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FLASH GENE
Symbol BMPER contributors: mct/ - updated : 18-09-2013
HGNC name BMP binding endothelial regulator
HGNC id 24154
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • five N-terminal well conserved cysteine repeat regions (CR1–5), which are involved in BMP binding
  • five tandem von Willebrand C-like domains at the N-terminal side, which are considered to form a BMP-binding site, one of five VWCs from chordin, can bind BMPs
  • five Chordin-like cysteine-rich domains
  • C-terminal containing a furin-like, a von Willebrand type D, and a trypsin inhibitor domain
    • HOMOLOGY
    interspecies ortholog to Drosophila melanogaster Crossveinless-2
    Homologene
    FAMILY
  • crossveinless 2 family
    • CATEGORY regulatory
    SUBCELLULAR LOCALIZATION extracellular
        intracellular
    intracellular,cytoplasm,organelle,membrane
    intracellular,cytoplasm,organelle,endoplasmic reticulum
    basic FUNCTION
  • involved in cell adhesion and, binding of sperm to zona pellucida
  • antagonizing bone morphogenetic protein signaling and endothelial cell differentiation
  • regulating BMP responsiveness of osteoblasts and chondrocytes and inhibitor of BMP function
  • with chordin, and CHRDL2, regulate BMP2 signaling by different recognition mechanisms
  • permissive and necessary role for SMAD1/5 phosphorylation and induces Erk1/2 activation (necessary for BMP4 to exert its activating role in endothelial function and to induce SMAD1/5 activation)
  • dose-dependent endothelial cell activator that plays a unique and pivotal role in fine-tuning BMP activity in angiogenesis
  • plays an important role in endothelial cell function and blood vessel formation (Helbing 2009)
  • key regulator of BMP4 activity and a prerequisite for BMP pathway activation by BMP4 in endothelial cells
  • requirement for BMPER-mediated signaling in vertebral development
  • is a new protective regulator of vascular inflammation that modulates leukocyte adhesion and migration
  • BMP modulator BMPER is highly expressed in malignant tumors and tumor growth is dependent on the presence of BMPER
  • was more potent at inhibiting BMP effects compared with TWSG1, and there was no evidence of a significant additive anti-BMP effect of BMPER and TWSG1 together
  • may play a role in suppressing hepcidin in other forms of severe chronic anemia with iron loading or in diseases where there is a significant amount of angiogenesis
  • mutual regulation by GDF2 and BMPER is essential in regulating the development of the vascular endothelium
  • critical regulator of BMP-mediated vascular inflammation and that the fine-tuning of BMP and BMPER levels is essential in the maintenance of normal vascular homeostasis
  • is a novel regulator of osteoblast-like differentiation of VSMCs
  • is a novel regulator of the osteoblast-like differentiation of human coronary artery SMCs
  • appears to play a role in regulating both vessel density and cardiac development
  • BMPER and TWSG1 maintain a fine-tuned equilibrium that controls BMP pathway activity and is necessary for vascular cell homeostasis
    • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
    INTERACTION
    DNA
    RNA
    small molecule
    protein
  • with BMP2, BMP4, and BMP6
  • downstream target of FOXO3a and consistently exerts activating effects on endothelial cell sprouting and migration
  • inhibited the effects of both BMP2 and BMP6 on hepcidin production, although the effect on BMP6 was less pronounced than that for BMP2
  • disrupts complex formation involving ALK2, ALK1, BMP4, and GDF2 required for the induction of both BMP antagonists
  • TWSG1 and BMPER interfere with each other to enhance proangiogenic events
    • cell & other
    REGULATION
    activated by Krüppel-like factor (KLF)15 (KLF15 is a transducer of endothelin-1 activity on BMPER expression)
    inhibited by endothelin-1 in a dose-dependent fashion and in parallel to KLF15
    ASSOCIATED DISORDERS
    corresponding disease(s) DIASD
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    SystemTypeDisorderPubmed
    miscelleaneousvascular 
    may be a potential target for prevention of vascular calcification
    ANIMAL & CELL MODELS