|Other Names||Melanoma-associated antigen 6, Cancer/testis antigen 16, CT16, MAGE-6 antigen, MAGE3B antigen, MAGEA6, MAGE6|
|Target/Specificity||The synthetic peptide sequence is selected from the C-terminus of human MAGEA6.|
|Format||The synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml deionized 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.|
|Function||Proposed to enhance ubiquitin ligase activity of RING- type zinc finger-containing E3 ubiquitin-protein ligases. May enhance ubiquitin ligase activity of TRIM28 and stimulate p53/TP53 ubiquitination by TRIM28. Proposed to act through recruitment and/or stabilization of the Ubl-conjugating enzyme (E2) at the E3:substrate complex. May play a role in tumor transformation or aspects of tumor progression. In vitro promotes cell viability in melanoma cell lines.|
|Tissue Location||Expressed in many tumors of several types, such as melanoma, head and neck squamous cell carcinoma, lung carcinoma and breast carcinoma, but not in normal tissues except for testes|
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Provided below are standard protocols that you may find useful for product applications.
MAGEA6 is a member of the MAGEA gene family. The members of this family have their entire coding sequences located in the last exon, and the encoded proteins show 50 to 80% sequence identity between each other. The promoters and first exons of the MAGEA genes show considerable variability, suggesting that the existence of this gene family enables the same function to be expressed under different transcriptional controls. The MAGEA genes are expressed at a high level in a number of tumors of various histologic types, and are silent in normal tissues with the exception of testis and placenta. The MAGEA genes are clustered on chromosome Xq28. They may be implicated in some hereditary disorders, such as dyskeratosis congenita.
Tatsumi, T., et al., Clin. Cancer Res. 9(3):947-954 (2003).Tatsumi, T., et al., J. Exp. Med. 196(5):619-628 (2002).Imai, Y., et al., Gene 160(2):287-290 (1995).Rogner, U.C., et al., Genomics 29(3):725-731 (1995).De Plaen, E., et al., Immunogenetics 40(5):360-369 (1994).
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