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GPR132

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Target id: 128

Nomenclature: GPR132

Family: Class A Orphans

Contents:

Gene and Protein Information Click here for help
class A G protein-coupled receptor
Species TM AA Chromosomal Location Gene Symbol Gene Name Reference
Human 7 380 14q32.33 GPR132 G protein-coupled receptor 132 27
Mouse 7 382 12 F1 Gpr132 G protein-coupled receptor 132
Rat 7 376 6q32 Gpr132 G protein-coupled receptor 132
Previous and Unofficial Names Click here for help
G protein-coupled receptor G2A | G2 accumulation protein
Database Links Click here for help
Specialist databases
GPCRdb gp132_human (Hs), gp132_mouse (Mm)
Other databases
Alphafold Q9UNW8 (Hs), Q9Z282 (Mm), D3ZIH1 (Rn)
ChEMBL Target CHEMBL3085618 (Hs)
Ensembl Gene ENSG00000183484 (Hs), ENSMUSG00000021298 (Mm), ENSRNOG00000013914 (Rn)
Entrez Gene 29933 (Hs), 56696 (Mm), 314480 (Rn)
Human Protein Atlas ENSG00000183484 (Hs)
KEGG Gene hsa:29933 (Hs), mmu:56696 (Mm), rno:314480 (Rn)
OMIM 606167 (Hs)
Pharos Q9UNW8 (Hs)
RefSeq Nucleotide NM_013345 (Hs), NM_019925 (Mm), NM_001170595 (Rn)
RefSeq Protein NP_037477 (Hs), NP_064309 (Mm), NP_001164066 (Rn)
UniProtKB Q9UNW8 (Hs), Q9Z282 (Mm), D3ZIH1 (Rn)
Wikipedia GPR132 (Hs)
Natural/Endogenous Ligands Click here for help
9-hydroxyoctadecadienoic acid
(lyso)phospholipid mediators, protons
Endogenous ligand
Protons

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Agonists
Key to terms and symbols View all chemical structures Click column headers to sort
Ligand Sp. Action Value Parameter Reference
NOX-6-7 Small molecule or natural product Ligand has a PDB structure Hs Agonist 7.3 pEC50 26
⤷ pEC50 7.3 (EC50 5x10-8 M) Efficacy 53% [26]
ONC212 Small molecule or natural product Hs Agonist 6.4 pEC50 14
⤷ pEC50 6.4 (EC50 4.05x10-7 M) [14]
Description: Measuring β-arrestin recruitment using the PathHunter assay system.
9-hydroxyoctadecadienoic acid Small molecule or natural product Ligand is endogenous in the given species Ligand has a PDB structure Hs Full agonist 5.7 pEC50 15
⤷ pEC50 5.7 (EC50 2x10-6 M) [15]
Agonist Comments
GPR132 has been reported to be activated by lysophosphatidylserine [30], by oxidized free fatty acids produced by oxidation and subsequent hydrolysis of phosphatidylcholine or cholesteryl linoleate [4] A report that the receptor was activated by lysophosphatidylcholine [8] was later retracted [28]. GPR4, GPR65, GPR68 and GPR132 are now thought to function as proton-sensing receptors detecting acidic pH [3,13,25].
Antagonists
Key to terms and symbols View all chemical structures Click column headers to sort
Ligand Sp. Action Value Parameter Reference
NOX-6-18 Small molecule or natural product Hs Antagonist 7.8 pIC50 26
⤷ pIC50 7.8 (IC50 1.7x10-8 M) [26]
Description: Efficacy 90%
Antagonist Comments
Lysophosphatidylcholine inhibited the pH-dependent activation of GPR132 in a dose dependent manner [13].
Primary Transduction Mechanisms Click here for help
Transducer Effector/Response
Other - See Comments
Comments:  GPR132 has been proposed to signal through Gα13 and Gαs [5,11]. Both pertussis toxin-sensitive and -insensitive G-proteins have been implicated in phospholipase C activation through GPR132 [13].
References:  11,30
Tissue Distribution Click here for help
Spleen, thymus, heart, lung
Species:  Human
Technique:  Northern blot
References:  27
Macrophages, monocytic THP-1 cells (low staining: Jurkat T cells, coronary artery smooth muscle cells, umbilical vein endothelial cells)
Species:  Human
Technique:  Immunohistochemistry
References:  24
Epidermis, normal epidermal keratinocytes, immortalized keratinocyte cell line (HaCaT)
Species:  Human
Technique:  Immunohistochemistry
References:  6
Peripheral blood leukocytes, heart, brain, kidney, placenta
Species:  Human
Technique:  RT-PCR
References:  16
Macrophages
Species:  Mouse
Technique:  Immunohistochemistry
References:  24
Spleen, thymus, T cells, B cells
Species:  Mouse
Technique:  Northern blot
References:  30
Tissue Distribution Comments
Colocalisation of GPR132 with macrophages identified in atherosclerotic plaques in humans and mice [24].

GPR132 is not expressed in human brain microvascular or dermal microvascular endothelial cells (RT-PCR) [12].

Expression Datasets Click here for help

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Log average relative transcript abundance in mouse tissues measured by qPCR from Regard, J.B., Sato, I.T., and Coughlin, S.R. (2008). Anatomical profiling of G protein-coupled receptor expression. Cell, 135(3): 561-71. [PMID:18984166] [Raw data: website]

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Functional Assay Comments
The reported action of LPC in stimulating macrophage and T-cell chemotaxis (via GPR132) [23], was replicated in vivo in one study [29] but not in others [17-18].
Physiological Functions Click here for help
Tumour suppressor promoting cell cycle arrest
Species:  Mouse
Tissue:  Lymphocytes
References:  10,27
Macrophage mediated neutrophil clearance
Species:  Mouse
Tissue:  Peritoneal cells
References:  4
Hepatobiliary bile salt, cholesterol, and phospholipid homeostasis
Species:  Mouse
Tissue:  Liver, gall bladder
References:  7
Physiological Consequences of Altering Gene Expression Click here for help
Lymphocytic infiltration, glomerular immune complex deposition, and anti-nuclear autoantibodies. T cells are hyperresponsive to TCR stimulation. Aged receptor knockout mice have secondary lymphoid organ enlargement associated with abnormal expansion of both T and B lymphocytes. Mice >1 year develop a slowly progressive wasting syndrome
Species:  Mouse
Tissue:  T and B lymphocytes
Technique:  Gene knockouts
References:  9
Overexpression of receptor in NIH-3T3 fibroblasts induces characteristics of oncogenic transformation. Loss of contact inhibition, survival and proliferation in the absence of anchorage or in reduced concentrations of growth factors, and tumor initiation in vivo
Species:  Mouse
Tissue:  Not specified
Technique:  NIH3T3 cell line
References:  30
Reduced plaque stability. Loss of GPR132 does not affect macrophage and T-cell infiltration, but does reduce collagen deposition in atherosclerotic plaques.
Species:  Mouse
Tissue:  Macrophages
Technique:  Gene knockouts
References:  18
Inhibition of LPC-induced chemotaxis. Wild-type but not GPR132 (G2A)-deficient mouse peritoneal macrophages migrated toward LPC.
Species:  Mouse
Tissue:  Macrophages
Technique:  RNA interference (RNAi)
References:  29
GPR132-deficient mice exhibit a similar incidence and onset of experimental autoimmune encephalomyelitis (EAE), and disease severity is only moderately reduced in knockout mice. Comparable numbers of T cells were generated in secondary lymphoid organs and spinal cords of knockout and WT mouse models of EAE
Species:  Mouse
Tissue:  T cells
Technique:  Gene knockouts
References:  17
Knockdown of GPR132 results in decreased migration to apoptotic culture supernatant and LysoPC
Species:  Human
Tissue:  THP-1 cells
Technique:  RNA interference (RNAi)
References:  21
GPR132 knockout ameliorates aortic atherosclerosis in low-density lipoprotein receptor knockout mice. Reduction in aortic lesion coverage, macrophage accumulation and T-cell recruitment
Species:  Mouse
Tissue:  Aorta
Technique:  Gene knockouts
References:  19
Increased cytokine secretion. Intracellular calcium mobilization and secretion of cytokines IL-6, IL-8, and GM-CSF are enhanced by receptor overexpression
Species:  Human
Tissue:  Keratinocytes
Technique:  Gene over expression
References:  6
Deletion of GPR132 in LDLR(-/-) mice increases the ApoA1, ApoE, and cholesterol content of plasma HDL fractions. GPR132 deficiency affects atherosclerosis in a tissue-specific manner. ApoE dependent pro-atherogenic phenotype is observed
Species:  Mouse
Tissue:  Hepatocytes, macrophages
Technique:  Gene knockouts
References:  20
Expanded population of leukemic cells. Shorter latency of BCR-ABL dependent chronic myeloid leukemia in receptor deficient mice
Species:  Mouse
Tissue:  Bone marrow leukocytes
Technique:  Targeting in embryonic stem cells
References:  10
Mildly cholestatic phenotype with altered hepatobiliary homeostasis and gall stone formation. Chow fed receptor knockout mice had reduced biliary phosphatidylcholine content, reduced hepatic gene expression of ATP-binding cassette B4, and increased expression of liver X receptor (LXR). Receptor knockout mice on a lithogenic diet had rapid gallstone formation, increased cholesterol saturation index, increased farnesoid X receptor expression, increased LXR expression, and a 90% reduction in cholesterol 7alpha-hydroxylase expression
Species:  Mouse
Tissue:  Liver
Technique:  Gene knockouts
References:  7
Absence of the GPR132 in mice promotes monocyte/endothelial interactions in aorta accompanied by 3-fold increase in interleukin-6 and monocyte chemoattractant protein-1 production and a dramatic increase in nuclear localization of the p65 subunit of nuclear factor κB. Proinflammatory signalling and increased monocyte/endothelial interactions in the aortic wall
Species:  Mouse
Tissue:  Aorta (monocytes, endothelial cells)
Technique:  Gene knockouts
References:  2
Reduced inhibition of DNA synthesis and cell cycle arrest. Receptor downregulation caused suppression of 9(S)-HODE-induced inhibitory effects on proliferation of keratinocytes.
Species:  Human
Tissue:  NHEK cells
Technique:  RNA interference (RNAi)
References:  6
Increased macrophage activation, accumulation and attenuated apoptosis, increased lesion size. GPR132 deficiency in mice reduces macrophage apoptosis and ability to engulf apoptotic cells in vitro, and promotes macrophage activation and atherosclerosis in vivo
Species:  Mouse
Tissue:  Peritoneal macrophages
Technique:  Not specified
References:  1
Physiological Consequences of Altering Gene Expression Comments
Studies of GPR132 knockout mice have produced conflicting results regarding the role of the receptor in attenuation of experimental autoimmune encephalomyelitis. One study suggested that GPR132 negatively regulates T-cell recruitment [9], whilst a more recent study concluded that the proposed anti-proliferative and chemotactic functions of the receptor are not manifested in vivo and therefore therapeutic targeting of G2A is unlikely to be beneficial in the treatment of multiple sclerosis [17]. Studies of GPR132 knockout mice have also produced conflicting results regarding the role of the receptor in protection from [1-2] or promotion of [19] atherosclerosis. One study investigating GPR132 knockout in LDLR-/- and ApoE-/- mice, suggested an ApoE-dependent function for GPR132 in the control of hepatic HDL metabolism that might contribute to proatherogenic action [20].
Phenotypes, Alleles and Disease Models Click here for help Mouse data from MGI

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Allele Composition & genetic background Accession Phenotype Id Phenotype Reference
Gpr132tm1Witt Gpr132tm1Witt/Gpr132tm1Witt
involves: 129X1/SvJ * BALB/c		 MGI:1890220  MP:0002722 abnormal immune system organ morphology PMID: 11371358 
Gpr132tm1Witt Gpr132tm1Witt/Gpr132tm1Witt
involves: 129X1/SvJ * BALB/c		 MGI:1890220  MP:0002339 abnormal lymph node morphology PMID: 11371358 
Gpr132tm1Witt Gpr132tm1Witt/Gpr132tm1Witt
involves: 129X1/SvJ * BALB/c		 MGI:1890220  MP:0003945 abnormal lymphocyte physiology PMID: 11371358 
Gpr132tm1Witt|Ldlrtm1Her Gpr132tm1Witt/Gpr132tm1Witt,Ldlrtm1Her/Ldlrtm1Her
B6.129-Ldlr Gpr132		 MGI:1890220  MGI:96765  MP:0002451 abnormal macrophage physiology PMID: 15834123 
Gpr132tm1Witt|Ldlrtm1Her Gpr132tm1Witt/Gpr132tm1Witt,Ldlrtm1Her/Ldlrtm1Her
B6.129-Ldlr Gpr132		 MGI:1890220  MGI:96765  MP:0005338 atherosclerotic lesions PMID: 15834123 
Gpr132tm1Witt Gpr132tm1Witt/Gpr132tm1Witt
involves: 129X1/SvJ * BALB/c		 MGI:1890220  MP:0005150 cachexia PMID: 11371358 
Gpr132tm1Witt Gpr132tm1Witt/Gpr132tm1Witt
involves: 129X1/SvJ * BALB/c		 MGI:1890220  MP:0009623 enlarged inguinal lymph nodes PMID: 11371358 
Gpr132tm1Witt Gpr132tm1Witt/Gpr132tm1Witt
involves: 129X1/SvJ * BALB/c		 MGI:1890220  MP:0000691 enlarged spleen PMID: 11371358 
Gpr132tm1Witt Gpr132tm1Witt/Gpr132tm1Witt
B6.129X1-Gpr132		 MGI:1890220  MP:0003799 impaired macrophage migration PMID: 15383458 
Gpr132tm1Witt Gpr132tm1Witt/Gpr132tm1Witt
involves: 129X1/SvJ * BALB/c		 MGI:1890220  MP:0004794 increased anti-nuclear antigen antibody level PMID: 11371358 
Gpr132tm1Witt Gpr132tm1Witt/Gpr132tm1Witt
involves: 129X1/SvJ * BALB/c		 MGI:1890220  MP:0005154 increased B cell proliferation PMID: 11371358 
Gpr132tm1Witt Gpr132tm1Witt/Gpr132tm1Witt
involves: 129X1/SvJ * BALB/c		 MGI:1890220  MP:0002495 increased IgA level PMID: 11371358 
Gpr132tm1Witt Gpr132tm1Witt/Gpr132tm1Witt
involves: 129X1/SvJ * BALB/c		 MGI:1890220  MP:0008499 increased IgG1 level PMID: 11371358 
Gpr132tm1Witt Gpr132tm1Witt/Gpr132tm1Witt
involves: 129X1/SvJ * BALB/c		 MGI:1890220  MP:0002461 increased immunoglobulin level PMID: 11371358 
Gpr132tm1Witt Gpr132tm1Witt/Gpr132tm1Witt
involves: 129X1/SvJ * BALB/c		 MGI:1890220  MP:0001846 increased inflammatory response PMID: 11371358 
Gpr132tm1Witt Gpr132tm1Witt/Gpr132tm1Witt
involves: 129X1/SvJ * BALB/c		 MGI:1890220  MP:0005348 increased T cell proliferation PMID: 11371358 
Gpr132tm1Witt Gpr132tm1Witt/Gpr132tm1Witt
involves: 129X1/SvJ * BALB/c		 MGI:1890220  MP:0001859 kidney inflammation PMID: 11371358 
Gpr132tm1Witt Gpr132tm1Witt/Gpr132tm1Witt
involves: 129X1/SvJ * BALB/c		 MGI:1890220  MP:0001860 liver inflammation PMID: 11371358 
Gpr132tm1Witt Gpr132tm1Witt/Gpr132tm1Witt
involves: 129X1/SvJ * BALB/c		 MGI:1890220  MP:0001861 lung inflammation PMID: 11371358 
Gene Expression and Pathophysiology Comments
GPR132 is believed to be a tumour suppressor gene which is upregulated in response to DNA damage. Loss upregulates oncogene expression (c-myc and BCR-ABL) associated with chronic myelogeneous leukemia [27].

GPR132 is implicated in the pathogenesis of cholesterol gallstone formation [7].
Biologically Significant Variants Click here for help
Type:  Splice variant
Species:  Human
Description:  Alternative splice variant of GPR132B (G2A-b) has a partially different N terminus compared with the GPR132A originally reported (G2A-a).
References:  16
Biologically Significant Variant Comments
An alternative splice variant of GPR132 (G2A-b) has a different N terminus to the isoform originally reported (G2A-a). The two splice variants show similar tissue distributions, but G2A-b is expressed more abundantly and produces higher basal rates of IP accumulation [16].
General Comments
Receptor is believed to be a proton sensor: transient expression of GPR132 causes significant activation of the zif 268 promoter and inositol phosphate (IP) accumulation at pH 7.6, and lowering extracellular pH augments the activation only in GPR132-expressing cells [13,15]. However, the histidine residues that were previously shown to be important for pH sensing by OGR1, GPR4, and TDAG8 were not conserved in GPR132 (G2A). In thymocytes and splenocytes explanted from receptor-deficient mice, TDAG8 was found to be critical for pH-dependent cAMP production, but GPR132 was found to be dispensable for this process [22].

References

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1. Bolick DT, Skaflen MD, Johnson LE, Kwon SC, Howatt D, Daugherty A, Ravichandran KS, Hedrick CC. (2009) G2A deficiency in mice promotes macrophage activation and atherosclerosis. Circ Res, 104 (3): 318-27. [PMID:19106413]

2. Bolick DT, Whetzel AM, Skaflen M, Deem TL, Lee J, Hedrick CC. (2007) Absence of the G protein-coupled receptor G2A in mice promotes monocyte/endothelial interactions in aorta. Circ Res, 100 (4): 572-80. [PMID:17255525]

3. Davenport AP, Alexander SP, Sharman JL, Pawson AJ, Benson HE, Monaghan AE, Liew WC, Mpamhanga CP, Bonner TI, Neubig RR et al.. (2013) International Union of Basic and Clinical Pharmacology. LXXXVIII. G protein-coupled receptor list: recommendations for new pairings with cognate ligands. Pharmacol Rev, 65 (3): 967-86. [PMID:23686350]

4. Frasch SC, Berry KZ, Fernandez-Boyanapalli R, Jin HS, Leslie C, Henson PM, Murphy RC, Bratton DL. (2008) NADPH oxidase-dependent generation of lysophosphatidylserine enhances clearance of activated and dying neutrophils via G2A. J Biol Chem, 283 (48): 33736-49. [PMID:18824544]

5. Frasch SC, Zemski-Berry K, Murphy RC, Borregaard N, Henson PM, Bratton DL. (2007) Lysophospholipids of different classes mobilize neutrophil secretory vesicles and induce redundant signaling through G2A. J Immunol, 178 (10): 6540-8. [PMID:17475884]

6. Hattori T, Obinata H, Ogawa A, Kishi M, Tatei K, Ishikawa O, Izumi T. (2008) G2A plays proinflammatory roles in human keratinocytes under oxidative stress as a receptor for 9-hydroxyoctadecadienoic acid. J Invest Dermatol, 128 (5): 1123-33. [PMID:18034171]

7. Johnson LE, Elias MS, Bolick DT, Skaflen MD, Green RM, Hedrick CC. (2008) The G protein-coupled receptor G2A: involvement in hepatic lipid metabolism and gallstone formation in mice. Hepatology, 48 (4): 1138-48. [PMID:18821587]

8. Kabarowski JH, Zhu K, Le LQ, Witte ON, Xu Y. (2001) Lysophosphatidylcholine as a ligand for the immunoregulatory receptor G2A. Science, 293 (5530): 702-5. [PMID:11474113]

9. Le LQ, Kabarowski JH, Weng Z, Satterthwaite AB, Harvill ET, Jensen ER, Miller JF, Witte ON. (2001) Mice lacking the orphan G protein-coupled receptor G2A develop a late-onset autoimmune syndrome. Immunity, 14 (5): 561-71. [PMID:11371358]

10. Le LQ, Kabarowski JH, Wong S, Nguyen K, Gambhir SS, Witte ON. (2002) Positron emission tomography imaging analysis of G2A as a negative modifier of lymphoid leukemogenesis initiated by the BCR-ABL oncogene. Cancer Cell, 1 (4): 381-91. [PMID:12086852]

11. Lin P, Ye RD. (2003) The lysophospholipid receptor G2A activates a specific combination of G proteins and promotes apoptosis. J Biol Chem, 278 (16): 14379-86. [PMID:12586833]

12. Lum H, Qiao J, Walter RJ, Huang F, Subbaiah PV, Kim KS, Holian O. (2003) Inflammatory stress increases receptor for lysophosphatidylcholine in human microvascular endothelial cells. Am J Physiol Heart Circ Physiol, 285 (4): H1786-9. [PMID:12805023]

13. Murakami N, Yokomizo T, Okuno T, Shimizu T. (2004) G2A is a proton-sensing G-protein-coupled receptor antagonized by lysophosphatidylcholine. J Biol Chem, 279 (41): 42484-91. [PMID:15280385]

14. Nii T, Prabhu VV, Ruvolo V, Madhukar N, Zhao R, Mu H, Heese L, Nishida Y, Kojima K, Garnett MJ et al.. (2019) Imipridone ONC212 activates orphan G protein-coupled receptor GPR132 and integrated stress response in acute myeloid leukemia. Leukemia, 33 (12): 2805-2816. [PMID:31127149]

15. Obinata H, Hattori T, Nakane S, Tatei K, Izumi T. (2005) Identification of 9-hydroxyoctadecadienoic acid and other oxidized free fatty acids as ligands of the G protein-coupled receptor G2A. J Biol Chem, 280 (49): 40676-83. [PMID:16236715]

16. Ogawa A, Obinata H, Hattori T, Kishi M, Tatei K, Ishikawa O, Izumi T. (2010) Identification and analysis of two splice variants of human G2A generated by alternative splicing. J Pharmacol Exp Ther, 332 (2): 469-78. [PMID:19855098]

17. Osmers I, Smith SS, Parks BW, Yu S, Srivastava R, Wohler JE, Barnum SR, Kabarowski JH. (2009) Deletion of the G2A receptor fails to attenuate experimental autoimmune encephalomyelitis. J Neuroimmunol, 207 (1-2): 18-23. [PMID:19135725]

18. Parks BW, Gambill GP, Lusis AJ, Kabarowski JH. (2005) Loss of G2A promotes macrophage accumulation in atherosclerotic lesions of low density lipoprotein receptor-deficient mice. J Lipid Res, 46 (7): 1405-15. [PMID:15834123]

19. Parks BW, Lusis AJ, Kabarowski JH. (2006) Loss of the lysophosphatidylcholine effector, G2A, ameliorates aortic atherosclerosis in low-density lipoprotein receptor knockout mice. Arterioscler Thromb Vasc Biol, 26 (12): 2703-9. [PMID:16990555]

20. Parks BW, Srivastava R, Yu S, Kabarowski JH. (2009) ApoE-dependent modulation of HDL and atherosclerosis by G2A in LDL receptor-deficient mice independent of bone marrow-derived cells. Arterioscler Thromb Vasc Biol, 29 (4): 539-47. [PMID:19164809]

21. Peter C, Waibel M, Radu CG, Yang LV, Witte ON, Schulze-Osthoff K, Wesselborg S, Lauber K. (2008) Migration to apoptotic "find-me" signals is mediated via the phagocyte receptor G2A. J Biol Chem, 283 (9): 5296-305. [PMID:18089568]

22. Radu CG, Nijagal A, McLaughlin J, Wang L, Witte ON. (2005) Differential proton sensitivity of related G protein-coupled receptors T cell death-associated gene 8 and G2A expressed in immune cells. Proc Natl Acad Sci USA, 102 (5): 1632-7. [PMID:15665078]

23. Radu CG, Yang LV, Riedinger M, Au M, Witte ON. (2004) T cell chemotaxis to lysophosphatidylcholine through the G2A receptor. Proc Natl Acad Sci USA, 101 (1): 245-50. [PMID:14681556]

24. Rikitake Y, Hirata K, Yamashita T, Iwai K, Kobayashi S, Itoh H, Ozaki M, Ejiri J, Shiomi M, Inoue N et al.. (2002) Expression of G2A, a receptor for lysophosphatidylcholine, by macrophages in murine, rabbit, and human atherosclerotic plaques. Arterioscler Thromb Vasc Biol, 22 (12): 2049-53. [PMID:12482833]

25. Seuwen K, Ludwig MG, Wolf RM. (2006) Receptors for protons or lipid messengers or both?. J Recept Signal Transduct Res, 26 (5-6): 599-610. [PMID:17118800]

26. Wang JL, Dou XD, Cheng J, Gao MX, Xu GF, Ding W, Ding JH, Li Y, Wang SH, Ji ZW et al.. (2023) Functional screening and rational design of compounds targeting GPR132 to treat diabetes. Nat Metab, 5 (10): 1726-1746. [PMID:37770763]

27. Weng Z, Fluckiger AC, Nisitani S, Wahl MI, Le LQ, Hunter CA, Fernal AA, Le Beau MM, Witte ON. (1998) A DNA damage and stress inducible G protein-coupled receptor blocks cells in G2/M. Proc Natl Acad Sci USA, 95 (21): 12334-9. [PMID:9770487]

28. Witte ON, Kabarowski JH, Xu Y, Le LQ, Zhu K. (2005) Retraction. Science, 307 (5707): 206. [PMID:15653487]

29. Yang LV, Radu CG, Wang L, Riedinger M, Witte ON. (2005) Gi-independent macrophage chemotaxis to lysophosphatidylcholine via the immunoregulatory GPCR G2A. Blood, 105 (3): 1127-34. [PMID:15383458]

30. Zohn IE, Klinger M, Karp X, Kirk H, Symons M, Chrzanowska-Wodnicka M, Der CJ, Kay RJ. (2000) G2A is an oncogenic G protein-coupled receptor. Oncogene, 19 (34): 3866-77. [PMID:10951580]

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