Demet Araç

Demet

Co-Chair

Department of Biochemistry and Molecular Biology
University of Chicago
929 E. 57th St.
GCIS W210
Chicago, IL 60637
USA

(P) +1-773-8342691
(E) arac@uchicago.edu
(W) website

Research Interests

The interplay of extracellular adhesion and intracellular signaling is essential for the development of all organs such as the brain, and is a key phenomenon that is disrupted in many human diseases. Adhesion GPCRs are cell-surface molecules that are believed to mediate intercellular communication via cell-cell and cell-matrix interactions. Genetic studies suggest critical roles for Adhesion GPCRs in development, immunity and especially in neurobiology (such as brain development, synapse maturation/elimination, myelination of neurons, central nervous system angiogenesis and neural tube development); and link them to numerous diseases including neurodevelopmental disorders, deafness, male infertility, schizophrenia, and immune disorders.

We are interested in understanding the mechanisms by which Adhesion GPCRs function in the brain by employing functional, structural, and protein engineering approaches to address major questions in the Adhesion GPCR field. We aim to understand the stepwise mechanical details of Adhesion GPCR activation that is believed to start with adhesion of a ligand to the extracellular region of the Adhesion GPCR, continue with transduction of the signal from the extracellular region to the transmembrane domain via the recently discovered GAIN domain, and end with the activation of the transmembrane domain by the tethered agonist peptide. We believe our structure/function relationship studies will elucidate the mechanistic details about the components that regulate Adhesion GPCR activity and reveal ways of manipulating their function.

Gabriela Aust

Research LaboratoriesCenter of Surgery
University of Leipzig
Liebigstr. 19
04103 Leipzig
Germany

(P) +49-341-9717555
(E) gabriela.aust@medizin.uni-leipzig.de


Research Interests

In 1994, we first described human CD97/ADGRE5, a member of the E (formerly EGF-TM7) subfamily of Adhesion GPCRs. During the next years we showed that, in contrast to the other subfamily E members, CD97 is broadly distributed and not restricted to the hematopoietic system. Especially malignant cells of epithelial and mesenchymal origin highly express CD97, whereas their corresponding normal counterparts often lack this receptor. The main focus of our work is the function of CD97 outside the immune system. Using transgenic mice, selectively expressing CD97 in enterocytes, we identified a role of CD97 in the strengthing of lateral cell contacts. We further showed that during colorectal carcinogenesis, CD97 appears in the cytoplasm. 

Our current studies are related to the intracellular signaling of CD97. We defined several intracellular interaction partners of CD97 and are just verifying the functional relevance of their binding to CD97. 

Beatriz Blanco-Redondo

RSI – Department of General Biochemistry
Leipzig University
Johannisallee 30, Haus J
04103 Leipzig
Germany

(E) Beatriz.Blanco-Redondo@medizin.uni-leipzig.de
(W) website

Research Interests
Our research focuses on characterizing three novel adhesion G protein-coupled receptors (aGPCRs) in Drosophila. Through molecular and biochemical analysis, we aim to elucidate the signaling pathways of mayo, an ancestral aGPCR, and remoulade, a homolog of the ADGRA family. Employing CRISPR techniques, we engineer a series of molecularly modified Drosophila transgenes. Notably, when mayo, an aGPCR expressed in the gut, is knocked out, we observe tachycardia in the flies, linked to increased extracellular potassium levels. However, its specific ligands, interactors, and signaling pathway remain unknown. Additionally, silencing remoulade specifically in the peripheral nervous system results in an elevated nocifensive response. Given remoulade’s similarity to the ADGRA family, we aim to investigate whether it activates a non-classical signaling pathway similar to that of ADGRA2 or if it follows an entirely distinct pathway.clinical manifestation linked to addiction.

Antony Boucard Jr.

Co-Chair

Department of Cell Biology
Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional (Cinvestav-IPN)
Avenido Instituto Politecnico Nacional 2508
Colonia Gustavo A. Madero
C.P. 07360
Mexico City
Mexico

(P) +52-55-3747-3800 ext 5561
(E) antony.boucard@cinvestav.mx
(W) website

Research Interests
My lab focuses mainly on molecular and cellular mechanisms underlying the function of adhesion GPCRs in the formation of synapses. Having a particular interest for a three-member family known as the latrophilins (ADGRL1,2,3), my group seeks to decipher the molecular code instructing adhesion events mediated by these aGPCRs. The pharmacology of latrophilins brings about a great deal of challenges given that they are highly polymorphic proteins expressed as various alternatively spliced isoforms thus potentially resulting in a differential modulation of cell signaling pathways. My team highlighted the importance of splicing events in biasing latrophilins’ regulation of cyclic AMP pathways and for determining the magnitude of ligand selectivity. Additionally, we are interested in understanding the pathophysiological relevance of latrophilins’ function in the development of neuropsychiatric disorders given their association with genetic susceptibility to neurodevelopmental disorders such as autism spectrum disorder or attention deficit hyperactivity disorder (ADHD) but also to a comorbid clinical manifestation linked to addiction.

Jörg Hamann

Department of Experimental Immunology
Academic University Medical Centers
University of Amsterdam
Meibergdreef 9
1105AZ Amsterdam
The Netherlands

(P) +31-20-5661719
(E) j.hamann@amsterdamumc.nl


Research Interests

My interest in Adhesion GPCRs started in the mid-90th with the expression cloning of CD97 and the identification of CD55 as its interacting partner. Since then, I have extensively studied the evolution, expression, structure, specificity, and functions of Adhesion GPCRs in immune cells. This work has focussed on the subfamily E members CD97 and EMR1 to 4, and more recently, on the subfamily G cluster GPR56/GPR97/GPR114. Using antibody application and gene targeting, we demonstrated roles of CD97 in granulocyte homeostasis and autoimmune pathogenesis. Moreover, we formally proved the interaction of CD97 with CD55 in vivo and showed that CD97 expression levels on circulating blood cells are regulated upon contact with CD55, possibly to restrict CD97-CD55-mediated cell adhesion to tissue sites. More recently, we reported the specific expression of GPR56 by cytotoxic lymphocytes and microglia and described a role of GPR56 in regulating immediate effector functions of NK cells.

Tobias Langenhan

Division of General Biochemistry
Rudolf-Schönheimer-Institute of Biochemistry
University of Leipzig
Johannisallee 30
04103 Leipzig
Germany

(P) +49-341-9722100
(E) tobias.langenhan@uni-leipzig.de
(W) website


Research Interests

My group is much interested in the physiological and molecular aspects of Adhesion GPCR signalling. We try to unravel, which stimuli Adhesion GPCR sense, how they are activated and which role proteolytic processing of Adhesion GPCR plays in this process. We primarily use Drosophila melanogaster as a genetic model to investigate these questions under in vivo conditions, but we also employ biochemistry, structural biology, biophysics and bioinformatics to dissect and characterise the physiological and molecular logic of Adhesion GPCR signals.

Previous experimental results have connected latrophilin, an evolutionarily old member of the Adhesion GPCR class, to synaptic function. In contrast, our recent studies on latrophilins demonstrated that latrophilin signalling is important for tissue polarity implicating latrophilin function in concerting developmental activities of large cell populations. We thus currently focus our investigations on the role of Adhesion GPCR in the nervous system, but we are also interested in their functions in other organs such as heart and kidney.

Ines Liebscher

Division of General Biochemistry
Rudolf-Schönheimer-Institute of Biochemistry
University of Leipzig
Johannisallee 30
04103 Leipzig
Germany

(P) +49-341-9722176
(E) ines.liebscher@medizin.uni-leipzig.de
(W) website


Research Interests

My group aims to unravel the function of aGPCRs on a molecular as well as on a physiological level. We have solved the signal transduction of several aGPCRs and described a tethered agonist activation mechanism, which allows now for in vitro and in vivo manipulation of this orphan receptor group through derived synthetic peptides. We could show that several aGPCRs can be activated through mechanical stimuli and/ or the interaction with the surrounding extracellular matrix components. We want to identify the G protein-dependent and -independent signaling cascades of aGPCRs and search for ways to specifically activate certain pathways at a time. We further employ receptor-deficient animal models to study the impact of aGPCR-deficiency on metabolism, cardiac and bone function.

Hsi-Hsien Lin

Department of Microbiology and Immunology
Chang Gung University
259 Wen-Hwa 1st Road, Kwei-Shan
Tao-Yuan
Taiwan, R.O.C.

(P) +886 3 2118800-ext3321
(E) hhlin@mail.cgu.edu.tw


Research Interests

– The role of EMR2 receptor in the cellular functions of macrophages
– The role of CD97 receptor in tumorigenesis
– Functional characterization of GPS auto-proteolysis in Adhesion GPCRs
– The role of GPR56 in NK cell function
– The role of GPR56 receptor in tumorigenesis
– Functional characterization of GPR56–ligand interaction

Signe Mathiasen

Department of Biomedical Sciences
University of Copenhagen
Faculty of Health Sciences
Blegdamsvej 3, DK-2200 Copenhagen
Denmark

(P) +45 61658536
(E) Signe.Mathiasen@sund.ku.dk
(W) website


Research Interests

In the lab we have a special focus on the adhesion GPCR ADGRL3 (historically latrophilin 3 or LPHN3).  We are interested in mapping ADGRL3’s basic biological functions, and especially to investigate the potential link between ligand binding, receptor activation and intracellular signalling. We aim to develop molecular scale tools to study the impact of mechanical stress across ADGRL3. To do so we combine a suite of molecular biology techniques and advanced GPCR signalling assays with the development of novel single molecule microscopy approaches.

Kelly Monk

Vollum Institute
Oregon Health & Science University, L474
3181 SW Sam Jackson Park Road
Portland, OR 97239
USA

(P) +1-503-494-2976
(E) monk@ohsu.edu
(W) website


Research Interests

We are interested in the function of Adhesion GPCRs in glial cell development and myelination, with a specific focus on myelinating glia. Myelin is the insulating membrane that surrounds neuronal projections called axons. Myelin is generated by specialized glial cells called Schwann cells in the peripheral nervous system and oligodendrocytes in the central nervous system. The importance of myelin is underscored in diseases in which it is disrupted, including numerous peripheral neuropathies and multiple sclerosis.

We became interested in the biology of Adhesion GPCRs through our discovery that GPR126 is essential for Schwann cell myelination in the peripheral nervous system. Using zebrafish and mouse models, and in collaboration with other members of the Adhesion GPCR Consortium, we are currently working to define domain-specific and cell type-specific functions of GPR126 in the peripheral nervous system as well as activating ligands and downstream signaling events. Excitingly, beyond GPR126, there are several Adhesion-GPCRs expressed in myelinating glia in both the central and peripheral nervous systems. Another major focus of the Monk lab, therefore, is to define the function of these Adhesion GPCRs in glial cell development, myelination, myelin maintenance, and regeneration.

Dimitris Placantonakis

Department of Neurosurgery
NYU School of Medicine
530 First Avenue – Skirball 8R-303
New York, NY 10016
USA

(P) +1-212-263-2441
(E) dimitris.placantonakis@nyulangone.org
(W) website


Research Interests

Dimitris Placantonakis is a neurosurgeon-scientist at NYU Grossman School of Medicine. His laboratory investigates the role of Adhesion GPCRs in glioblastoma, an aggressive brain malignancy. Areas of interest include activation mechanisms, extracellular ligands and intracellular interactors, signaling mechanisms and oncologic phenotypes. Besides the basic mechanistic studies, the laboratory is also interested in the clinical translation of Adhesion GPCRs as therapeutic targets in oncology.

Nicole Perry-Hauser

Columbia University
New York City, NY
USA

(E) nap2164@cumc.columbia.edu


Research Interests

Dr. Perry-Hauser will launch her independent research laboratory as a Lecturer (Research & Teaching Track) in the School of Molecular Biosciences at the University of Glasgow in March 2025. Currently, she serves as an Associate Research Scientist in Dr. Jonathan Javitch’s lab at Columbia University, where her work is supported by the Columbia University Institute for Developmental Sciences Award.

Dr. Perry-Hauser earned her PhD in Pharmacology from Vanderbilt University, where she studied under the mentorship of Drs. Vsevolod Gurevich and Tina Iverson. Her doctoral research focused on arrestins, adaptor proteins originally discovered for their role in the desensitization and internalization of G protein-coupled receptors (GPCRs). Driven by her passion for GPCR biology, Dr. Perry-Hauser joined Dr. Javitch’s lab in the Department of Psychiatry at Columbia University.

In her new lab, Dr. Perry-Hauser will continue to investigate the signaling pathways and mechanisms of adhesion GPCRs, focusing on their impact in neuropsychiatric disorders. Her research aims to bring forward new insights into the intricate molecular systems underlying these conditions.

Simone Prömel

Institute for Cell Biology
Heinrich Heine University
Universitätsstr. 1
40225 Düsseldorf
Germany

(P) +49-211-8113816
(E) proemel@hhu.de


Research Interests

We are interested in understanding how Adhesion GPCR signals are translated into physiological functions in different biological contexts. In order to delineate the molecular mechanisms that underlie Adhesion GPCR activation and activity, we use a broad range of cell biological, biochemical, and pharmacological methodologies. We further aim to link these molecular mechanisms to physiological functions in vivo by employing different model organisms as well as cell culture models.

Using the evolutionary conserved Adhesion GPCRs Latrophilins as prototypic members of the receptor class, our previous analyses have shown that the extraordinarily large N terminus of the receptors is a linchpin for different receptor functions. Thereby, an Adhesion GPCR does not only transduce classical G protein signals into cells, but also acts completely independently of its 7TM and C terminus, for instance to mediate signals on opposing cells. One main focus of our current research is to understand how and by which mechanisms different Adhesion GPCRs distinguish and integrate their different modes of function.

Nicole Scholz

Co-Chair

Institute for Biochemistry
University of Leipzig
Johannisallee 30
04104 Leipzig
Germany

(P) +1-410-614-3082
(E) nicole.scholz@medizin.uni-leipzig.de
(W) website


Research Interests

In the Scholz lab, we aim to understand physiological rationale of the vivid alternative splicing activities of Adhesion GPCR mRNAs and investigate if and how Adhesion GPCRs ‘talk’ to other cell surface molecules to enable neuronal mechanophysiology. Building on the knowledge of Adhesion GPCR function in physiological settings, we are also aiming to understand cellular processes that go wrong when Adhesion GPCRs fail to perform and especially if that entails faulty mechanical signature of cells and tissues contributing to mechanopathologies.

Greg Tall

Department of Pharmacology
University of Michigan
1240 MSRB 3
1150 W. Medical Center Dr.
Ann Arbor, MI 48109
USA

(P) +1-734-647-9824
(E) gregtall@umich.edu
(W) website

Research Interests

Our lab helped to discover a general activation mechanism of adhesion GPCRs in which dissociation of the extracellular NTF, perhaps by force, reveals the seven amino acid tethered-peptide-agonist that engages the 7TM domain to activate G protein signaling.  Our current work uses purified components in enzymatic assays and for structure determination, along with cell culture and mouse models to expand understanding of the mechanism by which NTF binding ligands and extracellular forces initiate the tethered agonist program. We have a particular focus on AGPCR-expressing cells in circulation that experience shear forces.

Kimberley Tolias

Departments of Neuroscience and
Biochemistry and Molecular Biology
Baylor College of Medicine
One Baylor Plaza
Room S607
Houston, TX 77030
USA

(P) +1-713-798-3981
(E) tolias@bcm.edu
(W) website
(W) website


Research Interests

We are interested in the function of Adhesion GPCRs in neuronal development and plasticity. The organization of neurons into complex brain circuits involves highly regulated steps including axon and dendritic growth and the formation and refinement of synapses, which mediate communication between neurons. Synapses continue to remodel throughout life, which is important for processes like learning and memory. Failure to properly form or maintain these synaptic connections and neural circuits underlies a wide array of neuropsychiatric disorders. We previously identified the Adhesion GPCR BAI1 (ADGRB1) as a critical regulator of dendritic arbor and excitatory synapse development and showed that BAI1 coordinates these processes through the differential activation of multiple Rho GTPase signaling pathways. We are continuing to investigate the specific roles BAI Adhesion GPCRs play in neuronal development, synaptic plasticity and behavior and to elucidate the mechanisms by which BAIs mediate their effects on these processes. Our long-term goal is to provide mechanistic insight into BAI1 Adhesion GPCR biology, which has potential implications for human health as BAIs are linked to autism spectrum disorder, schizophrenia, bipolar disorder, cognitive performance, and brain cancers.

Nathan Zaidman

Co-Chair

Department of Biochemistry & Molecular Biology
University of New Mexico
915 Camino De Salud NE
BRF 220
Albuquerque, NM 87131
USA

(P) +1-505-277-0682
(E) nzaidman@salud.unm.edu
(W) website


Research Interests

My introduction to Adhesion GPCRs came during my postdoctoral training in Jennifer Pluznick’s lab at Johns Hopkins University, where her group investigates understudied GPCRs in the kidney. My research in her lab is focused on ADGRF5/GPR116, and specifically identifying its significance in renal physiology. We discovered that Gpr116 is localized to acid secreting A-type intercalated cells of the collecting ducts and is a critical regulator of vacuolar-type H+-ATPase (V-ATPase) surface expression. Genetic deletion of GPR116 in mice causes a physiologically inappropriate distribution of proton pumps on the luminal membrane of A-type cells, leading to urine acidification and a subtle metabolic alkalosis. Furthermore, we revealed that in situ GPR116 activation with a synthetic agonist peptide inhibits proton flux in A-type cells, demonstrating that GPR116 is a critical negative regulator of V-ATPase proton pumps. My future research will continue our investigation of GPR116 and expand into other aGPCRs to determine their roles in renal physiology. I am also interested in transcriptional regulators of Adhseion GPCRs as well as identifying the endogenous activators of these receptors in the kidney.