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FLASH GENE
Symbol BCR contributors: mct/npt - updated : 21-05-2017
HGNC name breakpoint cluster region
HGNC id 1014
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • a region of homology to GDP-GTP exchangers like CDC24, for Rac and Rho (Arh) proteins, (signal transduction)
    • HOMOLOGY
    Homologene
    FAMILY
    CATEGORY enzyme , protooncogene
    SUBCELLULAR LOCALIZATION     intracellular
    intracellular,cytoplasm,cytosolic
    intracellular,nucleus
    text
  • BCR and its close relative active BCR-related (ABR) localize at excitatory synapses
    • basic FUNCTION
  • promoting the exchange of RAC or CDC42-bound GDP by GTP thereby activating them
  • displaying serine/threonine kinase activity
  • PCAF and BCR signalling are essential for apoptotic cell death (PCAF and BCR signalling control cooperatively pre-mature B cell apoptosis via both depletions of DFFA and BIRC2)
  • ABR and BCR are the only GTPase-activating proteins to date that specifically negatively regulate Rac function in primary macrophages
  • BCR and ABR cooperate in negatively regulating acute inflammatory responses
  • represses the expression of PEBP1, continuously activates pERK1/2, and suppresses FOXM1 expression, resulting in proliferation of CML cells (
  • BCR-ABL increases FBXO5 phosphorylation and stability to prevent SKP2 protein degradation via APC/CDH1-induced ubiquitination and to enhance proliferation of CML cells
  • functional interaction between BCR-ABL and mitosis dysfunctions, due to compromised mitotic checkpoints, may have important implications for the generation of aneuploidy and CML progression
  • BCR and ABR have novel roles in the regulation of synaptic Rac1 signaling, synaptic plasticity, and learning and memory, and that excessive Rac1 activity negatively affects synaptic and cognitive functions
  • also acts via PPARG independent signaling
  • a RAC1 GTPase-activating protein that plays a key role in neuronal development
  • is involved in the regulation of neuronal development via control of the BCR GTPase-activating domain function by PTPRT
    • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling signal transduction
    a component
  • proximal BCR-ABL1 signaling network shows a modular and layered organization with an inner core of three leukemia transformation-relevant adaptor protein complexes (GRB2/GAB2/SHC1 complex, CRK complex and DOK1/DOK2 complex)
  • BCR-ABL1 suppresses autophagy through ATF5-mediated regulation of MTOR transcription
    • INTERACTION
    DNA
    RNA
    small molecule
    protein
  • binding of the adaptor protein GRB2 to Tyr177 of BCR-ABL1 is crucial for the leukemic transformation of cells by BCR-ABL1
  • TGM2 bound to the Rac-binding pocket in the GTPase-activating domains of BCR and ABR, blocked BCR activity and, through this mechanism, increased levels of active GTP-bound Rac and EGF-stimulated membrane ruffling
  • BCR-ABL fusion oncogene frequently found in chronic myeloid leukemia (CML) cells can up-regulate SKP2 expression via transcriptional activation
  • directly interact with DLG4, an abundant postsynaptic scaffolding protein
  • binds to DDX39B and binding of DDX39B to BCR is critical for BCR induced DNA synthesis in vascular smooth muscle cells (VSMC)
  • DDX329B/BCR interaction is important for BCR induced DNA synthesis
  • signaling cascades driven by the BCR and TLR9 have a newly identified meeting point at TBX21(
  • HAP1 interacts with BCR on microtubules to regulate neuronal differentiation
  • RICTOR positively regulates the early events of BCR signaling
    • cell & other
    REGULATION
    Other functional involvement of LRRK1 in the balance of BCR-ABL1-mediated MAP-kinase signaling
    Janus kinase 2 regulates BCR-ABL signaling in chronic myeloid leukemia
    function of the BCR GTPase-activating domain could be modulated by protein tyrosine phosphatase receptor T (PTPRT), which is expressed principally in the brain
    ASSOCIATED DISORDERS
    corresponding disease(s) BCR-ABL , DEL22Q11D
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    tumoral fusion      
    BCR-JAK2 fusion result of a t(9;22)(p24;q11.2) translocation in chronic myeloid leukemia
    tumoral fusion      
    fused with FGFR1 in t(8;22) (p11;q11) in myelo proliferative disorder and with PDGFRA in t(4;22) (q12;q11) in atypical chronic myeloid leukemia
    tumoral fusion      
    with ABL1, in reciprocal translocation between chromosomes 22 and 9 produces the Philadelphia chromosome, which is often found in patients with chronic myelogenous leukemia
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    SystemTypeDisorderPubmed
    cardiovascularaquired 
    BCR/DDX39B interaction may be a target for inhibiting pathological VSMC proliferation
    cancerhemopathy 
    targeting ROR1 simultaneously with inhibition of B-cell receptor (BCR) signaling is more effective in killing ROR1-positive leukemia cells
    ANIMAL & CELL MODELS