OR2T2 (NM 001004136) Human Untagged Clone – SC300610
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Copy Number Variation in Fetal Alcohol Spectrum Disorder
Biochemistry and Cell Biology Copy number variation in fetal alcohol spectrum disorder Journal: Biochemistry and Cell Biology Manuscript ID bcb-2017-0241.R1 Manuscript Type: Article Date Submitted by the Author: 09-Nov-2017 Complete List of Authors: Zarrei, Mehdi; The Centre for Applied Genomics Hicks, Geoffrey G.; University of Manitoba College of Medicine, Regenerative Medicine Reynolds, James N.; Queen's University School of Medicine, Biomedical and Molecular SciencesDraft Thiruvahindrapuram, Bhooma; The Centre for Applied Genomics Engchuan, Worrawat; Hospital for Sick Children SickKids Learning Institute Pind, Molly; University of Manitoba College of Medicine, Regenerative Medicine Lamoureux, Sylvia; The Centre for Applied Genomics Wei, John; The Centre for Applied Genomics Wang, Zhouzhi; The Centre for Applied Genomics Marshall, Christian R.; The Centre for Applied Genomics Wintle, Richard; The Centre for Applied Genomics Chudley, Albert; University of Manitoba Scherer, Stephen W.; The Centre for Applied Genomics Is the invited manuscript for consideration in a Special Fetal Alcohol Spectrum Disorder Issue? : Keyword: Fetal alcohol spectrum disorder, FASD, copy number variations, CNV https://mc06.manuscriptcentral.com/bcb-pubs Page 1 of 354 Biochemistry and Cell Biology 1 Copy number variation in fetal alcohol spectrum disorder 2 Mehdi Zarrei,a Geoffrey G. Hicks,b James N. Reynolds,c,d Bhooma Thiruvahindrapuram,a 3 Worrawat Engchuan,a Molly Pind,b Sylvia Lamoureux,a John Wei,a Zhouzhi Wang,a Christian R. 4 Marshall,a Richard F. Wintle,a Albert E. Chudleye,f and Stephen W. Scherer,a,g 5 aThe Centre for Applied Genomics and Program in Genetics and Genome Biology, The Hospital 6 for Sick Children, Toronto, Ontario, Canada 7 bRegenerative Medicine Program, University of Manitoba, Winnipeg, Canada 8 cCentre for Neuroscience Studies, Queen's University, Kingston, Ontario, Canada. -
Whole Exome Sequencing in Families at High Risk for Hodgkin Lymphoma: Identification of a Predisposing Mutation in the KDR Gene
Hodgkin Lymphoma SUPPLEMENTARY APPENDIX Whole exome sequencing in families at high risk for Hodgkin lymphoma: identification of a predisposing mutation in the KDR gene Melissa Rotunno, 1 Mary L. McMaster, 1 Joseph Boland, 2 Sara Bass, 2 Xijun Zhang, 2 Laurie Burdett, 2 Belynda Hicks, 2 Sarangan Ravichandran, 3 Brian T. Luke, 3 Meredith Yeager, 2 Laura Fontaine, 4 Paula L. Hyland, 1 Alisa M. Goldstein, 1 NCI DCEG Cancer Sequencing Working Group, NCI DCEG Cancer Genomics Research Laboratory, Stephen J. Chanock, 5 Neil E. Caporaso, 1 Margaret A. Tucker, 6 and Lynn R. Goldin 1 1Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD; 2Cancer Genomics Research Laboratory, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD; 3Ad - vanced Biomedical Computing Center, Leidos Biomedical Research Inc.; Frederick National Laboratory for Cancer Research, Frederick, MD; 4Westat, Inc., Rockville MD; 5Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD; and 6Human Genetics Program, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD, USA ©2016 Ferrata Storti Foundation. This is an open-access paper. doi:10.3324/haematol.2015.135475 Received: August 19, 2015. Accepted: January 7, 2016. Pre-published: June 13, 2016. Correspondence: [email protected] Supplemental Author Information: NCI DCEG Cancer Sequencing Working Group: Mark H. Greene, Allan Hildesheim, Nan Hu, Maria Theresa Landi, Jennifer Loud, Phuong Mai, Lisa Mirabello, Lindsay Morton, Dilys Parry, Anand Pathak, Douglas R. Stewart, Philip R. Taylor, Geoffrey S. Tobias, Xiaohong R. Yang, Guoqin Yu NCI DCEG Cancer Genomics Research Laboratory: Salma Chowdhury, Michael Cullen, Casey Dagnall, Herbert Higson, Amy A. -
Sean Raspet – Molecules
1. Commercial name: Fructaplex© IUPAC Name: 2-(3,3-dimethylcyclohexyl)-2,5,5-trimethyl-1,3-dioxane SMILES: CC1(C)CCCC(C1)C2(C)OCC(C)(C)CO2 Molecular weight: 240.39 g/mol Volume (cubic Angstroems): 258.88 Atoms number (non-hydrogen): 17 miLogP: 4.43 Structure: Biological Properties: Predicted Druglikenessi: GPCR ligand -0.23 Ion channel modulator -0.03 Kinase inhibitor -0.6 Nuclear receptor ligand 0.15 Protease inhibitor -0.28 Enzyme inhibitor 0.15 Commercial name: Fructaplex© IUPAC Name: 2-(3,3-dimethylcyclohexyl)-2,5,5-trimethyl-1,3-dioxane SMILES: CC1(C)CCCC(C1)C2(C)OCC(C)(C)CO2 Predicted Olfactory Receptor Activityii: OR2L13 83.715% OR1G1 82.761% OR10J5 80.569% OR2W1 78.180% OR7A2 77.696% 2. Commercial name: Sylvoxime© IUPAC Name: N-[4-(1-ethoxyethenyl)-3,3,5,5tetramethylcyclohexylidene]hydroxylamine SMILES: CCOC(=C)C1C(C)(C)CC(CC1(C)C)=NO Molecular weight: 239.36 Volume (cubic Angstroems): 252.83 Atoms number (non-hydrogen): 17 miLogP: 4.33 Structure: Biological Properties: Predicted Druglikeness: GPCR ligand -0.6 Ion channel modulator -0.41 Kinase inhibitor -0.93 Nuclear receptor ligand -0.17 Protease inhibitor -0.39 Enzyme inhibitor 0.01 Commercial name: Sylvoxime© IUPAC Name: N-[4-(1-ethoxyethenyl)-3,3,5,5tetramethylcyclohexylidene]hydroxylamine SMILES: CCOC(=C)C1C(C)(C)CC(CC1(C)C)=NO Predicted Olfactory Receptor Activity: OR52D1 71.900% OR1G1 70.394% 0R52I2 70.392% OR52I1 70.390% OR2Y1 70.378% 3. Commercial name: Hyperflor© IUPAC Name: 2-benzyl-1,3-dioxan-5-one SMILES: O=C1COC(CC2=CC=CC=C2)OC1 Molecular weight: 192.21 g/mol Volume -
Clinical, Molecular, and Immune Analysis of Dabrafenib-Trametinib
Supplementary Online Content Chen G, McQuade JL, Panka DJ, et al. Clinical, molecular and immune analysis of dabrafenib-trametinib combination treatment for metastatic melanoma that progressed during BRAF inhibitor monotherapy: a phase 2 clinical trial. JAMA Oncology. Published online April 28, 2016. doi:10.1001/jamaoncol.2016.0509. eMethods. eReferences. eTable 1. Clinical efficacy eTable 2. Adverse events eTable 3. Correlation of baseline patient characteristics with treatment outcomes eTable 4. Patient responses and baseline IHC results eFigure 1. Kaplan-Meier analysis of overall survival eFigure 2. Correlation between IHC and RNAseq results eFigure 3. pPRAS40 expression and PFS eFigure 4. Baseline and treatment-induced changes in immune infiltrates eFigure 5. PD-L1 expression eTable 5. Nonsynonymous mutations detected by WES in baseline tumors This supplementary material has been provided by the authors to give readers additional information about their work. © 2016 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/30/2021 eMethods Whole exome sequencing Whole exome capture libraries for both tumor and normal samples were constructed using 100ng genomic DNA input and following the protocol as described by Fisher et al.,3 with the following adapter modification: Illumina paired end adapters were replaced with palindromic forked adapters with unique 8 base index sequences embedded within the adapter. In-solution hybrid selection was performed using the Illumina Rapid Capture Exome enrichment kit with 38Mb target territory (29Mb baited). The targeted region includes 98.3% of the intervals in the Refseq exome database. Dual-indexed libraries were pooled into groups of up to 96 samples prior to hybridization. -
1 Copper-Mediated Thiol Potentiation and Mutagenesis-Guided Modeling Suggest a Highly Conserved Copper Binding Motif in Human OR
Copper-mediated thiol potentiation and mutagenesis-guided modeling suggest a highly conserved copper binding motif in human OR2M3 Franziska Haag1, Lucky Ahmed2, Krystle Reiss2, Eric Block3, Victor S. Batista2 and Dietmar Krautwurst1 1Leibniz-Institute for Food Systems Biology at the Technical University of Munich, Lise-Meitner-Str. 34, D-85354 Freising, Germany 2Department of Chemistry, Yale University, New Haven, CT 06520, United States 3Department of Chemistry, University at Albany, State University of New York, Albany, NY 12222, United States Contents: Table S1: Oligonucleotides for molecular cloning of odorant receptors investigated. ........................... 2 Table S2: Oligonucleotides for Homo sapiens OR2M3 site-directed mutagenesis. ................................ 2 Table S3: Oligonucleotides for Homo sapiens OR2W1 site-directed mutagenesis. ................................ 4 Table S4: Vector internal oligonucleotides for pi2-dk (39aa rho-tag). .................................................... 4 Table S5: NCBI reference sequences of olfactory receptor genes investigated. ..................................... 5 Table S6: EC50 values and relative amplitudes for 3-mercapto-2-methylpentan-1-ol on OR2M3 wild type in the absence and presence of different heavy metals. ................................................................ 7 Table S7: EC50 values and relative amplitudes for OR2M3 wild type in the absence and presence of different concentrations of Cu2+. ........................................................................................................... -
The Hypothalamus As a Hub for SARS-Cov-2 Brain Infection and Pathogenesis
bioRxiv preprint doi: https://doi.org/10.1101/2020.06.08.139329; this version posted June 19, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. The hypothalamus as a hub for SARS-CoV-2 brain infection and pathogenesis Sreekala Nampoothiri1,2#, Florent Sauve1,2#, Gaëtan Ternier1,2ƒ, Daniela Fernandois1,2 ƒ, Caio Coelho1,2, Monica ImBernon1,2, Eleonora Deligia1,2, Romain PerBet1, Vincent Florent1,2,3, Marc Baroncini1,2, Florence Pasquier1,4, François Trottein5, Claude-Alain Maurage1,2, Virginie Mattot1,2‡, Paolo GiacoBini1,2‡, S. Rasika1,2‡*, Vincent Prevot1,2‡* 1 Univ. Lille, Inserm, CHU Lille, Lille Neuroscience & Cognition, DistAlz, UMR-S 1172, Lille, France 2 LaBoratorY of Development and PlasticitY of the Neuroendocrine Brain, FHU 1000 daYs for health, EGID, School of Medicine, Lille, France 3 Nutrition, Arras General Hospital, Arras, France 4 Centre mémoire ressources et recherche, CHU Lille, LiCEND, Lille, France 5 Univ. Lille, CNRS, INSERM, CHU Lille, Institut Pasteur de Lille, U1019 - UMR 8204 - CIIL - Center for Infection and ImmunitY of Lille (CIIL), Lille, France. # and ƒ These authors contriButed equallY to this work. ‡ These authors directed this work *Correspondence to: [email protected] and [email protected] Short title: Covid-19: the hypothalamic hypothesis 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.06.08.139329; this version posted June 19, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. -
Supplemental Table 1 (S1). the Chromosomal Regions and Genes Exhibiting Loss of Heterozygosity That Were Shared Between the HLRCC-Rccs of Both Patients 1 and 2
BMJ Publishing Group Limited (BMJ) disclaims all liability and responsibility arising from any reliance Supplemental material placed on this supplemental material which has been supplied by the author(s) J Clin Pathol Supplemental Table 1 (S1). The chromosomal regions and genes exhibiting loss of heterozygosity that were shared between the HLRCC-RCCs of both Patients 1 and 2. Chromosome Position Genes 1 p13.1 ATP1A1, ATP1A1-AS1, LOC101929023, CD58, IGSF3, MIR320B1, C1orf137, CD2, PTGFRN, CD101, LOC101929099 1 p21.1* COL11A1, LOC101928436, RNPC3, AMY2B, ACTG1P4, AMY2A, AMY1A, AMY1C, AMY1B 1 p36.11 LOC101928728, ARID1A, PIGV, ZDHHC18, SFN, GPN2, GPATCH3, NR0B2, NUDC, KDF1, TRNP1, FAM46B, SLC9A1, WDTC1, TMEM222, ACTG1P20, SYTL1, MAP3K6, FCN3, CD164L2, GPR3, WASF2, AHDC1, FGR, IFI6 1 q21.3* KCNN3, PMVK, PBXIP1, PYGO2, LOC101928120, SHC1, CKS1B, MIR4258, FLAD1, LENEP, ZBTB7B, DCST2, DCST1, LOC100505666, ADAM15, EFNA4, EFNA3, EFNA1, SLC50A1, DPM3, KRTCAP2, TRIM46, MUC1, MIR92B, THBS3, MTX1, GBAP1, GBA, FAM189B, SCAMP3, CLK2, HCN3, PKLR, FDPS, RUSC1-AS1, RUSC1, ASH1L, MIR555, POU5F1P4, ASH1L-AS1, MSTO1, MSTO2P, YY1AP1, SCARNA26A, DAP3, GON4L, SCARNA26B, SYT11, RIT1, KIAA0907, SNORA80E, SCARNA4, RXFP4, ARHGEF2, MIR6738, SSR2, UBQLN4, LAMTOR2, RAB25, MEX3A, LMNA, SEMA4A, SLC25A44, PMF1, PMF1-BGLAP 1 q24.2–44* LOC101928650, GORAB, PRRX1, MROH9, FMO3, MIR1295A, MIR1295B, FMO6P, FMO2, FMO1, FMO4, TOP1P1, PRRC2C, MYOC, VAMP4, METTL13, DNM3, DNM3-IT1, DNM3OS, MIR214, MIR3120, MIR199A2, C1orf105, PIGC, SUCO, FASLG, TNFSF18, TNFSF4, LOC100506023, LOC101928673, -
An Evolutionary Medicine Perspective on Neandertal Extinction
Supplementary Information (Figures and Tables) for: An evolutionary medicine perspective on Neandertal extinction Alexis P. Sullivan1, Marc de Manuel3, Tomas Marques-Bonet3,4,5, & George H. Perry1,2 Departments of 1Biology and 2Anthropology, Pennsylvania State University, University Park, PA 16802, USA 3Institut de Biologia Evolutiva (CSIC/UPF), Parque de Investigación Biomédica de Barcelona (PRBB), Barcelona, Catalonia 08003, Spain 4CNAG-CRG, Centre for Genomic Regulation (CRG), Barcelona Institute of Science and Technology (BIST), Baldiri i Reixac 4, 08028 Barcelona, Spain 5Catalan Institution of Research and Advanced Studies (ICREA), Passeig de Lluís Companys, 23, 08010, Barcelona, Spain Corresponding Author: George H. Perry E-mail: [email protected] Supplemental Figure 1: Innate immune system gene permutation analyses – 10,000 sets of 73 randomly selected genes containing nonsynonymous SNPs Supplemental Figure 2: Virus-interacting protein gene permutation analyses – 10,000 sets of 164 randomly selected genes containing nonsynonymous SNPs Supplemental Figure 3: MHC gene permutation analyses – 10,000 sets of 13 randomly selected genes containing nonsynonymous SNPs Supplemental Figure 4: Patterns of Neandertal and modern human nonsynonymous SNP diversity in MHC genes (n = 13) excluding the Altai Neandertal and one random modern human per population Supplemental Figure 5: Significantly enriched gene ontology categories (red) among top 1% ape diversity genes Supplemental Table 1: A comparison of genome-wide nonsynonymous SNPs versus total (nonsynonymous -
Us 2018 / 0305689 A1
US 20180305689A1 ( 19 ) United States (12 ) Patent Application Publication ( 10) Pub . No. : US 2018 /0305689 A1 Sætrom et al. ( 43 ) Pub . Date: Oct. 25 , 2018 ( 54 ) SARNA COMPOSITIONS AND METHODS OF plication No . 62 /150 , 895 , filed on Apr. 22 , 2015 , USE provisional application No . 62/ 150 ,904 , filed on Apr. 22 , 2015 , provisional application No. 62 / 150 , 908 , (71 ) Applicant: MINA THERAPEUTICS LIMITED , filed on Apr. 22 , 2015 , provisional application No. LONDON (GB ) 62 / 150 , 900 , filed on Apr. 22 , 2015 . (72 ) Inventors : Pål Sætrom , Trondheim (NO ) ; Endre Publication Classification Bakken Stovner , Trondheim (NO ) (51 ) Int . CI. C12N 15 / 113 (2006 .01 ) (21 ) Appl. No. : 15 /568 , 046 (52 ) U . S . CI. (22 ) PCT Filed : Apr. 21 , 2016 CPC .. .. .. C12N 15 / 113 ( 2013 .01 ) ; C12N 2310 / 34 ( 2013. 01 ) ; C12N 2310 /14 (2013 . 01 ) ; C12N ( 86 ) PCT No .: PCT/ GB2016 /051116 2310 / 11 (2013 .01 ) $ 371 ( c ) ( 1 ) , ( 2 ) Date : Oct . 20 , 2017 (57 ) ABSTRACT The invention relates to oligonucleotides , e . g . , saRNAS Related U . S . Application Data useful in upregulating the expression of a target gene and (60 ) Provisional application No . 62 / 150 ,892 , filed on Apr. therapeutic compositions comprising such oligonucleotides . 22 , 2015 , provisional application No . 62 / 150 ,893 , Methods of using the oligonucleotides and the therapeutic filed on Apr. 22 , 2015 , provisional application No . compositions are also provided . 62 / 150 ,897 , filed on Apr. 22 , 2015 , provisional ap Specification includes a Sequence Listing . SARNA sense strand (Fessenger 3 ' SARNA antisense strand (Guide ) Mathew, Si Target antisense RNA transcript, e . g . NAT Target Coding strand Gene Transcription start site ( T55 ) TY{ { ? ? Targeted Target transcript , e . -
Integrated Analysis of Optical Mapping and Whole-Genome Sequencing Reveals Intratumoral Genetic Heterogeneity in Metastatic Lung Squamous Cell Carcinoma
681 Original Article Integrated analysis of optical mapping and whole-genome sequencing reveals intratumoral genetic heterogeneity in metastatic lung squamous cell carcinoma Yizhou Peng1,2, Chongze Yuan1,2, Xiaoting Tao1,2, Yue Zhao1,2, Xingxin Yao1,2, Lingdun Zhuge1,2, Jianwei Huang3, Qiang Zheng2,4, Yue Zhang3, Hui Hong1,2, Haiquan Chen1,2, Yihua Sun1,2 1Department of Thoracic Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China; 2Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China; 3Berry Genomics Corporation, Beijing 100015, China; 4Department of Pathology, Fudan University Shanghai Cancer Center, Shanghai 200032, China Contributions: (I) Conception and design: Y Peng, C Yuan, H Chen, Y Sun; (II) Administrative support: H Chen, Y Sun; (III) Provision of study materials or patients: X Tao, X Yao, Q Zheng, H Chen, Y Sun; (IV) Collection and assembly of data: J Huang, Y Zhang; (V) Data analysis and interpretation: Y Peng, Y Zhao, L Zhuge, J Huang, Y Zhang; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors. Correspondence to: Yihua Sun; Haiquan Chen. Department of Thoracic Surgery, Fudan University Shanghai Cancer Center, 270 Dong-An Road, Shanghai 200032, China. Email: [email protected]; [email protected]. Background: Intratumoral heterogeneity is a crucial factor to the outcome of patients and resistance to therapies, in which structural variants play an indispensable but undiscovered role. Methods: We performed an integrated analysis of optical mapping and whole-genome sequencing on a primary tumor (PT) and matched metastases including lymph node metastasis (LNM) and tumor thrombus in the pulmonary vein (TPV). Single nucleotide variants, indels and structural variants were analyzed to reveal intratumoral genetic heterogeneity among tumor cells in different sites. -
High-Throughput Inference of Pairwise Coalescence Times Identifies Signals of Selection and Enriched Disease Heritability
bioRxiv preprint doi: https://doi.org/10.1101/276931; this version posted March 7, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. High-throughput inference of pairwise coalescence times identifies signals of selection and enriched disease heritability Pier Francesco Palamara1,2,3, Jonathan Terhorst4, Yun S. Song5,6, Alkes L. Price2,3 1 - Department of Statistics, University of Oxford, Oxford, UK 2 - Department of Epidemiology, Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA, USA 3 - Program in Medical and Population Genetics, Broad Institute of MIT and Harvard, Cambridge, MA, USA 4 - Department of Statistics, University of Michigan, Ann Arbor, MI, USA 5 - Department of Statistics, Computer Science Division, University of California, Berkeley, Berkeley, CA, USA 6 - Chan Zuckerberg Biohub, San Francisco, CA 94158, USA Correspondence: [email protected], [email protected] Abstract 1 Interest in reconstructing demographic histories has motivated the development of methods to 2 estimate locus-specific pairwise coalescence times from whole-genome sequence data. We 3 developed a new method, ASMC, that can estimate coalescence times using only SNP array data, 4 and is 2-4 orders of magnitude faster than previous methods when sequencing data are available. 5 We were thus able to apply ASMC to 113,851 phased British samples from the UK Biobank, 6 aiming to detect recent positive selection by identifying loci with unusually high density of very 7 recent coalescence times. -
Explorations in Olfactory Receptor Structure and Function by Jianghai
Explorations in Olfactory Receptor Structure and Function by Jianghai Ho Department of Neurobiology Duke University Date:_______________________ Approved: ___________________________ Hiroaki Matsunami, Supervisor ___________________________ Jorg Grandl, Chair ___________________________ Marc Caron ___________________________ Sid Simon ___________________________ [Committee Member Name] Dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Neurobiology in the Graduate School of Duke University 2014 ABSTRACT Explorations in Olfactory Receptor Structure and Function by Jianghai Ho Department of Neurobiology Duke University Date:_______________________ Approved: ___________________________ Hiroaki Matsunami, Supervisor ___________________________ Jorg Grandl, Chair ___________________________ Marc Caron ___________________________ Sid Simon ___________________________ [Committee Member Name] An abstract of a dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Neurobiology in the Graduate School of Duke University 2014 Copyright by Jianghai Ho 2014 Abstract Olfaction is one of the most primitive of our senses, and the olfactory receptors that mediate this very important chemical sense comprise the largest family of genes in the mammalian genome. It is therefore surprising that we understand so little of how olfactory receptors work. In particular we have a poor idea of what chemicals are detected by most of the olfactory receptors in the genome, and for those receptors which we have paired with ligands, we know relatively little about how the structure of these ligands can either activate or inhibit the activation of these receptors. Furthermore the large repertoire of olfactory receptors, which belong to the G protein coupled receptor (GPCR) superfamily, can serve as a model to contribute to our broader understanding of GPCR-ligand binding, especially since GPCRs are important pharmaceutical targets.