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ep3 receptor  (Schmid GmbH)

 
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    Schmid GmbH ep3 receptor
    Ep3 Receptor, supplied by Schmid GmbH, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ep3+receptor/p300+protein/pm38697857-241-7-19
    Average 90 stars, based on 1 article reviews
    ep3 receptor - by Bioz Stars, 2026-09
    90/100 stars

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    Article Title: Effects of prostaglandin E2 on cells cultured from the rat organum vasculosum laminae terminalis and median preoptic nucleus.
    Article Snippet: 25 Abstract—The time course of the induction of enzymes responsible for the formation of prostaglandin E2 (PGE2) after an inflammatory insult, in relation to the concomitant febrile response, suggests that peripherally generated PGE2 is involved in the induction of the early phase of fever, while centrally produced PGE2 exerts pyrogenic capacities during the later stages of fever within the hypothalamic median preoptic nucleus (MnPO).. The actions of peripherally derived PGE2 on the brain might occur at the level of the organum vasculosum laminae terminalis (OVLT), which lacks a tight blood–brain barrier and is implicated in fever, while the effects of PGE2 within the MnPO might interfere with glutamatergic neurotransmission within a recently characterized central efferent pathway for the activation of cold-defence reactions.. Using the fura-2 ratio imaging technique we, therefore, measured changes of the intracellular Ca concentration in primary neuroglial microcultures of rat OVLT and MnPO stimulated with PGE2 and/or glutamate.

    Article Title: Prostaglandin E2 in the Tumor Microenvironment, a Convoluted Affair Mediated by EP Receptors 2 and 4.
    Article Snippet: For humans, eight different isoforms of the EP3 receptor are known (Adam et al., 1994; Kotani et al., 1995; Schmid et al., 1995; Bilson et al., 2004), whereas for mice, only three have been published (Irie et al., 1993; Sugimoto et al., 1993).



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    Overview of prostanoid receptors and pharmacology.
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    Overview of prostanoid receptors and pharmacology.

    Journal: Frontiers in Neural Circuits

    Article Title: Prostaglandin E2 Exerts Biphasic Dose Response on the PreBötzinger Complex Respiratory-Related Rhythm

    doi: 10.3389/fncir.2022.826497

    Figure Lengend Snippet: Overview of prostanoid receptors and pharmacology.

    Article Snippet: The following drugs were used: EP1 antagonist GW848867X (Cayman Chemicals, Ann Arbor, MI, United States, 50 nM), EP2 Antagonist PF-04418948 (Cayman Chemical, 500 nM), EP3 antagonist DG041 (Tocris, Bristol, United Kingdom, 40 nM), EP4 antagonist MK2894 (APExBIO, Houston, TX, United States, 100 nM), Prostaglandin E2 (Sigma-Aldrich, St. Louis, MO, United States, 1 nM-1 μM), Prostaglandin F receptor antagonist AL-8810 (Cayman Chemical, 1 μM), Prostaglandin D2 receptor antagonist Setipiprant (Cayman Chemical, 500 nM), Non-selective EP2/3/4 agonist 11-deoxy PGE1 (Cayman Chemical, 10 nM), EP2R agonist Butaprost (Cayman Chemical, 5 μM), EP3 receptor agonist Sulprostone (Cayman Chemical, 1 μM).

    Techniques:

    Integrated XII motor output in preBötC slices after exposure to prostanoid receptor agonists. (A) Examples of integrated hypoglossal motor output (XII) of slices exposed to EP2R agonist Butaprost (500 nM), EP3R agonist Sulprostone (1 μM) and non-selective prostanoid receptor agonist 11-deoxy PGE1 (10 nM) (150 s shown per condition). (B) Activating prostanoid receptors with selective agonists modulates burst period of XII motor output. Exposure to EP2R agonist Butaprost decreases burst period (–28% below control, p < 0.01), while EP3R agonist Sulprostone increases burst period (+21% above control, p < 0.0001). Non-selective prostanoid receptor agonist 11-deoxy PGE1 does not change the burst period. (C) EP2R agonist Butaprost decreases average burst amplitude (–35% below control, p < 0.001). (D) EP3R agonist Sulprostone decreases burst width (–9% below control, p < 0.01). (E,F) EP2R agonist Butaprost decreases XII burst area (–44% below control, p < 0.001) and the CV of the burst period (–0.07 below control, p < 0.05) (* p < 0.05, ** p < 0.01, **** p < 0.0001).

    Journal: Frontiers in Neural Circuits

    Article Title: Prostaglandin E2 Exerts Biphasic Dose Response on the PreBötzinger Complex Respiratory-Related Rhythm

    doi: 10.3389/fncir.2022.826497

    Figure Lengend Snippet: Integrated XII motor output in preBötC slices after exposure to prostanoid receptor agonists. (A) Examples of integrated hypoglossal motor output (XII) of slices exposed to EP2R agonist Butaprost (500 nM), EP3R agonist Sulprostone (1 μM) and non-selective prostanoid receptor agonist 11-deoxy PGE1 (10 nM) (150 s shown per condition). (B) Activating prostanoid receptors with selective agonists modulates burst period of XII motor output. Exposure to EP2R agonist Butaprost decreases burst period (–28% below control, p < 0.01), while EP3R agonist Sulprostone increases burst period (+21% above control, p < 0.0001). Non-selective prostanoid receptor agonist 11-deoxy PGE1 does not change the burst period. (C) EP2R agonist Butaprost decreases average burst amplitude (–35% below control, p < 0.001). (D) EP3R agonist Sulprostone decreases burst width (–9% below control, p < 0.01). (E,F) EP2R agonist Butaprost decreases XII burst area (–44% below control, p < 0.001) and the CV of the burst period (–0.07 below control, p < 0.05) (* p < 0.05, ** p < 0.01, **** p < 0.0001).

    Article Snippet: The following drugs were used: EP1 antagonist GW848867X (Cayman Chemicals, Ann Arbor, MI, United States, 50 nM), EP2 Antagonist PF-04418948 (Cayman Chemical, 500 nM), EP3 antagonist DG041 (Tocris, Bristol, United Kingdom, 40 nM), EP4 antagonist MK2894 (APExBIO, Houston, TX, United States, 100 nM), Prostaglandin E2 (Sigma-Aldrich, St. Louis, MO, United States, 1 nM-1 μM), Prostaglandin F receptor antagonist AL-8810 (Cayman Chemical, 1 μM), Prostaglandin D2 receptor antagonist Setipiprant (Cayman Chemical, 500 nM), Non-selective EP2/3/4 agonist 11-deoxy PGE1 (Cayman Chemical, 10 nM), EP2R agonist Butaprost (Cayman Chemical, 5 μM), EP3 receptor agonist Sulprostone (Cayman Chemical, 1 μM).

    Techniques: