PMID- 31336833
OWN - NLM
STAT- MEDLINE
DCOM- 20191227
LR  - 20200225
IS  - 1422-0067 (Electronic)
IS  - 1422-0067 (Linking)
VI  - 20
IP  - 14
DP  - 2019 Jul 12
TI  - Chemotactic Ligands that Activate G-Protein-Coupled Formylpeptide Receptors.
LID - 10.3390/ijms20143426 [doi]
LID - 3426
AB  - Leukocyte infiltration is a hallmark of inflammatory responses. This process 
      depends on the bacterial and host tissue-derived chemotactic factors interacting 
      with G-protein-coupled seven-transmembrane receptors (GPCRs) expressed on the 
      cell surface. Formylpeptide receptors (FPRs in human and Fprs in mice) belong to 
      the family of chemoattractant GPCRs that are critical mediators of myeloid cell 
      trafficking in microbial infection, inflammation, immune responses and cancer 
      progression. Both murine Fprs and human FPRs participate in many 
      patho-physiological processes due to their expression on a variety of cell types 
      in addition to myeloid cells. FPR contribution to numerous pathologies is in part 
      due to its capacity to interact with a plethora of structurally diverse 
      chemotactic ligands. One of the murine Fpr members, Fpr2, and its endogenous 
      agonist peptide, Cathelicidin-related antimicrobial peptide (CRAMP), control 
      normal mouse colon epithelial growth, repair and protection against 
      inflammation-associated tumorigenesis. Recent developments in FPR (Fpr) and 
      ligand studies have greatly expanded the scope of these receptors and ligands in 
      host homeostasis and disease conditions, therefore helping to establish these 
      molecules as potential targets for therapeutic intervention.
FAU - Krepel, Stacey A
AU  - Krepel SA
AD  - Cancer and Inflammation Program, Center for Cancer Research, National Cancer 
      Institute at Frederick, Frederick, MD 21702, USA.
FAU - Wang, Ji Ming
AU  - Wang JM
AD  - Cancer and Inflammation Program, Center for Cancer Research, National Cancer 
      Institute at Frederick, Frederick, MD 21702, USA. wangji@mail.nih.gov.
LA  - eng
GR  - HSN261200800001E/National Cancer Institute/
PT  - Journal Article
PT  - Review
DEP - 20190712
PL  - Switzerland
TA  - Int J Mol Sci
JT  - International journal of molecular sciences
JID - 101092791
RN  - 0 (Bacterial Proteins)
RN  - 0 (Chemotactic Factors)
RN  - 0 (Ligands)
RN  - 0 (Peptides)
RN  - 0 (Receptors, Formyl Peptide)
RN  - 0 (Receptors, G-Protein-Coupled)
RN  - 0 (Viral Proteins)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Bacterial Proteins/chemistry/metabolism
MH  - Chemotactic Factors/*metabolism
MH  - Chemotaxis
MH  - Chemotaxis, Leukocyte/immunology
MH  - Drug Discovery
MH  - Host-Pathogen Interactions/genetics/immunology
MH  - Humans
MH  - Leukocytes/immunology/metabolism
MH  - Ligands
MH  - Peptides/chemistry/metabolism
MH  - Receptors, Formyl Peptide/agonists/*metabolism
MH  - Receptors, G-Protein-Coupled/agonists/metabolism
MH  - Signal Transduction
MH  - Viral Proteins/chemistry/metabolism
PMC - PMC6678346
OTO - NOTNLM
OT  - diseases
OT  - formyl peptide receptors
OT  - ligands
COIS- The authors declare no conflict of interest.
EDAT- 2019/07/25 06:00
MHDA- 2019/12/28 06:00
PMCR- 2019/07/01
CRDT- 2019/07/25 06:00
PHST- 2019/06/19 00:00 [received]
PHST- 2019/07/03 00:00 [revised]
PHST- 2019/07/05 00:00 [accepted]
PHST- 2019/07/25 06:00 [entrez]
PHST- 2019/07/25 06:00 [pubmed]
PHST- 2019/12/28 06:00 [medline]
PHST- 2019/07/01 00:00 [pmc-release]
AID - ijms20143426 [pii]
AID - ijms-20-03426 [pii]
AID - 10.3390/ijms20143426 [doi]
PST - epublish
SO  - Int J Mol Sci. 2019 Jul 12;20(14):3426. doi: 10.3390/ijms20143426.