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FLASH GENE
Symbol BID contributors: mct/pgu - updated : 18-09-2015
HGNC name BH3 interacting domain death agonist
HGNC id 1050
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • eight alpha helices, containing from the N terminal
  • three BCL2 homology domain
    • mono polymer heteromer , dimer
    HOMOLOGY
    interspecies homolog to murine Bid
    Homologene
    FAMILY
  • BCL-2 family of cell death regulators
    • CATEGORY transcription factor
    SUBCELLULAR LOCALIZATION     intracellular
    intracellular,cytoplasm,organelle,mitochondria,outer
    intracellular,cytoplasm,organelle,membrane
    intracellular,cytoplasm,cytosolic
    text
  • expressed in cytosol and translocated to mitochondria after proteolytic activation by CASP8
  • truncated BID (tBID) translocates to the mitochondria, facilitates the release of cytochrome c, and activates the intrinsic pathways
  • binds to the membrane, and undergoes slow structural rearrangements that result in an equilibrium between two major tBID conformations on the membrane
    • basic FUNCTION
  • death agonist (inducing apoptosis), inducing mitochondrial damage by caspase-8 cleavage
  • acting downstream of MAPK8 in TNF signaling to mitochondria
  • important role in activating the mitochondrial apoptosis pathway after death receptor engagement, particularly in hepatocytes
  • regulates hepatocyte proliferation by positively affecting [Ca(2+)](ER) homeostasis, which could be important for liver regeneration and carcinogenesis
  • having a unique role in signaling of apoptosis, because it links the death receptor signaling pathway to the mitochondrial signaling pathway mediated by BCL2 proteins
  • mediator of mitochondrial damage induced by caspase-8 (CASP8)
  • a pro-apoptotic BCL-2 family member playing an essential role in initiating this program
  • involved in the Bak/Bax-dependent mitochondrial cell death pathway
  • putative cathepsin B target in SPARC-induced apoptosis
  • novel role of BID in inflammation and immunity independent of its apoptotic function
  • potential proximal regulator of the NOD1 signalling complex
  • involved in tumor necrosis factor death receptor I (TNFRI)-mediated destructive signal transduction pathways such as cell dysfunction or neurodegeneration in the temporal cortex of patients with Parkinson disease
    • CELLULAR PROCESS cell life, cell death/apoptosis
    nucleotide, transcription
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
  • heterodimerizing with either agonists (BAX) or antagonists (BCL2) of apoptosis
  • cleaved in response to apoptotic stimuli into two fragments, p7 and tBid (p15), that are held together by strong hydrophobic interactions until the complex binds to membranes (9)
    • INTERACTION
    DNA
    RNA
    small molecule
    protein
  • MAPK8, DIABLO for TNF-mediated CASP8 cleavage and apoptosis
  • GZMK directly processes BID to release cytochrome c and endonuclease G leading to mitochondria-dependent cell death
  • preferentially associated with the CK2alpha (CSNK2A1) subunit
  • BID, BCL2L11, and BBC3 are required to activate BAX- and BAK1-dependent mitochondrial apoptosis
  • CAV1 regulates hyperoxia/ROS-induced apoptosis through interactions with FAS and BID, probably via FAS palmitoylation and CAV1 Y14 phosphorylation, respectively
  • interacts with NOD1, NOD2 and the IKB kinase (IKK) complex, impacting NFKB and extracellular signal-regulated kinase (ERK) signalling
  • BID associates with RPA1 and stimulates the recruitment and/or stabilization of ATR-ATRIP to the DNA damage sensor complex
  • activates BAK1 to mitochondrial outer-membrane permeabilization (MOMP), which leads to apoptosis
  • KAT2B and TADA3 regulate BID processing via PACS2, to modulate the mitochondrial cell death pathway in response to GZMB
  • role for MOAP1 in FAS signaling in the liver by promoting MTCH2-mediated BID recruitment to mitochondria
  • ANXA1 interacted with the BID (BH3-interacting-domain death agonist) promoter directly
    • cell & other
    REGULATION
    activated by CASP8
    Other regulated in part by alternative splicing
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    constitutional       loss of function
    loss of BID function impaired the ability of NOD2 but not TLR3 to trigger tissue repair responses upon injury
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    SystemTypeDisorderPubmed
    cancerreproductivebreast
    with its substrate CTSB were shown to be molecular links between apoptosis and autophagy in breast cancer MCF-7 cells exposed to the cytostatic drug, camptothecin
    ANIMAL & CELL MODELS
  • Bid-/- mice are unresponsive to local or systemic exposure to NOD agonists or their protective effect in experimental colitis