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FLASH GENE
Symbol KLRB1 contributors: mct - updated : 04-04-2014
HGNC name killer cell lectin-like receptor subfamily B, member 1
HGNC id 6373
DNA
TYPE functioning gene
STRUCTURE 12.63 kb     6 Exon(s)
10 Kb 5' upstream gene genomic sequence study
motif Viral sequence   long terminal repeat
text structure specific HERV-K LTR within intron 2
MAPPING cloned Y linked N status confirmed
RNA
TRANSCRIPTS type messenger
identificationnb exonstypebpproduct
ProteinkDaAAspecific expressionYearPubmed
6 - 740 25.28 225 - 1997 9162104
EXPRESSION
Type
   expressed in (based on citations)
organ(s)
cells
SystemCellPubmedSpeciesStageRna symbol
Lymphoid/Immunenatural killer Homo sapiens
Lymphoid/ImmuneT cell Homo sapiens
cell lineage
cell lines
fluid/secretion
at STAGE
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • an extracytoplasmic carbohydrate recognition domain homologous with C type lectin superfamily member, like Ly-49
  • one C-type lectin-like domain in the extracellular region responsible for the ligand recognition, that bound directly to CLEC2D
  • mono polymer homomer , dimer
    HOMOLOGY
    Homologene
    FAMILY
  • natural killer cell lectin-like receptor family
  • subfamily B
  • CATEGORY antigen , receptor
    SUBCELLULAR LOCALIZATION     plasma membrane
    text type II integral membrane protein
    basic FUNCTION
  • triggering cellular activation of NK cells and target lysis
  • its signaling in NK cells involves the activation of acid sphingomyelinase
  • role for CLEC2D/KLRB1 in modulating immune responses to pathogens
  • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
    INTERACTION
    DNA
    RNA
    small molecule
    protein
  • KLRB1 and ENTPD1 have direct interactions that are further linked with acid sphingomyelinase (ASM)
  • cell & other
    REGULATION
    induced by RORC (marker of all IL17-producing T-cell subsets and is induced by RORC)
    Other regulated by IL2 and IL12
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    constitutional     --over  
    in multiple sclerosis
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    ANIMAL & CELL MODELS