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EGLN2/PHD1 Antibody [Alexa Fluor® 405]

Novus Biologicals, part of Bio-Techne | Catalog # NBP3-05472AF405

Novus Biologicals, part of Bio-Techne

Key Product Details

Species Reactivity

Human

Applications

Immunocytochemistry/ Immunofluorescence, Western Blot

Label

Alexa Fluor 405 (Excitation = 405 nm, Emission = 421 nm)

Antibody Source

Polyclonal Rabbit IgG

Concentration

Please see the vial label for concentration. If unlisted please contact technical services.

Product Specifications

Immunogen

Partial synthetic peptide made to an N-terminal portion of the human EGLN2 / PHD1 protein (between amino acids 10-75) [UniProt Q96KS0]

Clonality

Polyclonal

Host

Rabbit

Isotype

IgG

Applications for EGLN2/PHD1 Antibody [Alexa Fluor® 405]

Application
Recommended Usage

Immunocytochemistry/ Immunofluorescence

Optimal dilutions of this antibody should be experimentally determined.

Western Blot

Optimal dilutions of this antibody should be experimentally determined.
Application Notes
Optimal dilution of this antibody should be experimentally determined.

Formulation, Preparation, and Storage

Purification

Immunogen affinity purified

Formulation

50mM Sodium Borate

Preservative

0.05% Sodium Azide

Concentration

Please see the vial label for concentration. If unlisted please contact technical services.

Shipping

The product is shipped with polar packs. Upon receipt, store it immediately at the temperature recommended below.

Stability & Storage

Store at 4C in the dark.

Background: EGLN2/PHD1

HIF prolyl hydroxylase 1 (HPH-3 or EGLN2) is a prolyl hydroxylase that modifies HIF-alpha. Classic prolyl hydroxylases are found in the endoplasmic reticulum and modify collagen, whereas HIF is 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 is an essential component of the pathway through which cells sense oxygen. In the presence of oxygen, HPHs convert specific prolyl residues in HIF-alpha to hydroxyproline, leading to HIF-alpha destruction. Low oxygen levels, sensed at the cellular level, cause the HIF conversion to be reduced so that HIF is stable and there is increased angiogenesis.

Long Name

Egl Nine Homolog 2/Prolyl Hydroxylase Domain-containing Protein 1

Alternate Names

EIT6, HIFPH1, HPH-1, HPH-3, PHD1

Gene Symbol

EGLN2

Additional EGLN2/PHD1 Products

Product Documents for EGLN2/PHD1 Antibody [Alexa Fluor® 405]

Certificate of Analysis

To download a Certificate of Analysis, please enter a lot number in the search box below.

Product Specific Notices for EGLN2/PHD1 Antibody [Alexa Fluor® 405]

Alexa Fluor (R) products are provided under an intellectual property license from Life Technologies Corporation. The purchase of this product conveys to the buyer the non-transferable right to use the purchased product and components of the product only in research conducted by the buyer (whether the buyer is an academic or for-profit entity). The sale of this product is expressly conditioned on the buyer not using the product or its components, or any materials made using the product or its components, in any activity to generate revenue, which may include, but is not limited to use of the product or its components: (i) in manufacturing; (ii) to provide a service, information, or data in return for payment; (iii) for therapeutic, diagnostic or prophylactic purposes; or (iv) for resale, regardless of whether they are resold for use in research. For information on purchasing a license to this product for purposes other than as described above, contact Life Technologies Corporation, 5791 Van Allen Way, Carlsbad, CA 92008 USA or outlicensing@lifetech.com. This conjugate is made on demand. Actual recovery may vary from the stated volume of this product. The volume will be greater than or equal to the unit size stated on the datasheet.

This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.

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