|Jmol-3D images||Image 1|
|Molar mass||436.52 g/mol|
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Except where noted otherwise, data are given for materials in their standard state (at 25 °C (77 °F), 100 kPa)
LPA acts as a potent mitogen due to its activation of three high-affinity G-protein-coupled receptors called LPA1, LPA2, and LPA3 (also known as EDG2, EDG4, and EDG7). Additional, newly identified LPA receptors include LPA4 (p2y9/GPR23), LPA5 (GPR92) and LPA6 (GPR87).
Because of its ability to stimulate cell proliferation, aberrant LPA-signaling has been linked to cancer in numerous ways. Dysregulation of autotaxin or the LPA receptors can lead to hyperproliferation, which may contribute to oncogenesis and metastasis.
LPA may be the cause of pruritus (itching) in individuals with cholestatic (impaired bile flow) diseases.
Downstream of LPA receptor activation, the small GTPase Rho can be activated, subsequently activating Rho kinase. This can lead to the formation of stress fibers and cell migration through the inhibition of myosin light-chain phosphatase.
There are a number of potential routes to its biosynthesis, but the most well-characterized is by the action of a lysophospholipase D called autotaxin, which removes the choline group from lysophosphatidylcholine.
Lysophosphatidic acid is also an intermediate in the synthesis of phosphatidic acid.
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- Park, S Y; Jeong, K J; Panupinthu, N; Yu, S; Lee, J; Han, J W; Kim, J M; Lee, J-S et al. (2010). "Lysophosphatidic acid augments human hepatocellular carcinoma cell invasion through LPA1 receptor and MMP-9 expression". Oncogene 30 (11): 1351–9. doi:10.1038/onc.2010.517. PMID 21102517.