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FLASH GENE
Symbol LTBR contributors: SGE/npt - updated : 31-05-2010
HGNC name lymphotoxin beta receptor (TNFR superfamily, member 3)
HGNC id 6718
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • extracytoplasmic cysteine-rich pseudorepeats
  • a small cytoplasmic domain with the serine/threonine kinase but lacking the DEATH domain
  • four TNFR-CYS repeats
  • conjugated GlycoP
    HOMOLOGY
    Homologene
    FAMILY
  • tumor necrosis factor receptor TNFR superfamily
  • CATEGORY receptor
    SUBCELLULAR LOCALIZATION     plasma membrane
    text type 1 transmembrane protein
    basic FUNCTION
  • specifically binding to the lymphotoxin membrane form and thus playing a role in the development and organization of lymphoid tissues and transformed cells
  • promoting apoptosis via TRAF3 and TRAF5
  • is required for liver regeneration, hepatitis and hepatic lipid metabolism (Tumanov 2007)
  • CELLULAR PROCESS cell life, cell death/apoptosis
    PHYSIOLOGICAL PROCESS development
    PATHWAY
    metabolism
    signaling
    a component
  • self-associating
  • INTERACTION
    DNA
    RNA
    small molecule
    protein
  • interacting with TRAF2 and TNFSF14 (TRAF2, an important effector molecule of TNF signaling, plays a critical, nonredundant role in TNFSF14-LTBR signaling)
  • interacts with HCV core protein
  • receptor for the heterotrimeric lymphotoxin containing LTA and LTB, and for TNFSF14
  • interacting with TRAF3, TRAF4, TRAF5
  • ZMYND11 abrogates LTBR function through a protein-protein interaction
  • cell & other
    REGULATION
    Other negatively regulated by TRAF3 (Bista 2010)
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Susceptibility
    Variant & Polymorphism
    Candidate gene
  • constitutively inducing NF-KappaB activation and it may be associated with autonomous growth of melanoma cells (Dhawan 2008)
  • Marker
    Therapy target
    ANIMAL & CELL MODELS
  • engagment of Ltbr by Tnfsf14 is essential for both intestinal inflammation and hyperserum IgA syndrome in a murine model that spontaneously develops T cell-mediated intestinal inflammation (Wang 2004)