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FLASH GENE
Symbol ADGRG6 contributors: mct/npt/pgu - updated : 14-11-2023
HGNC name adhesion G protein-coupled receptor G6
HGNC id 13841
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • a long extracellular N-terminal region and
  • C1r-C1s, Uegf and Bmp1 (CUB) and pentraxin (PTX)-like modules
  • a mucin-like spacer
  • a seven transmembrane domain (7tm_2)
  • a conserved GAIN domain
  • a GPCR proteolytic site (GPS) domains and heptahelical transmembrane domain shared by all GPCRs
    • HOMOLOGY
    interspecies homolog to rattus Gpr126 (84,68 pc)
    homolog to murine Gpr126 (84.19 pc)
    Homologene
    FAMILY
  • G-protein coupled receptor 2 family
  • LN-TM7 subfamily
  • adhesion GPCR (aGPCR) family of proteins
    • CATEGORY receptor membrane G
    SUBCELLULAR LOCALIZATION     plasma membrane
    basic FUNCTION
  • may be involved in neuropeptide signaling pathway
  • playing an important role in cell-adhesion and potentially in inflammation and coagulation
  • regulates the proliferation of pulmonary arterial smooth muscle cells and airway smooth muscle cells
  • required autonomously in Schwann cells for myelination
  • drives the differentiation of promyelinating Schwann cells by elevating cAMP levels, thereby triggering SLC22a16 expression and myelination
  • potentially equired for embryonic viability and cardiovascular development
  • essential for myelination and other aspects of peripheral nerve development in mammals
  • new roles in axonal sorting, formation of mature non-myelinating Schwann cells and organization of the perineurium
  • is required for proper trabeculation, contraction, and energy metabolism of the heart
  • acts as a receptor to drive myelin gene expression in PNS Schwann cells, whereas in the heart, the N-terminus of GPR126 acts as a ligand or coreceptor activating an unknown receptor
  • directly increases cAMP by coupling to heterotrimeric G-proteins
  • functions potentially in Schwann cells for proper development and myelination and these functions are mediated via G-protein-signaling pathways
  • modulates both physiological and pathological angiogenesis through VEGFA signaling, providing a potential target for the treatment of angiogenesis-related diseases
  • is critical for myelination of peripheral nerves
  • has also been implicated in bone mineralization
  • ADGRG6 is essential for Schwann cells (SCs) development and myelination
  • adhesion G protein-coupled receptor essential for Schwann cell (SC) myelination with important contributions to repair after nerve crush injury
  • ADGRG6 contributes to the terminal Schwann cell response at the neuromuscular junction following peripheral nerve injury
  • ADGRG6 extracellular regions (ECRs) utilizes a multi-faceted dynamic approach to regulate receptor function and provide relevant insights for ECR-targeted drug design
  • ADGRG6 is essential for placental development
  • possible role of ADGRG6 in kidney physiology
  • critical developmental roles in Schwann cell maturation and its mediated myelination in the peripheral nervous system
  • is likely involved in mounting an epithelial inflammatory response to smoke exposure
    • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling signal transduction
    a component
    INTERACTION
    DNA
    RNA
    small molecule
    protein
    cell & other
  • ADGRG6-expressing cells are known to be exposed to mechanical stimuli
    • REGULATION
    ASSOCIATED DISORDERS
    corresponding disease(s) AMCN4
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    constitutional     --low  
    in type 2 alveolar epithelial cells is decreased in chronic obstructive pulmonary disease (COPD)
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    SystemTypeDisorderPubmed
    respiratorylungchr.Bronchopathy obstructive
    as likely a novel therapeutic target for COPD
    neurologyacquired 
    represents an attractive potential target to stimulate repair in myelin disease or following nerve injury
    ANIMAL & CELL MODELS
  • Gpr126 deletion causes heart phenotypes in mice causing embryonic lethality
  • a mutation in Gpr126 causes a severe congenital hypomyelinating peripheral neuropathy in mice
  • Gpr126-/- mice have a lethal arthrogryposis phenotype
  • Gpr126-null mice with a heterozygous placenta survive but exhibit GPR126-defective peripheral nervous system (PNS) phenotype