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Details for receptor: Probable G-protein coupled receptor 132

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EndoNet ID: ENR01323

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Synonyms

  • G2A
  • G2 accumulation protein
  • Probable G-protein coupled receptor 132
  • G-protein coupled receptor 132
  • GPR132

General information

  • Belongs to the G-protein coupled receptor 1 family.
  • Induction by stress and DNA-damaging agents. [1]

Links to other resources

UniProt Q9UNW8
Ensembl ENST00000392585

Subunit information

Isoform 1 (1 times)

Sequence 
MCPMLLKNG YNGNATPVT TTAPWASLG 
LSAKTCNNV SFEESRIVL VVVYSAVCT 
LGVPANCLT AWLALLQVL QGNVLAVYL 
LCLALCELL YTGTLPLWV IYIRNQHRW 
TLGLLACKV TAYIFFCNI YVSILFLCC 
ISCDRFVAV VYALESRGR RRRRTAILI 
SACIFILVG IVHYPVFQT EDKETCFDM 
LQMDSRIAG YYYARFTVG FAIPLSIIA 
FTNHRIFRS IKQSMGLSA AQKAKVKHS 
AIAVVVIFL VCFAPYHLV LLVKAAAFS 
YYRGDRNAM CGLEERLYT ASVVFLCLS 
TVNGVADPI IYVLATDHS RQEVSRIHK 
GWKEWSMKT DVTRLTHSR DTEELQSPV 
ALADHYTFS RPVHPPGSP CPAKRLIEE 
SC
UniProt Q9UNW8-1

Isoform 2 (1 times)

Sequence 
MLQMDSRIA GYYYARFTV GFAIPLSII 
AFTNHRIFR SIKQSMGLS AAQKAKVKH 
SAIAVVVIF LVCFAPYHL VLLVKAAAF 
SYYRGDRNA MCGLEERLY TASVVFLCL 
STVNGVADP IIYVLATDH SRQEVSRIH 
KGWKEWSMK TDVTRLTHS RDTEELQSP 
VALADHYTF SRPVHPPGS PCPAKRLIE 
ESC
UniProt Q9UNW8-2

Binding hormones

  • Sphingosylphosphorylcholine
    • Was originally thought to be a receptor for sphingosylphosphorylcholine (SPC), However, this work has been retracted. [2]
  • lysophosphatidylcholine
    (trough: blood
    )
    • Was originally thought to be a receptor for lysophosphatidylcholine (LPC). However, this work has been retracted. [2]

Anatomical structures with this receptor

  • macrophage

    Induced phenotypes

    • regulation of innate immune response
      • Innate immune responses of macrophages may be regulated via G2A in response to local fluctuations in lysolipids encountered during infection and inflammation. It is possible that LPC produced at sites of inflammation and from disintegrating apoptotic/necrotic cell membranes may be a novel “molecular pattern” recognized by G2A to modulate innate immune processes and the initiation and/or resolution of inflammatory responses. [3]
    • atherosclerosis
      • The key role of LPC as a major antigenic component of oxLDL has implicated this bioactive lipid in atherosclerosis, the primary cause of heart disease and stroke. [3]
      • Aspects of immune function as potential targets of LPC action play some role in atherogenesis. Macrophage responses to oxLDL such as migration and activation are likely determined to a significant extent by its LPC content, and may therefore be mediated to some degree via G2A and/or GPR4. [3]

  • spleen

    Induced phenotypes

    • lymphocyte homeostasis
      • Disruption of G2A in mice leads to immunological disorders. The G2A(-/-) mice develop enlarged spleens with abnormal expansion of both T- and B-lymphocytes. [4]

  • thymus

  • heart

  • lung

  • bone_marrow

  • lymph_node

    Induced phenotypes

    • lymphocyte homeostasis
      • Disruption of G2A in mice leads to immunological disorders. The G2A(-/-) mice develop enlarged lymph nodes with abnormal expansion of both T- and B-lymphocytes. [4]

  • lymphocyte

    Induced phenotypes

    • regulation of actin cytoskeleton organization
      • G2A may relay signals regulating APC migration between tissue and lymph in response to LPC produced at inflammatory sites through its effects on actin cytoskeleton reorganization. [5]
    • lymphocyte homeostasis
      • Old G2A-deficient mice (older than 1 year) develop a late-onset autoimmune syndrome, indicating that G2A plays a role in the control of lymphocyte homeostasis. [4]

  • T-lymphocyte

    Induced phenotypes

    • Systemic lupus erythematosus
      • Further complexity is introduced by the broad cellular involvement in SLE and the presence of related LPC receptors in multiple immune cell types. [3]
      • Several studies suggest that endogenously produced LPC may influence T cell responses and that receptor-mediated signals are involved. [3]
      • Increased levels of antibodies against LPC in patients with Systemic Lupus Erythematosus and the development of systemic autoimmune disease in G2A-deficient animals suggest a pathophysiological connection. How the pathology of this disease could relate to this receptor/ligand pair is likely to be complex considering the multiple susceptibility factors involved in SLE. [3]
    • modulation of T cell response
      • Genetic ablation of G2A function in mice has revealed a role for G2A in the homeostatic regulation of lymphocyte pools and the maintenance of immunological tolerance. G2A-deficient mice T lymphocytes exhibit hyperproliferative responses to antigen receptor stimulation. [4]
    • regulation of T cell activation
      • APC/T lymphocyte interactions within lymph nodes may be modulated by autocrine/paracrine production of LPC through G2A to influence the threshold for T cell activation. [3]

  • dendritic_cell_in_lymphoid_tissues

    Induced phenotypes

    • regulation of innate immune response
      • Innate immune responses of dendritic cells may be regulated via G2A in response to local fluctuations in lysolipids encountered during infection and inflammation. It is possible that LPC produced at sites of inflammation and from disintegrating apoptotic/necrotic cell membranes may be a novel “molecular pattern” recognized by G2A to modulate innate immune processes and the initiation and/or resolution of inflammatory responses. [3]
Reference