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Bioss
PHD3 Polyclonal Antibody
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Product Details
BS-0532R
Applications
Tested Dilution
Publications
Product Specifications
Species Reactivity
Human,
Mouse,
Rat
Host/Isotype
Rabbit
/ IgG
Class
Polyclonal
Type
Antibody
Immunogen
KLH conjugated synthetic peptide derived from PHD3.
Conjugate
Form
Liquid
Concentration
1 mg/mL
Purification
Protein A
Storage buffer
0.01M TBS, pH 7.4, with 50% glycerol, 1% BSA
Contains
0.02% ProClin 300
Storage conditions
-20°C
Shipping conditions
Ambient (domestic); Wet ice (international)
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 homolog 3, mitochondrial; egl nine-like protein 3 isoform; egl-9 family hypoxia-inducible factor 3; factor-responsive smooth muscle protein; 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; SM-20
Gene Aliases: 2610021G09Rik; AI505553; AI648162; EGLN3; Hif-p4h-3; HIFP4H3; HIFPH3; PHD-3; PHD3; SM-20; Sm20
UniProt ID: (Human) Q9H6Z9, (Mouse) Q91UZ4, (Rat) Q62630
Entrez Gene ID: (Human) 112399, (Mouse) 112407, (Rat) 54702
iron ion binding
protein binding
oxidoreductase activity, acting on paired donors, with incorporation or reduction of molecular oxygen, 2-oxoglutarate as one donor, and incorporation of one atom each of oxygen into both donors
L-ascorbic acid binding
peptidyl-proline 4-dioxygenase activity
oxidoreductase activity
oxidoreductase activity, acting on paired donors, with incorporation or reduction of molecular oxygen
peptidyl-proline dioxygenase activity
metal ion binding
dioxygenase activity
response to hypoxia
apoptotic process
cellular response to DNA damage stimulus
protein hydroxylation
peptidyl-proline hydroxylation to 4-hydroxy-L-proline
peptidyl-proline hydroxylation
regulation of cell proliferation
regulation of neuron apoptotic process
oxidation-reduction process
activation of cysteine-type endopeptidase activity involved in apoptotic process
regulation of transcription from RNA polymerase II promoter in response to hypoxia
Performance Guarantee
If an Invitrogen™ antibody doesn't perform as described on our website or datasheet,we'll replace the product at no cost to you, or provide you with a credit for a future purchase.*
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