Invitrogen

Human PHD3 (aa 212-239) Control Fragment Recombinant Protein

Name: Human PHD3 (aa 212-239) Control Fragment Recombinant Protein
Brand: Invitrogen
SKU: RP-107385

Datasheet

Tech Support

Datasheet

Tech Support

Product Details

RP-107385

Applications

Tested Dilution

Publications

Control (Ctrl)

Assay-dependent

Blocking Assay (BLOCK)

Assay-dependent

Product Specifications

Species

Human

Expression System

E. coli

Amino acid sequence

YFDAEERAEAKKKFRNLTRKTESALTED

Tag

His-ABP-tag

Class

Recombinant

Type

Protein

Purity

>80% by SDS-PAGE and Coomassie blue staining

Conjugate

Unconjugated Unconjugated Unconjugated

Form

Liquid

Concentration

≥5.0 mg/mL

Purification

purified

Storage buffer

1M urea/PBS, pH 7.4

Contains

no preservative

Storage conditions

-20°C, Avoid Freeze/Thaw Cycles

Product Specific Information

Highest antigen sequence indentity to the following orthologs: Mouse (93%), Rat (93%).

This recombinant protein control fragment may be used for blocking experiments. In IHC/ICC and WB experiments, we recommend a 100x molar excess of the protein fragment control based on the concentration and the molecular weight. Pre-incubate the antibody-protein control fragment mixture for 30 min at room temperature.

Target Information

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. EGLN3 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. 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. Target proteins are preferentially recognized via a LXXLAP motif.

For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.

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Bioinformatics

Protein Aliases: Egl nine homolog 3; egl nine-like protein 3 isoform; egl-9 family hypoxia-inducible factor 3; FLJ21620; HIF prolyl hydroxylase 3; HIF-PH3; HIF-prolyl hydroxylase 3; HPH-1; HPH-3; Hypoxia-inducible factor prolyl hydroxylase 3; MGC125998; MGC125999; P4H3; PHD3; Prolyl hydroxylase domain-containing protein 3; Prolyl hydroxylase EGLN3