|Other Names||NKG2D ligand 4, N2DL-4, NKG2DL4, Lymphocyte effector toxicity activation ligand, RAE-1-like transcript 4, RL-4, Retinoic acid early transcript 1E, RAET1E, LETAL, N2DL4, ULBP4|
|Format||Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Synonyms||LETAL, N2DL4, ULBP4|
|Function||Ligand for the KLRK1 receptor. Delivers activating signals to NK cells and promotes tumor immune surveillance by inducing the expansion of anti-tumor cytotoxic lymphocytes.|
|Cellular Location||Membrane; Single-pass type I membrane protein|
|Tissue Location||Predominantly expressed in the skin, but also expressed in testis and trachea. Up-regulated in tumor cells of different origins. Expression progressively decreased after treatment of tumor cells with retinoic acid|
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Members of the RAET1 family, such as RAET1E, are majorhistocompatibility complex (MHC) class I-related genes locatedwithin a 180-kb cluster on chromosome 6q24.2-q25.3. RAET1 proteinscontain MHC class I-like alpha-1 and alpha-2 domains. RAET1E andRAET1G (MIM 609244) differ from the other RAET1 proteins (e.g.,RAET1I, or ULBP1; MIM 605697) in that they have type Imembrane-spanning sequences at their C termini rather thanglycosylphosphatidylinositol anchor sequences. RAET1E is a ligandfor NKG2D (KLRK1; MIM 611817), which is expressed on the surface ofseveral types of immune cells and is involved in innate andadaptive immune responses (summary by Radosavljevic et al. (2002)[PubMed 11827464] and Cao et al. (2007) [PubMed17470428]).
McGilvray, R.W., et al. Int. J. Cancer 127(6):1412-1420(2010)Antoun, A., et al. Hum. Immunol. 71(6):610-620(2010)Davila, S., et al. Genes Immun. 11(3):232-238(2010)Romphruk, A.V., et al. Immunogenetics 61(9):611-617(2009)Kong, Y., et al. Blood 114(2):310-317(2009)
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