Egl Nine Homolog 3 (C. Elegans) (EGLN3) antibody

Details for Product No. ABIN250181
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Antigen
Synonyms zgc:77019, wu:fj78a08, EGLN3, phd3, PHD-3, PHD3, SM-20, 2610021G09Rik, AI505553, AI648162, Hif-p4h-3, Phd3, HIFP4H3, HIFPH3
Reactivity
Human
(61), (34), (25), (17), (15), (14), (6), (1), (1), (1)
Host
Rabbit
(51), (14), (6)
Clonality
Polyclonal
Conjugate
Un-conjugated
(7), (7), (4), (4), (4), (4), (1), (1), (1), (1), (1), (1), (1), (1), (1), (1), (1)
Application
Western Blotting (WB), Immunoelectron Microscopy (IEM), Immunocytochemistry (ICC), Immunofluorescence (IF), Immunohistochemistry (Paraffin-embedded Sections) (IHC (p)), Immunoprecipitation (IP)
(60), (23), (11), (10), (10), (2), (1), (1), (1)
Pubmed 10 references available
Quantity 0.025 mL
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Catalog No. ABIN250181
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Immunogen Synthetic peptide corresponding to residues between 50-100 of human PHD3/HIF Prolyl Hydroxylase 3 using the numbering given in entry NP_071356.1 (GeneID 112399).
Cross-Reactivity (Details) Mouse reactivity reported in scientific literature (PMID: 24037093)
Purification affinity purified
Alternative Name EGLN3 / PHD3
Background HIF prolyl hydroxylase 3 is a prolyl hydroxylase that modifies HIF-alpha. Classic prolylhydroxylases are found in the endoplasmic reticulum and modify collagen, whereas HIFis an intracellular protein and the HPH sites do not resemble those modifying collagen. HIF is a transcriptional complex that plays a critical role in oxygen homeostasis. HPH isan essential component of the pathway through which cells sense oxygen. In thepresence of oxygen, HPHs convert specific prolyl residues in HIF-alpha tohydroxyproline, leading to HIF-alpha destruction. Low oxygen levels, sensed at thecellular level, cause the HIF conversion to be reduced so that HIF is stable and there isincreased angiogenesis.HPH-1, specifically, catalyzes the posttranslational formation of 4-hydroxyproline in HIFalpha proteins. It hydroxylates HIF-1 alpha at Pro(564) and HIF-2 alpha. It targets HIFthrough the hydroxylation for proteasomal degradation via the von Hippel-Lindau ubiquitylation complex. It may also play a role in cell growth regulation in muscle cellsand in apoptosis in neuronal tissues, promoting cell death through a caspase-dependentmechanism. Alternate Names: anti-EGL9 homolog of C. elegans 3 antibody, anti-EGLN3 antibody, anti-Factorresponsive smooth muscle protein antibody, anti-HIF Prolyl Hydroxylase 3 antibody,anti-HIFP4H3 antibody, anti-HIFPH3 antibody, anti-P4H3 antibody, anti-ProlylHydroxylase Domain Containing Protein 3 antibody, anti-SM20 antibody, anti-PHD3antibody, anti-EGLN3 antibody.
Gene Symbol: EGLN3
Gene ID 112399
NCBI Accession NP_071356
Application Notes This PHD3/HIF Prolyl Hydroxylase 3 antibody is useful for Immunocytochemistry/Immunofluorescence and Western blot, where a band can be seen at 27-30 kDa. Use in Immunohistochemistry-Paraffin and Electron Microscopy reported in scientific literature (PMID 17003483) Use in chromatin immunoprecipitation reported in scientific literature (PMID 24367580)
Recommended dilutions: Electron Microscopy, Immunocytochemistry/Immunofluorescence 1:500, Immunohistochemistry-Paraffin, Immunoprecipitation, Western Blot 1:1000-1:2000
Restrictions For Research Use only
Format Liquid
Concentration 1 mg/mL
Buffer Tris-citrate/Phosphate, pH 7-8, Sodium Azide
Preservative Sodium azide
Precaution of Use WARNING: Reagents contain sodium azide. Sodium azide is very toxic if ingested or inhaled. Avoid contact with skin, eyes, or clothing. Wear eye or face protection when handling. If skin or eye contact occurs, wash with copious amounts of water. If ingested or inhaled, contact a physician immediately. Sodium azide yields toxic hydrazoic acid under acidic conditions. Dilute azide-containing compounds in running water before discarding to avoid accumulation of potentially explosive deposits in lead or copper plumbing.
Handling Advice Do not freeze.
Storage 4 °C
General Bruick, McKnight: "A conserved family of prolyl-4-hydroxylases that modify HIF." in: Science (New York, N.Y.), Vol. 294, Issue 5545, pp. 1337-40, 2001 (PubMed).

Ivan, Haberberger, Gervasi et al.: "Biochemical purification and pharmacological inhibition of a mammalian prolyl hydroxylase acting on hypoxia-inducible factor." in: Proceedings of the National Academy of Sciences of the United States of America, Vol. 99, Issue 21, pp. 13459-64, 2002 (PubMed).

Asikainen, Schneider, Waleh et al.: "Activation of hypoxia-inducible factors in hyperoxia through prolyl 4-hydroxylase blockade in cells and explants of primate lung." in: Proceedings of the National Academy of Sciences of the United States of America, Vol. 102, Issue 29, pp. 10212-7, 2005 (PubMed).

Jokilehto, Rantanen, Luukkaa et al.: "Overexpression and nuclear translocation of hypoxia-inducible factor prolyl hydroxylase PHD2 in head and neck squamous cell carcinoma is associated with tumor aggressiveness." in: Clinical cancer research : an official journal of the American Association for Cancer Research, Vol. 12, Issue 4, pp. 1080-7, 2006 (PubMed).

Asikainen, Waleh, Schneider et al.: "Enhancement of angiogenic effectors through hypoxia-inducible factor in preterm primate lung in vivo." in: American journal of physiology. Lung cellular and molecular physiology, Vol. 291, Issue 4, pp. L588-95, 2006 (PubMed).

Li, Yi, Sundy et al.: "Expression and actions of HIF prolyl-4-hydroxylase in the rat kidneys." in: American journal of physiology. Renal physiology, Vol. 292, Issue 1, pp. F207-16, 2007 (PubMed).

Fu, Menzies, Freeman et al.: "EGLN3 prolyl hydroxylase regulates skeletal muscle differentiation and myogenin protein stability." in: The Journal of biological chemistry, Vol. 282, Issue 17, pp. 12410-8, 2007 (PubMed).

Bai, Zeng, Hu et al.: "Expression and characteristic of synthetic human epidermal growth factor (hEGF) in transgenic tobacco plants." in: Biotechnology letters, Vol. 29, Issue 12, pp. 2007-12, 2007 (PubMed).

Rantanen, Pursiheimo, Hoegel et al.: "Prolyl hydroxylase PHD3 activates oxygen-dependent protein aggregation." in: Molecular biology of the cell, Vol. 19, Issue 5, pp. 2231-40, 2008 (PubMed).

Ginouvès, Ilc, Macías et al.: "PHDs overactivation during chronic hypoxia \desensitizes\" HIFalpha and protects cells from necrosis."" in: Proceedings of the National Academy of Sciences of the United States of America, Vol. 105, Issue 12, pp. 4745-50, 2008 (PubMed).

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