title: Dissecting signaling and functions of adhesion G protein-coupled receptors.
abstract: G protein-coupled receptors (GPCRs) comprise an expanded superfamily of receptors in the human genome. Adhesion class G protein-coupled receptors (adhesion-GPCRs) form the second largest class of GPCRs. Despite the abundance, size, molecular structure, and functions in facilitating cell and matrix contacts in a variety of organ systems, adhesion-GPCRs are by far the most poorly understood GPCR class. Adhesion-GPCRs possess a unique molecular structure, with extended N-termini containing various adhesion domains. In addition, many adhesion-GPCRs are autoproteolytically cleaved into an N-terminal fragment (NTF, NT, α-subunit) and C-terminal fragment (CTF, CT, β-subunit) at a conserved GPCR autoproteolysis-inducing (GAIN) domain that contains a GPCR proteolysis site (GPS). These two features distinguish adhesion-GPCRs from other GPCR classes. Though active research on adhesion-GPCRs in diverse areas, such as immunity, neuroscience, and development and tumor biology has been intensified in the recent years, the general biological and pharmacological properties of adhesion-GPCRs are not well known, and they have not yet been used for biomedical purposes. The "6th International Adhesion-GPCR Workshop," held at the Institute of Physiology of the University of Würzburg on September 6-8, 2012, assembled a majority of the investigators currently actively pursuing research on adhesion-GPCRs, including scientists from laboratories in Europe, the United States, and Asia. The meeting featured the nascent mechanistic understanding of the molecular events driving the signal transduction of adhesion-GPCRs, novel models to evaluate their functions, and evidence for their involvement in human disease.
authors.affiliation: Stanford University, Stanford, California, USA.
authors.forename: Demet
authors.initials: D
authors.lastname: Araç
authors.forename: Gabriela
authors.initials: G
authors.lastname: Aust
authors.forename: Davide
authors.initials: D
authors.lastname: Calebiro
authors.forename: Felix B
authors.initials: FB
authors.lastname: Engel
authors.forename: Caroline
authors.initials: C
authors.lastname: Formstone
authors.forename: André
authors.initials: A
authors.lastname: Goffinet
authors.forename: Jörg
authors.initials: J
authors.lastname: Hamann
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Kittel
authors.forename: Ines
authors.initials: I
authors.lastname: Liebscher
authors.forename: Hsi-Hsien
authors.initials: HH
authors.lastname: Lin
authors.forename: Kelly R
authors.initials: KR
authors.lastname: Monk
authors.forename: Alexander
authors.initials: A
authors.lastname: Petrenko
authors.forename: Xianhua
authors.initials: X
authors.lastname: Piao
authors.forename: Simone
authors.initials: S
authors.lastname: Prömel
authors.forename: Helgi B
authors.initials: HB
authors.lastname: Schiöth
authors.forename: Thue W
authors.initials: TW
authors.lastname: Schwartz
authors.forename: Martin
authors.initials: M
authors.lastname: Stacey
authors.forename: Yuri A
authors.initials: YA
authors.lastname: Ushkaryov
authors.forename: Manja
authors.initials: M
authors.lastname: Wobus
authors.forename: Uwe
authors.initials: U
authors.lastname: Wolfrum
authors.forename: Lei
authors.initials: L
authors.lastname: Xu
authors.forename: Tobias
authors.initials: T
authors.lastname: Langenhan
mesh_terms: D002448:Cell Adhesion; D006801:Humans; D008024:Ligands; D008954:Models, Biological; D059748:Proteolysis; D043562:Receptors, G-Protein-Coupled / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D008024:Ligands; D043562:Receptors, G-Protein-Coupled