SHP/NR0B2/Nuclear Receptor SHP Antibody (OTI7B5) [Alexa Fluor® 350]

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.

SHP (short heterodimer partner) is a bile acid-dependent orphan NR0 Knirps-Like receptor with dimerization and ligand-binding domains but not the conventional DNA-binding domain. SHP has been shown to inhibit the transcriptional activity of other nuclear receptors, including thyroid hormone receptor, constitutive androstane receptor, and retinoic acid receptors. SHP affects hepatic cholesterol catabolism based on a two-step mechanism dependent on both coactivator competition and direct transcriptional repression by mediating the repression of CYP7A1, the rate-limiting enzyme for bile acid synthesis. Mutations in the SHP gene contribute to increased body weight, indicating a possible role of SHP in the development of early-onset diabetes (maturity-onset diabetes of the young, MODY). Loss of SHP in mice caused abnormal accumulation and increased synthesis of bile acids due to derepression of rate-limiting CYP7A1 and CYP8B1 hydroxylase enzymes in the biosynthetic pathway. SHP expression has been documented in human liver, adrenal, spleen, and pancreas. ESTs have been isolated from cancerous human kidney, lung, and stomach, as well as normal human heart, kidney, liver, and liver/spleen. Caution: The nuclear receptor SHP should not be confused with the tyrosine phosphatases SHP-1 and SHP-2.

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.

Array NBP2-74172AF350

• SHP/NR0B2/Nuclear Receptor SHP Antibodies
• SHP/NR0B2/Nuclear Receptor SHP ELISA Kits
• SHP/NR0B2/Nuclear Receptor SHP Lysate
• SHP/NR0B2/Nuclear Receptor SHP Protein