Overview
- Peptide (C)TEQVRSGNEIT(S)YEN, corresponding to amino acid residues 153-167 of human FFAR2 (Accession O15552). 2nd extracellular loop.
- Human HT-29 colon adenocarcinoma, HL-60 promyelocytic leukemia, THP-1 monocytic leukemia, and LoVo colorectal adenocarcinoma cell lysates (1:200-1:1000).
Western blot analysis of human HT-29 colon adenocarcinoma cell line (lanes 1 and 5), human HL-60 promyelocytic leukemia cell line (lanes 2 and 6), human THP-1 monocytic leukemia cell line (lane 3 and 7) and human LoVo colorectal adenocarcinoma cell line (lanes 4 and 8) lysates:1-4. Anti-Human GPR43/FFAR2 (extracellular) Antibody (#AFR-015), (1:200).
5-8. Anti-Human GPR43/FFAR2 (extracellular) Antibody, preincubated with Human GPR43/FFAR2 (extracellular) Blocking Peptide (#BLP-FR015).
- Human THP-1 monocytic leukemia cells (2.5 µg).
Free fatty acids (FFAs) are essential nutrients that are also involved in signal transduction through FFA receptors, members of the G-protein coupled receptor superfamily.
FFAR2/GPR43 is an FFA receptor that is activated specifically by short fatty acids (acetate, propionate and butyrate), that are the products of bacterial fermentation in the gut1.
GPR43 is expressed in adipose tissue, intestines, and immune tissues2 and its stimulation by interaction with short fatty acids inhibits cAMP production, activates the extracellular signal-regulated kinase (ERK) cascade via interactions with the Gi/o family of G-proteins. This increases intracellular Ca2+ levels, and promotes activation of the mitogen-activated protein kinase (MAPK) cascade through interactions with the Gq family of G-proteins1.
These processes, mediated by GPR43 receptor regulate the host energy homeostasis and hence GPR43 is shown to be related to metabolic disorders, such as obesity and diabetes1.
Because of its pivotal role in energy homeostasis and in regulating many cellular processes, GPR43 has many phenotypic effects: mutant mice are hyper susceptible to developing intestinal carcinogenesis3, Klebsiella pneumoniae infection4 and to increased differentiation of bone marrow cells into osteoclasts5. Studies have shown the role of GPR43 in regulating inflammatory responses, which can lead to colitis and asthma6,7. The various activities mediated by GPR43 makes it an appealing therapeutic target.
