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LPAR1  -  lysophosphatidic acid receptor 1

Bos taurus

 
 
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Disease relevance of EDG2

  • Although a pertussis toxin-sensitive G-protein has been reported to transmit the inhibitory signals between the LPA receptor and adenylyl cyclase, the observed upregulation of the enzyme activity in luteal cells is not abolished after pre-treating the cells with the toxin, suggesting that a different mechanism is operative in these cells [1].
 

High impact information on EDG2

  • The LPA-induced attenuation of steroid production occurs only in the mid-cycle corpus luteum and is associated with a transient endogenous expression of mRNA for the lysophosphatidic acid A2 (LPA2) receptor (with no concomitant changes in the expression of LPA1 receptor) [2].
  • Lysophosphatidylglycerol (LPG), a competitive inhibitor of the putative LPA receptor, inhibited the calcium releasing activity of LPA, but not that of LPS and SPC, suggesting that these lysophospholipids interact with different receptors and that desensitization is due to interactions in downstream signaling pathways [3].

References

  1. Functional lysophosphatidic acid receptor in bovine luteal cells. Budnik, L.T., Mukhopadhyay, A.K. FEBS Lett. (1997) [Pubmed]
  2. Differential effects of lysolipids on steroid synthesis in cells expressing endogenous LPA2 receptor. Budnik, L.T., Brunswig-Spickenheier, B. J. Lipid Res. (2005) [Pubmed]
  3. Effect of lysophospholipids on signaling in the human Jurkat T cell line. Xu, Y., Casey, G., Mills, G.B. J. Cell. Physiol. (1995) [Pubmed]
 
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