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Egln3 (BC022961) Mouse Tagged ORF Clone Lentiviral Particle
CAT＃: MR200563L4V
- LentiORF®
-
Lenti ORF particles, Egln3 (GFP-tagged) - Mouse EGL nine homolog 3 (C. elegans) (cDNA clone MGC:36685 IMAGE:5371854), 200ul, >10^7 TU/mL
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CNY 7,505.00
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Specifications
| Product Data | |
| Product Name | Egln3 (BC022961) Mouse Tagged ORF Clone Lentiviral Particle |
| Synonyms | SM-20 |
| Vector | pLenti-C-mGFP-P2A-Puro |
| ACCN | BC022961 |
| ORF Size | 357 bp |
| Sequence Data |
The ORF insert of this clone is exactly the same as(MR200563).
|
| OTI Disclaimer | The molecular sequence of this clone aligns with the gene accession number as a point of reference only. However, individual transcript sequences of the same gene can differ through naturally occurring variations (e.g. polymorphisms), each with its own valid existence. This clone is substantially in agreement with the reference, but a complete review of all prevailing variants is recommended prior to use. More info |
| OTI Annotation | This clone was engineered to express the complete ORF with an expression tag. Expression varies depending on the nature of the gene. |
| Reference Data | |
| RefSeq | BC022961 |
| RefSeq Size | 2156 bp |
| RefSeq ORF | 359 bp |
| Locus ID | 112407 |
| Gene Summary | Plays a crucial role in DNA damage response (DDR) by hydroxylating TELO2, promoting its interaction with ATR which is required for activation of the ATR/CHK1/p53 pathway (By similarity). Cellular oxygen sensor that catalyzes, under normoxic conditions, the post-translational formation of 4-hydroxyproline in hypoxia-inducible factor (HIF) alpha proteins. Hydroxylates a specific proline found in each of the oxygen-dependent degradation (ODD) domains (N-terminal, NODD, and C-terminal, CODD) of HIF1A. Also hydroxylates HIF2A. Has a preference for the CODD site for both HIF1A and HIF2A. Hydroxylation on the NODD site by EGLN3 appears to require prior hydroxylation on the CODD site. Hydroxylated HIFs are then targeted for proteasomal degradation via the von Hippel-Lindau ubiquitination complex. Under hypoxic conditions, the hydroxylation reaction is attenuated allowing HIFs to escape degradation resulting in their translocation to the nucleus, heterodimerization with HIF1B, and increased expression of hypoxy-inducible genes. ELGN3 is the most important isozyme in limiting physiological activation of HIFs (particularly HIF2A) in hypoxia. Also hydroxylates PKM in hypoxia, limiting glycolysis. Under normoxia, hydroxylates and regulates the stability of ADRB2. Regulator of cardiomyocyte and neuronal apoptosis. In cardiomyocytes, inhibits the anti-apoptotic effect of BCL2 by disrupting the BAX-BCL2 complex. In neurons, has a NGF-induced proapoptotic effect, probably through regulating CASP3 activity. Also essential for hypoxic regulation of neutrophilic inflammation. Target proteins are preferentially recognized via a LXXLAP motif.[UniProtKB/Swiss-Prot Function] |
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