Egln3 (BC022961) Mouse Recombinant Protein
CAT#: TP500563
Purified recombinant protein of Mouse EGL nine homolog 3 (C. elegans) (cDNA clone MGC:36685 IMAGE:5371854), complete cds, with C-terminal MYC/DDK tag, expressed in HEK293T cells, 20ug
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CNY 1,050.00
Specifications
Product Data | |
Species | Mouse |
Expression Host | HEK293T |
Expression cDNA Clone or AA Sequence |
>MR200563 protein sequence
Red=Cloning site Green=Tags(s) MVACYPGNGTGYVRHVDNPNGDGRCITCIYYLNKNWDAKLHGGVLRIFPEGKSFVADVEPIFDRLLFFWS DRRNPHEVQPSYATRYAMTVWYFDAEERAEAKKKFRNLTRKTESALAKD TRTRPLEQKLISEEDLAANDILDYKDDDDKV |
Tag | C-MYC/DDK |
Predicted MW | 13.8 kDa |
Concentration | >0.05 µg/µL as determined by microplate BCA method |
Purity | > 80% as determined by SDS-PAGE and Coomassie blue staining |
Buffer | 25 mM Tris-HCl, 100 mM glycine, pH 7.3, 10% glycerol |
Note | For testing in cell culture applications, please filter before use. Note that you may experience some loss of protein during the filtration process. |
Storage | Store at -80°C after receiving vials. |
Stability | Stable for 12 months from the date of receipt of the product under proper storage and handling conditions. Avoid repeated freeze-thaw cycles. |
Reference Data | |
Locus ID | 112407 |
UniProt ID | Q91UZ4 |
Refseq Size | 2156 |
Cytogenetics | 12 C1 |
Refseq ORF | 357 |
Synonyms | SM-20 |
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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