Fixed-term

Details Chronic and allergic pulmonary aspergillosis syndromes complicate asthma, COPD and bronchiectasis, leading to symptoms, admissions and mortality. Antifungal treatment with azoles is the mainstay of treatment, however response rates are suboptimal, eg 60% in CPA suggesting that concomitant patient of microbial factors may have an impact. Several phenotypes of allergic bronchopulmonary aspergillosis (ABPA) and chronic pulmonary aspergillosis (CPA) exist, yet treatment recommendations are not individualised. Atopy, bronchiectasis, COPD, or concomitant infection may affect antifungal treatment response resulting in deterioration, hospital admissions and mortality. In addition, patients with chronic lung disease may not have the full criteria for diagnosis of ABPA or CPA, but may have evidence of Aspergillus lung colonisation; some evidence indicates that these patients have worse outcomes, however no treatment recommendation exists. This project will explore the potential for a personalised approach to management of aspergillosis in chronic lung disease via 2 distinct workstreams. Workstream 1: Real-world large scale data analysis: By accessing data from a large primary care database, this workstream will explore the effect of antifungal treatment on the outcomes of patients with chronic lung disease, when prescribed for indications outside well defined aspergillosis infection syndromes. The student will use advanced statistical methods and will be supported by supervisors experienced in such analyses. Workstream 2: Prospective precision medicine trial: This workstream will explore the role of patient factors and biomarkers in the response to antifungal treatment in ABPA and CPA. Antifungals have a role in ABPA and CPA, although several phenotypes of these diseases exist, justifying the need for personalised treatment in these patients. A prospective trial of assessment of antifungal treatment response in patients with ABPA and CPA will be undertaken. The use of biomarkers such as aspergillus serology, FeNO, peripheral eosinophil count, volatile organic compounds will be explored as potential predictors of treatment response. Eligibility Candidates are expected to hold (or be about to obtain) a minimum upper second-class honours degree (or equivalent) in Medicine, Biology or a related area / subject. Candidates with a clinical background, such as in respiratory medicine or infectious disease, a laboratory background in microbiology or chemistry and/or with experience in mathematics or statistics are encouraged to apply. How to Apply For information on how to apply for this project, please visit the Faculty of Biology, Medicine and Health Doctoral Academy website (https://www.bmh.manchester.ac.uk/study/research/apply/). Informal enquiries may be made directly to the primary supervisor.  On the online application form select PhD Infectious Diseases. Equality, Diversity & Inclusion Equality, diversity and inclusion is fundamental to the success of The University of Manchester, and is at the heart of all of our activities. The full Equality, diversity and inclusion statement can be found on the website Website Funding Notes Applications are invited from self-funded students. This project has a Band 2 fee. Details of our different fee bands can be found on our website: https://www.bmh.manchester.ac.uk/study/research/fees/ References Kosmidis C, Smith H, Mollett G, Harris C, Akili S, Bazaz R. Predictive factors for treatment response and mortality in chronic pulmonary aspergillosis. Mycoses. 2023 Nov;66(11):960-968. doi: 10.1111/myc.13641. Epub 2023 Aug 8. PMID: 37553558. Sengupta A, Ray A, Upadhyay AD, Izumikawa K, Tashiro M, Kimura Y, Bongomin F, Su X, Maitre T, Cadranel J, de Oliveira VF, Iqbal N, Irfan M, Uzunhan Y, Aguilar-Company J, Munteanu O, Beardsley J, Furuuchi K, Takazono T, Ito A, Kosmidis C, Denning DW. Mortality in chronic pulmonary aspergillosis: a systematic review and individual patient data meta-analysis. Lancet Infect Dis. 2025 Mar;25(3):312-324. doi: 10.1016/S1473-3099(24)00567-X. Epub 2024 Nov 29. Erratum in: Lancet Infect Dis. 2025 Mar;25(3):e137. doi: 10.1016/S1473-3099(25)00098-2. PMID: 39617023. Apply Now

Details The mineral and bone disorders of chronic kidney disease (CKD-MBD) cause vascular calcification and cardiovascular mortality in patients suffering advanced renal disease. CKD-MBD involves hyperphosphataemia (high serum phosphate) and secondary hyperparathyroidism (SHPT; excess parathyroid hormone release) which increase mortality in dialysis patients. However, the mechanism by which hyperphosphataemia increases parathyroid hormone (PTH) secretion remains unknown. The calcium-sensing receptor (CaR) is the key controller of PTH secretion, and we have identified CaR as the likely parathyroid phosphate sensor (Centeno et al., 2019). Specifically, raising phosphate concentration within the pathophysiologic range for CKD appears to inhibit CaR activity by non-competitive antagonism. More recently, we reported that a calcimimetic drug (that lowers PTH secretion in CKD) sees its effect impaired when the patient also has hyperphosphataemia (Goodman et al., 2022). Therefore, to better treat CKD-MBD we need to understand how hyperphosphataemia inhibits the calcium-sensing receptor – the critical controller of PTH secretion. Another feature of CKD-MBD is vitamin D3 deficiency which is itself a common public health problem worldwide that is increasingly believed to contribute not only to decreased bone mineralisation but potentially to other serious medical conditions. Interestingly, there is even increasing evidence of links between obesity and vitamin D3 deficiency. However, the mechanisms underlying these associations remain poorly understood. This project will thus also look at the cellular actions of 1,25(OH)2 vitamin D3 formation on cells/tissues of the endocrine system. The techniques involved in this project include hormone assay, live cell calcium imaging, kinase assays and transfection with siRNAs for the selective knockdown of calciotropic signal regulators. We will also perform ex vivo hormone assays on transgenic mouse parathyroid glands (modified by CRISPR/Cas9). Candidates are expected to hold (or be about to obtain) a minimum 2:1 Bachelors Degree with Honours (or equivalent) in a related area/subject. Candidates with Masters-level experience in molecular and/or in vivo techniques are strongly encouraged to apply. Eligibility  Applicants must have obtained or be about to obtain a minimum Upper Second class UK honours degree, or the equivalent qualifications gained outside the UK, in a relevant discipline.    Before you Apply  Applicants must make direct contact with preferred supervisors before applying. It is your responsibility to make arrangements to meet with potential supervisors, prior to submitting a formal online application. How to Apply  To be considered for this project you MUST submit a formal online application form – on the application form select PhD Pharmacology Programme. Full details on how to apply can be found on the Website: How to apply for postgraduate research at The University of Manchester If you have any queries regarding making an application please contact our admissions team FBMH.doctoralacademy.admissions@manchester.ac.uk Equality, Diversity and Inclusion   Equality, diversity and inclusion is fundamental to the success of The University of Manchester, and is at the heart of all of our activities. The full Equality, diversity and inclusion statement can be found on the website: Equality, diversity and inclusion (EDI | Postgraduate Research | Biology, Medicine and Health | University of Manchester Funding Notes Applications are invited from self-funded students. This project has a Band 3 (high) fee. Details of our different fee bands can be found on our website https://www.bmh.manchester.ac.uk/study/research/fees/ References [1] Centeno PP, Herberger A, Mun H-C, Tu C, Nemeth EF, Chang W, Conigrave AD, Ward DT (2019) Phosphate acts directly on the calcium-sensing receptor to stimulate parathyroid hormone secretion. Nature Communications. 10, 4693. [2] Goodman WG, Ward DT, Martin KJ, Drayer D, Moore C, Xu J, Lai J, Chon Y, Nemeth EF (2022) Activation of the Calcium Receptor by Calcimimetic Agents is Preserved Despite Modest Attenuating Effects of Hyperphosphatemia. Journal of the American Society of Nephrology. 33, 201-212. [3] Campion KL, McCormick WD, Warwicker J, Bin Khayat ME, Atkinson-Dell R, Steward MC, Delbridge LW, Mun H-C, Conigrave AD, Ward DT. (2015) Pathophysiological Changes in Extracellular pH Modulate Parathyroid Calcium-Sensing Receptor Activity and Secretion via a Histidine-Independent Mechanism. Journal of the American Society of Nephrology. 26, 2163-2171. [4] Centeno PP, Binmahfouz LS, Alghamdi K, Ward DT (2023) Inhibition of the Calcium-Sensing Receptor by Extracellular Phosphate Ions and by Intracellular Phosphorylation. Frontiers in Physiology. 14, 1154374. [5] Leach K, Hannan FM, Josephs TM, Keller AN, Møller TC, Ward DT, Kallay E, Mason RS, Thakker RV, Riccardi D, Conigrave AD, Bräuner-Osborne H. (2020) International Union of Basic and Clinical Pharmacology: Calcium-sensing receptor Nomenclature, Pharmacology, and Function. Pharmacological Reviews 72, 558-604 Apply Now

Details Sporothrix species, particularly S. schenckii and S. brasiliensis, are thermally dimorphic fungi responsible for sporotrichosis; a chronic subcutaneous infection with zoonotic potential and rising antifungal resistance. Despite its clinical importance, the molecular mechanisms underlying skin colonisation, tissue invasion, and host-pathogen interactions remain poorly defined. This project will establish a next-generation skin-on-a-chip infection platform for Sporothrix, identify genetic pathways essential for skin tropism, and implement CRISPR-Cas9 genome editing to functionally validate novel antifungal targets. Objective 1: Developing a Microfluidic Skin-on-a-Chip Model for Sporothrix Infection The first objective will engineer a dynamic, multilayered human skin-on-a-chip system to study Sporothrix skin colonisation and host responses under physiologically relevant conditions. Unlike static skin models, the chip will integrate a microfluidic system to simulate perfusion, nutrient gradients, and immune cell recruitment, enabling real-time monitoring of infection dynamics. The chip will incorporate a layered structure: primary human keratinocytes (epidermis), fibroblasts embedded in collagen (dermis), and optional endothelial cells to mimic microvascular interfaces. Infection progression will be tracked using live-cell microscopy, CFU quantification, histology and immunofluorescence for fungal structures and host markers. Cytokine release and barrier integrity (via TEER) will be monitored over time. Training will include microfluidic chip assembly, cell co-culture techniques, live-cell infection imaging, and host response assays. Objective 2: Identifying Genetic Determinants of Skin Colonisation and Pathogenicity in Sporothrix Species This objective will define the fungal genetic programs activated during skin infection using the skin-on-a-chip model. S. schenckii and S. brasiliensis will be harvested at defined infection stages, and fungal RNA will be extracted for transcriptomic profiling. Particular focus will be given to genes involved in thermal dimorphism, adhesion, stress resistance, and secretion of virulence-associated proteins. Comparative transcriptomics will highlight differentially expressed genes between the two species and between environmental and host-associated states. Genes highly induced during skin invasion. Bioinformatic pipelines will integrate transcriptomic data with orthology mapping to identify potential druggable targets. These will inform CRISPR-based functional studies in Objective 3. Training will include dual RNA-seq, fungal transcriptomics during infection, and comparative genome analysis. Objective 3: Establishing CRISPR-Cas9 Genome Editing in Sporothrix The third objective will develop CRISPR-Cas9 genome editing for Sporothrix to functionally interrogate genes identified in Objective 2. Due to low transformation efficiency and dimorphism, Sporothrix remains genetically intractable. This project will adapt a ribonucleoprotein (RNP)-based CRISPR approach, utilising transient Cas9 delivery with species-optimised sgRNAs and homologous repair templates.We will first optimise transformation via electroporation or PEG-mediated protoplast fusion, testing selectable markers (hph, nat1) and homologous recombination rates. Mutant validation will involve PCR genotyping and phenotyping in both filamentous and yeast phases. Knockout strains will be assessed in the skin-on-a-chip model for changes in colonisation, invasion depth, stress resistance, and immunogenicity. Mutants with attenuated virulence or hypersensitivity to antifungals will be screened for drug-target feasibility under host-relevant conditions. Training will include sgRNA design, fungal transformation optimisation, and CRISPR-based functional screening in organotypic models. Candidates are expected to hold (or be about to obtain) a minimum 2:1 Bachelors Degree with Honours (or equivalent) in a related subject. Candidates with experience in fungal biology or with an interest in infection biology are encouraged to apply. Eligibility  Applicants must have obtained or be about to obtain a minimum Upper Second class UK honours degree, or the equivalent qualifications gained outside the UK, in a relevant discipline.    Before you Apply  Applicants must make direct contact with preferred supervisors before applying. It is your responsibility to make arrangements to meet with potential supervisors, prior to submitting a formal online application. How to Apply  To be considered for this project you MUST submit a formal online application form – on the application form select PhD Molecular Biology Programme. Full details on how to apply can be found on the Website: How to apply for postgraduate research at The University of Manchester If you have any queries regarding making an application please contact our admissions team FBMH.doctoralacademy.admissions@manchester.ac.uk Equality, Diversity and Inclusion   Equality, diversity and inclusion is fundamental to the success of The University of Manchester, and is at the heart of all of our activities. The full Equality, diversity and inclusion statement can be found on the website: Equality, diversity and inclusion (EDI | Postgraduate Research | Biology, Medicine and Health | University of Manchester Funding Notes Applications are invited from self-funded students. This project has a Band 3 (high) fee. Details of our different fee bands can be found on our website https://www.bmh.manchester.ac.uk/study/research/fees/ Apply Now

Details Complex somatic structural variations (SVs) in genomic regions such as centromeres and telomeres play a crucial role in driving many genetic disorders. For example, large SVs in centromeric regions contribute to chromosomal instability (CIN) and therapy resistance in cancers like glioblastoma and lung cancer. Despite their importance, these repetitive regions remain insufficiently explored due to the limitations of current sequencing technologies, restricting our understanding of key somatic mutations, mobile genetic elements (MGEs), and critical biomarkers for early diagnosis. Traditional methods struggle to accurately analyze complex structural variations (SVs) in centromeres, telomeres, and extrachromosomal DNA (ecDNA) due to the repetitive and intricate nature of these genomic regions. This project will bridge these gaps by employing graph-based models and integrating long-read sequencing with Hi-C data from bulk and/or single-cell datasets at a personalized, chromosome-specific base level. Our approach will overcome the limitations of traditional linear genome analysis, enabling precise mapping of SVs and chromosome-level interactions, with the scalability to analyze thousands of genomes efficiently. By focusing on complex somatic SVs including chromothripsis, chromoplexy, and ecDNA, we aim to uncover a comprehensive somatic SV landscape essential for understanding the mechanisms driving cancer progression. Specific Aims Aim 1: Develop a graph-based method for accurately analyzing repetitive genomic regions to advance early disease diagnostics – Create a graph-based method using long-read sequencing and Hi-C data to detect somatic variations in complex, repetitive regions like centromeres and telomeres. – Identify and characterize classes of inter- and intra-chromosomal structural variations, including chromothripsis and chromoplexy, and assess their functional consequences. Aim 2: Investigate the role of extrachromosomal DNA (ecDNA) in disease progression – Develop a toolkit feature that captures the circular nature of ecDNA to explore its role in disease progression and gene amplification. Aim 3: Comprehensively unravel the processes of clonal evolution in personalized cancer – Generate and validate a personalized set of structural variations in cancer cell lines, using the tools developed in Aims 1 and 2, across both commercially available and patient-derived cell lines. – By using a graph-based approach, we can precisely map centromeric disruptions, such as alpha-satellite DNA instability and EGFR amplification, in brain, lung, and oesophageal cancers, providing insights into clonal evolution and resistance mechanisms. This method overcomes the limitations of linear reference genomes, enabling personalized treatment strategies by accurately tracking structural variations and predicting tumor responses to therapies, ultimately improving patient outcomes. Outcomes This project will deliver a comprehensive map of structural variations (SVs) in centromeric and telomeric regions, advancing our understanding of how these variations drive cancer progression and rare diseases. By developing graph-based methods, we will enable the detection of previously hidden SVs, supporting early diagnostics and personalized treatments tailored to each patient’s unique genetic profile. The project’s insights into chromosomal instability, gene amplification, immune evasion, and the regulatory roles of mobile genetic elements will deepen our knowledge of fundamental disease mechanisms. The project will illuminate the broader implications of SVs on genome evolution, gene regulation, and disease mechanisms. Through collaborations with healthcare partners, we aim to integrate these innovations into clinical pipelines, improving outcomes for conditions with significant unmet needs. The PGR will receive comprehensive support and training designed to foster expertise in genomics and disease biology. Complementing the set of technical skills, the PGR will develop essential professional skills in project management, academic writing, and data visualization, with access to workshops, writing retreats, and industry-focused seminars. This holistic training approach will equip the PGR with the knowledge and skills needed to make significant contributions to clinical applications. Students are expected to be highly motivated to work on challenging research questions in an international team and collaborative environment. See our latest publications here: https://scholar.google.com/citations?hl=en&user=_Sn07lgAAAAJ&view_op=list_works&sortby=pubdate. https://scholar.google.co.uk/citations?hl=en&user=gt9DERIAAAAJ&view_op=list_works&sortby=pubdate. Our investigation will also focus on somatic instability and clonal evolution in nervous tissue by analysing repeat expansions in genes like HTT (Huntington’s Disease) and DMPK (Myotonic Dystrophy). Eligibility Applicants must have obtained or be about to obtain a minimum Upper Second class UK honours degree, or the equivalent qualifications gained outside the UK, in a relevant discipline. How to Apply For information on how to apply for this project, please visit the Faculty of Biology, Medicine and Health Doctoral Academy website (https://www.bmh.manchester.ac.uk/study/research/apply/). Informal enquiries may be made directly to the primary supervisor. On the online application form please select PhD Bioinformatics. Equality, Diversity & Inclusion Equality, diversity and inclusion is fundamental to the success of The University of Manchester, and is at the heart of all of our activities. The full Equality, diversity and inclusion statement can be found on the website https://www.bmh.manchester.ac.uk/study/research/apply/equality-diversity-inclusion/ Funding Notes Applications are invited from self-funded students. Apply Now

Details Background: Translation of mRNA into proteins is a critical cellular process for normal development and function. An increasing number of genetic disorders caused by variants in genes encoding translation factors are now known. We recently described a novel human disorder called Faundes-Banka Syndrome (OMIM #619376) caused by mutations in the translation factor EIF5A1 gene resulting in developmental problems, small head size and craniofacial defects in children. Using yeast and zebrafish model systems we showed how EIF5A1 mutations lead to impaired eIF5A function and cause phenotypes consistent with the human disorder. Interestingly, in the same model systems we have shown that a specific food supplement (spermidine) may be a potential treatment for this disease. We have now also found patients with related neurodevelopmental disorders that have mutations in other related translation factor genes. Project: This project aims to improve diagnosis, mechanistic understanding and treatment of one or more neurodevelopmental disorder caused by defects in the protein synthesis machinery by – 1. Computationally Investigating the landscape of variants in genes encoding members of protein synthesis machinery in large whole exome or genome datasets from healthy and disease populations to Identify novel genetic variants and/or disorders. 2. Investigate functional impact of selected novel variants by developing a whole animal model (zebrafish), using CRISPR, combined with neurodevelopmental phenotypic and biochemical characterisation via fluorescent microscopy, RNA-seq, mass spectrometry and biochemical assays of global and specific protein synthesis functions. 3. Investigate treatment in neurodevelopmental disease zebrafish models caused by variants in protein synthesis genes using pharmacological and genetic approaches. Outcome: The student will contribute to providing novel insights into a human disorder at the interface of fundamental biology and translational precision medicine. The student will learn several fundamental interdisciplinary and quantitative skills, as well as gaining significant experience of studying whole organism physiology in context of human disease Candidates are expected to hold (or be about to obtain) a minimum 2:1 Bachelors Degree with Honours (or equivalent) in a related area/subject.  Candidates with experience in zebrafish modelling or with an interest in neurodevelopmental disease and genetics are encouraged to apply. Before you Apply  Applicants must make direct contact with preferred supervisors before applying. It is your responsibility to make arrangements to meet with potential supervisors, prior to submitting a formal online application. How to Apply  To be considered for this project you MUST submit a formal online application form – on the application form select PhD Medical Genetics Programme. Full details on how to apply can be found on the Website: How to apply for postgraduate research at The University of Manchester If you have any queries regarding making an application please contact our admissions team FBMH.doctoralacademy.admissions@manchester.ac.uk Equality, Diversity and Inclusion   Equality, diversity and inclusion is fundamental to the success of The University of Manchester, and is at the heart of all of our activities. The full Equality, diversity and inclusion statement can be found on the website: Equality, diversity and inclusion (EDI | Postgraduate Research | Biology, Medicine and Health | University of Manchester Funding Notes Applications are invited from self-funded students. This project has a Band 3 (high) fee. Details of our different fee bands can be found on our website https://www.bmh.manchester.ac.uk/study/research/fees/ References 1. Park MH, Kar RK, Banka S, Ziegler A, Chung WK. (2021) Post-translational formation of hypusine in eIF5A: implications in human neurodevelopment. Amino Acids. doi: 10.1007/s00726-021-03023-6 2. V Faundes, MD Jennings, S Crilly, S Legraie, S Cuvertino, SJ Davies, A Douglas, A Fry, V Harrison, J Amiel, D Lehalle, WG Newman, P Newkirk, J Ranells, M Splitt, The Deciphering Developmental Disorders (DDD) Study, CT Gordon, PR Kasher*, GD Pavitt*, S Banka* (2021). Impaired eIF5A function causes a Mendelian disorder that is partially rescued in model systems by spermidine. Nature Communications 12:833. doi: 10.1038/s41467-021-21053-2.

Details The regulation of parathyroid hormone (PTH) secretion is of fundamental importance for calcium homeostasis and in mineral conditions affecting bone and the kidneys. Whilst it is clear that the calcium-sensing receptor (CaR) represents the key controller of PTH secretion by suppressing its secretion, the way the CaR works remains unclear. Indeed, it is still not clear how elevated intracellular calcium concentration (Ca2+i) appears to suppress PTH secretion in parathyroid gland while stimulating hormone / neurotransmitter secretion in many other cell-types. Furthermore, the pulsatility of PTH secretion, which is vital for bone formation, remains poorly understood. Therefore, this project aims to shed light on both the basic physiology of mammalian calcium homeostasis as well as helping us to understand the development of osteoporosis and CKD-MBD (bone mineral disease of chronic kidney disease). This project involves live cell imaging (including intracellular calcium imaging), and ex vivo hormone assays, as well as cell transfection with receptors, signalling modulators and siRNAs for selectively knocking down expression of CaR signal regulators. Candidates are expected to hold (or be about to obtain) a minimum 2:1 Bachelors Degree with Honours (or equivalent) in a related area/subject. Candidates with Masters-level experience in molecular and/or in vivo techniques are strongly encouraged to apply. Before you Apply Applicants must make direct contact with preferred supervisors before applying. It is your responsibility to make arrangements to meet with potential supervisors, prior to submitting a formal online application. How to Apply To be considered for this project you MUST submit a formal online application form – on the application form select PhD Endocrinology Programme. Full details on how to apply can be found on the Website: How to apply for postgraduate research at The University of Manchester If you have any queries regarding making an application please contact our admissions team FBMH.doctoralacademy.admissions@manchester.ac.uk Equality, Diversity and Inclusion Equality, diversity and inclusion is fundamental to the success of The University of Manchester, and is at the heart of all of our activities. The full Equality, diversity and inclusion statement can be found on the website: Equality, diversity and inclusion (EDI | Postgraduate Research | Biology, Medicine and Health | University of Manchester Funding Notes Applications are invited from self-funded students. This project has a Band 3 (high) fee. Details of our different fee bands can be found on our website https://www.bmh.manchester.ac.uk/study/research/fees/ References [1] Centeno PP, Herberger A, Mun H-C, Tu C, Nemeth EF, Chang W, Conigrave AD, Ward DT (2019) Phosphate acts directly on the calcium-sensing receptor to stimulate parathyroid hormone secretion. Nature Communications. 10, 4693. [2] Goodman WG, Ward DT, Martin KJ, Drayer D, Moore C, Xu J, Lai J, Chon Y, Nemeth EF (2022) Activation of the Calcium Receptor by Calcimimetic Agents is Preserved Despite Modest Attenuating Effects of Hyperphosphatemia. Journal of the American Society of Nephrology. 33, 201-212. [3] Campion KL, McCormick WD, Warwicker J, Bin Khayat ME, Atkinson-Dell R, Steward MC, Delbridge LW, Mun H-C, Conigrave AD, Ward DT. (2015) Pathophysiological Changes in Extracellular pH Modulate Parathyroid Calcium-Sensing Receptor Activity and Secretion via a Histidine-Independent Mechanism. Journal of the American Society of Nephrology. 26, 2163-2171. [4] Centeno PP, Binmahfouz LS, Alghamdi K, Ward DT (2023) Inhibition of the Calcium-Sensing Receptor by Extracellular Phosphate Ions and by Intracellular Phosphorylation. Frontiers in Physiology. 14, 1154374. [5] Leach K, Hannan FM, Josephs TM, Keller AN, Møller TC, Ward DT, Kallay E, Mason RS, Thakker RV, Riccardi D, Conigrave AD, Bräuner-Osborne H. (2020) International Union of Basic and Clinical Pharmacology: Calcium-sensing receptor Nomenclature, Pharmacology, and Function. Pharmacological Reviews 72, 558-604