Sumit Bandekar
Communications Secretary
K99 Postdoctoral Scholar, Araç Laboratory
Department of Biochemistry and Molecular Biology
University of Chicago
USA
(E) sjbandekar@uchicago.edu
Research Interests
As a postdoctoral scholar in the lab of Demet Araç, I study the structural basis of how adhesion GPCRs are regulated by their extracellular regions. Specifically, I focus on how conformational dynamics in the extracellular region can regulate adhesion GPCR function. My focus is on ADGRC1 which directs planar cell polarity and ADGRG6 which regulates peripheral nervous system myelination. In each case I have used structural methods to show how defined compact conformations in the extracellular region can regulate receptor function. With my own funding (K99/R00) in hand, I hope to open my independent research lab soon and establish exciting new frontiers in the aGPCR world.
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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.
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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.
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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.
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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.
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Dimitris Placantonakis
Workshop Officer
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.
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Nicole Perry-Hauser
Communications Officer
Glasgow University
School of Molecular Biosciences
Scotland
(E) Nicole.Perry-Hauser@glasgow.ac.uk
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.
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Xianhua Piao
Newborn Brain Research Institute
University of California, San Francisco
35 Medical Center Way, RMB, PodD, 1036
San Francisco, CA 94143
USA
(P) +1-415-502-3460
(E) xianhua.piao@ucsf.edu
(W) website
Research Interests
We are interested in the role of adhesion GPCRs in brain development and malformation. Genetic studies have identified mutations in a specific adhesion GPCR, GPR56, which is the underlying cause of a severe human brain malformation called bilateral frontoparietal polymicrogyria (BFPP). Our subsequent studies revealed that GPR56 interacts with its ligand, collagen III, in the developing brain to regulate the integrity of the pial basement membrane and the proper positioning of the migrating neurons.
In parallel, we are examining how GPR56 signaling regulates myelination. Brain MRIs of patients with BFPP reveal associated myelination defects in the region of periventricular white matter. Oligodendrocytes are largely responsible for the development of myelin in those areas. It is possible that GPR56 signaling affects the interaction of oligodendrocytes and the axons, thus regulating myelination in the central nervous system.
We are also investigating the functional domains of the GPR56 molecule, the ligand(s) that activate GPR56, and the signal transduction events that are triggered by GPR56 activation. Ultimately, we hope that our work will delineate novel signaling pathways that control the development of the mammalian brain and shed light on the intrinsic causes of brain malformations.
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Simone Prömel
Workshop Officer
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.
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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.
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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.
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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.
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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.
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