- Peptide (C)RSQQHRQGRSHHLE, corresponding to amino acid residues 233-246 of rat Prostaglandin F2-α receptor (Accession P43118). Intracellular, 3rd loop.
- Rat and mouse brain lysates, and human U-87 MG glioblastoma cell lysate (1:200-1:1000).
- Western blot analysis of rat brain (lanes 1 and 4), mouse brain (lanes 2 and 5) and human U-87 MG glioblastoma cell line (lanes 3 and 6) lysates:1-3. Anti-Prostaglandin F2-α Receptor/PTGFR Antibody (#APR-067), (1:200).
4-6. Anti-Prostaglandin F2-α Receptor/PTGFR Antibody, preincubated with Prostaglandin F2-α Receptor/PTGFR Blocking Peptide (#BLP-PR067).
- Mouse brain sections (1:200).
Prostaglandins (PGs) are key lipid mediators derived from arachidonic acid that are involved in numerous physiological and pathological processes including inflammation and cardiovascular homeostasis. Each PG acts on its specific and distinct cell surface G-protein coupled receptor (GPCR) or peroxisome proliferator-activated receptor (PPAR)1.
All prostaglandins are composed of a cyclopentanone nucleus with two side chains. Currently, three classes of prostaglandins are recognized, and these are categorized on the basis of the number of double bonds present within the prostaglandin molecule and on the fatty acid from which they are derived.
Prostaglandin F2α (PGF2α) and its receptor (FP) are required for female reproductive functions such as luteolysis and parturition2. PGF2α was shown to be an important regulator of corpora luteal (CL) function, uterine contractility, ovulation, and embryo attachment in female swine. High affinity PGF2α receptors are present in the CL at all stages of the estrous cycle3.
Apart from its pivotal role in parturition, PGF2α and its receptor are been implicated in blood pressure regulation4, atherosclerosis and other inflammation-related disorders5, cardiovascular diseases6 and bone development7. Prostaglandin F2α analogs were the first prostaglandin agonists introduced for glaucoma treatment, its mechanism of action includes reduction of intracellular pressure by increasing the uveoscleral outflow8.