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SK-MEL-19

RRID:CVCL_6025

Organism

Homo sapiens

Comments

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; DepMap). Sequence variation: Homozygous for CDKN2A deletion (PubMed=17260012). Sequence variation: TP53 p.Asn131Lys (c.390C>A) (DepMap). Omics: Array-based CGH. Omics: Deep exome analysis. Omics: SNP array analysis. Omics: Transcriptome analysis. DT Created: 04-04-12; Last updated: 05-07-19; Version: 23

Proper Citation

RRID:CVCL_6025

Category

Cancer cell line DT Created: 04-04-12; Last updated: 05-07-19; Version: 23

Sex

DT Created: 04-04-12; Last updated: 05-07-19; Version: 23

Synonyms

SK-Mel-19, SKMEL-19, SkMEL-19, SK-MEL19, SK-Mel19, Sk Mel19, SKMEL19, AL-Mel DT Created: 04-04-12, Last updated: 05-07-19, Version: 23

Cross References

Cell_Model_Passport; SIDM01423 ChEMBL-Cells; CHEMBL3307448 ChEMBL-Targets; CHEMBL614915 Cosmic; 685202 Cosmic; 721841 Cosmic; 886830 Cosmic; 923385 Cosmic; 933126 Cosmic; 1047686 Cosmic; 1060427 Cosmic; 1122255 Cosmic; 1669136 DepMap; ACH-002005 GEO; GSM156032 GEO; GSM555122 GEO; GSM555175 GEO; GSM784508 Lonza; 1332 Wikidata; Q54953894 DT Created: 04-04-12; Last updated: 05-07-19; Version: 23

Hierarchy

DT Created: 04-04-12; Last updated: 05-07-19; Version: 23

Originate from Same Individual

DT Created: 04-04-12; Last updated: 05-07-19; Version: 23

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:


Abstract:

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)