2CH3K9 (both of which demethylate histone 3 at lysine 9). Contributions of histone demethylase activity to tumor development, decreases in cell proliferation, and hormone-dependent transcriptional activation have been observed.
References
Ota, T., et al., Nat. Genet. 36(1):40-45 (2004).
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