PRAME (preferentially expressed antigen of melanoma) is a protein that in humans is encoded by the PRAME gene.[3][4][5] Five alternatively spliced transcript variants encoding the same protein have been observed for this gene.[5]

PRAME
Identifiers
AliasesPRAME, CT130, MAPE, OIP-4, OIP4, preferentially expressed antigen in melanoma, PRAME nuclear receptor transcriptional regulator
External IDsOMIM: 606021; HomoloGene: 48404; GeneCards: PRAME; OMA:PRAME - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

n/a

RefSeq (protein)

n/a

Location (UCSC)Chr 22: 22.55 – 22.56 Mbn/a
PubMed search[2]n/a
Wikidata
View/Edit Human

Function

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This gene encodes an antigen that is predominantly expressed in human melanomas and that is recognized by cytolytic T lymphocytes. It is not expressed in normal tissues, except testis. This expression pattern is similar to that of other CT antigens, such as MAGE, BAGE and GAGE. However, unlike these other CT antigens, this gene is also expressed in acute leukemias. The overexpression of PRAME in tumor tissues and relative low levels in normal somatic tissues make it an attractive target for cancer therapy. In recent years, immunotherapy has spearheaded a new era of cancer therapy resulting in the development of numerous novel antigen-specific immunotherapy approaches. Studies on PRAME-specific immunotherapy primarily involve vaccines and cellular immunotherapies.[6]

PRAME can inhibit retinoic acid signaling and retinoic acid mediated differentiation and apoptosis.[7] PRAME overexpression in triple negative breast cancer has also been found to promote cancer cell motility through induction of the epithelial-to-mesenchymal transition.[8]

References

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  1. ^ a b c ENSG00000275013 GRCh38: Ensembl release 89: ENSG00000185686, ENSG00000275013Ensembl, May 2017
  2. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  3. ^ Ikeda H, Lethé B, Lehmann F, van Baren N, Baurain JF, de Smet C, Chambost H, Vitale M, Moretta A, Boon T, Coulie PG (Feb 1997). "Characterization of an antigen that is recognized on a melanoma showing partial HLA loss by CTL expressing an NK inhibitory receptor". Immunity. 6 (2): 199–208. doi:10.1016/S1074-7613(00)80426-4. PMID 9047241.
  4. ^ Dunham I, Shimizu N, Roe BA, Chissoe S, Hunt AR, Collins JE, Bruskiewich R, Beare DM, Clamp M, Smink LJ, Ainscough R, Almeida JP, Babbage A, Bagguley C, Bailey J, Barlow K, Bates KN, Beasley O, Bird CP, Blakey S, Bridgeman AM, Buck D, Burgess J, Burrill WD, O'Brien KP (Dec 1999). "The DNA sequence of human chromosome 22". Nature. 402 (6761): 489–95. Bibcode:1999Natur.402..489D. doi:10.1038/990031. PMID 10591208.
  5. ^ a b "Entrez Gene: PRAME preferentially expressed antigen in melanoma".
  6. ^ Al-Khadairi G, Decock J (July 2019). "Cancer Testis Antigens and Immunotherapy: Where Do We Stand in the Targeting of PRAME?". Cancers. 11 (7): 984. doi:10.3390/cancers11070984. PMC 6678383. PMID 31311081.
  7. ^ Epping MT, Wang L, Edel MJ, Carlée L, Hernandez M, Bernards R (September 2005). "The human tumor antigen PRAME is a dominant repressor of retinoic acid receptor signaling". Cell. 122 (6): 835–47. doi:10.1016/j.cell.2005.07.003. hdl:1874/17819. PMID 16179254. S2CID 18144920.
  8. ^ Al-Khadairi G, Naik A, Thomas R, Al-Sulaiti B, Rizly S, Decock J (January 2019). "PRAME promotes epithelial-to-mesenchymal transition in triple negative breast cancer". Journal of Translational Medicine. 17 (1): 9. doi:10.1186/s12967-018-1757-3. PMC 6317205. PMID 30602372.

Further reading

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