NKp80/KLRF1 Proteins, cDNA Clones Research Reagents

KLRF1 (Killer Cell Lectin Like Receptor F1, also known as NKp80; CLEC5C), located on 12p13.31, is a Protein Coding gene. The gene produces a 26563 Da protein composed of 231 amino acids. KLRF1, an activating homodimeric C-type lectin-like receptor (CTLR), is expressed on nearly all natural killer (NK) cells and stimulates their cytotoxicity and cytokine release. The encoded protein has a 42-amino acid cytoplasmic region; a 23-amino acid transmembrane segment; and a 166-amino acid extracellular region. The related pathways of KLRF1 include Hematopoietic Stem Cells and Lineage-specific Markers and the Innate Immune System.

NKp80/KLRF1 Protein (1)

    NKp80/KLRF1 cDNA Clone (26)


    NKp80/KLRF1 qPCR Primer (1)

    NKp80/KLRF1 Lysate (1)

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      NKp80/KLRF1 Background

      NKp80, also known as KLRF1, is an activating homodimeric C-type lectin-like receptor that is expressed on nearly all-natural killer cells and stimulates their cytotoxicity and cytokine release. NKp80 stimulates cytotoxicity upon engagement of its genetically linked ligand: myeloid-specific CTLR activation-induced C-type lectin (AICL). NKp80, but not NKp80 mutated at tyrosine 7 (NKp80/Y7F), is tyrosine phosphorylated. Accordingly, NKp80/Y7F, but not NKp80/Y3F or NKp80/Y37F, failed to induce cytotoxicity. NKp80 phosphopeptides comprising the Hemi-ITAM-like sequence surrounding tyrosine 7 bound Lck- and Syk-family kinases; accordingly, cross-linking of NKp8, but not NKp80/Y7F, induced Syk phosphorylation. Moreover, inhibition of Syk kinase, but not ZAP-7 kinase, impaired cytotoxic responses through NKp80. Atypical residues in the Hemi-ITAM-like motif of NKp80 cause an altered stoichiometry of phosphorylation but did not substantially affect NK cytotoxicity. Altogether, these results show that NKp80 uses an atypical Hemi-ITAM and Syk kinase to trigger cellular cytotoxicity.

      NKp80/KLRF1 References

      • Kuttruff S. et al., 2009, Blood. 113 (2): 358-69.
      • Dennehy KM. et al., 2011, J Immunol. 186 (2): 657-61.
      • Roda-Navarro P. et al., 2000, Eur J Immunol. 30 (2): 568-76.

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