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Homo sapiens


From: Memorial Sloan Kettering Cancer Center; New York; USA. Characteristics: Pigmented. Sequence variation: BRAF p.Val600Glu (c.1799T>A) (PubMed=17260012; PubMed=21725359; PubMed=24576830). Sequence variation: Homozygous for CDKN2A deletion (PubMed=17260012). Omics: Array-based CGH. Omics: SNP array analysis. Omics: Transcriptome analysis.

Proper Citation



Cancer cell line




SK-Mel-19, SKMEL-19, SkMEL-19, SK-MEL19, SK-Mel19, Sk Mel19, SKMEL19, AL-Mel

Cross References

ChEMBL-Cells; CHEMBL3307448 ChEMBL-Targets; CHEMBL614915 Cosmic; 685202 Cosmic; 721841 Cosmic; 886830 Cosmic; 923385 Cosmic; 933126 Cosmic; 1047686 Cosmic; 1060427 Cosmic; 1122255 Cosmic; 1669136 GEO; GSM156032 GEO; GSM555122 GEO; GSM555175 GEO; GSM784508 Lonza; 1332 Wikidata; Q54953894

Publications that use this research resource

Empty conformers of HLA-B preferentially bind CD8 and regulate CD8+ T cell function.

  • Geng J
  • Elife
  • 2018 May 9

Literature context: oma cell line SK-mel-19 (SK19) (RRID:CVCL_6025) (Yang et al., 2003) and ecotro


When complexed with antigenic peptides, human leukocyte antigen (HLA) class I (HLA-I) molecules initiate CD8+ T cell responses via interaction with the T cell receptor (TCR) and co-receptor CD8. Peptides are generally critical for the stable cell surface expression of HLA-I molecules. However, for HLA-I alleles such as HLA-B*35:01, peptide-deficient (empty) heterodimers are thermostable and detectable on the cell surface. Additionally, peptide-deficient HLA-B*35:01 tetramers preferentially bind CD8 and to a majority of blood-derived CD8+ T cells via a CD8-dependent binding mode. Further functional studies reveal that peptide-deficient conformers of HLA-B*35:01 do not directly activate CD8+ T cells, but accumulate at the immunological synapse in antigen-induced responses, and enhance cognate peptide-induced cell adhesion and CD8+ T cell activation. Together, these findings indicate that HLA-I peptide occupancy influences CD8 binding affinity, and reveal a new set of regulators of CD8+ T cell activation, mediated by the binding of empty HLA-I to CD8.

Funding information:
  • NIAID NIH HHS - R01 AI044115()
  • NIH Office of the Director - AI044115()
  • NIH Office of the Director - R01AI044115()
  • PHS HHS - P01-155258(United States)