Imperial College London

DrAylinHanyaloglu

Faculty of MedicineDepartment of Surgery & Cancer

Senior Lecturer
 
 
 
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Contact

 

+44 (0)20 7594 2128a.hanyaloglu Website

 
 
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Assistant

 

Miss Kiran Dosanjh +44 (0)20 7594 2176

 
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Location

 

2006Institute of Reproductive and Developmental BiologyHammersmith Campus

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Summary

 

Publications

Publication Type
Year
to

36 results found

Hanyaloglu AC, Grammatopoulos DK, 2017, Pleiotropic GPCR signaling in health and disease., Mol Cell Endocrinol, Vol: 449, Pages: 1-2

JOURNAL ARTICLE

Jonas KC, Hanyaloglu AC, 2017, Impact of G protein-coupled receptor heteromers in endocrine systems, MOLECULAR AND CELLULAR ENDOCRINOLOGY, Vol: 449, Pages: 21-27, ISSN: 0303-7207

JOURNAL ARTICLE

Sposini S, Hanyaloglu AC, 2017, Spatial encryption of G protein-coupled receptor signaling in endosomes; Mechanisms and applications., Biochem Pharmacol, Vol: 143, Pages: 1-9

Within any cellular signaling system membrane trafficking is a critical mechanism for cells to translate complex networks into specific downstream responses, including the signal pathways activated by the superfamily of G protein-coupled receptors (GPCRs). Classically, membrane trafficking is viewed as a mechanism to regulate ligand sensitivity of a target tissue by controlling the level of surface receptors. Recent studies, however, have not only highlighted that GPCR trafficking is a tightly regulated process critical for spatio-temporal control of signaling, but that heterotrimeric G protein signaling can also be reactivated or continue to signal from distinct endocytic compartments, and even endosomal microdomains. The significance of spatio-temporal control will be discussed, not only with respect to how these novel molecular pathways impact our basic understanding of cellular regulation, but also our view of how aberrant signaling can result in disease. Furthermore, these mechanisms offer the potential application for novel therapeutic strategies to identify GPCR compounds with high specificity in their actions.

JOURNAL ARTICLE

Babinsky VN, Hannan FM, Gorvin CM, Howles SA, Nesbit MA, Rust N, Hanyaloglu AC, Hu J, Spiegel AM, Thakker RVet al., 2016, Allosteric Modulation of the Calcium-sensing Receptor Rectifies Signaling Abnormalities Associated with G-protein α-11 Mutations Causing Hypercalcemic and Hypocalcemic Disorders., J Biol Chem, Vol: 291, Pages: 10876-10885

Germline loss- and gain-of-function mutations of G-protein α-11 (Gα11), which couples the calcium-sensing receptor (CaSR) to intracellular calcium (Ca(2+) i) signaling, lead to familial hypocalciuric hypercalcemia type 2 (FHH2) and autosomal dominant hypocalcemia type 2 (ADH2), respectively, whereas somatic Gα11 mutations mediate uveal melanoma development by constitutively up-regulating MAPK signaling. Cinacalcet and NPS-2143 are allosteric CaSR activators and inactivators, respectively, that ameliorate signaling disturbances associated with CaSR mutations, but their potential to modulate abnormalities of the downstream Gα11 protein is unknown. This study investigated whether cinacalcet and NPS-2143 may rectify Ca(2+) i alterations associated with FHH2- and ADH2-causing Gα11 mutations, and evaluated the influence of germline gain-of-function Gα11 mutations on MAPK signaling by measuring ERK phosphorylation, and assessed the effect of NPS-2143 on a uveal melanoma Gα11 mutant. WT and mutant Gα11 proteins causing FHH2, ADH2 or uveal melanoma were transfected in CaSR-expressing HEK293 cells, and Ca(2+) i and ERK phosphorylation responses measured by flow-cytometry and Alphascreen immunoassay following exposure to extracellular Ca(2+) (Ca(2+) o) and allosteric modulators. Cinacalcet and NPS-2143 rectified the Ca(2+) i responses of FHH2- and ADH2-associated Gα11 loss- and gain-of-function mutations, respectively. ADH2-causing Gα11 mutations were demonstrated not to be constitutively activating and induced ERK phosphorylation following Ca(2+) o stimulation only. The increased ERK phosphorylation associated with ADH2 and uveal melanoma mutants was rectified by NPS-2143. These findings demonstrate that CaSR-targeted compounds can rectify signaling disturbances caused by germline and somatic Gα11 mutations, which respectively lead to calcium disorders and tumorigenesis; and that ADH2-causing Gα11 mutatio

JOURNAL ARTICLE

Jonas KC, Huhtaniemi I, Hanyaloglu AC, 2016, Single-molecule resolution of G protein-coupled receptor (GPCR) complexes, Editors: Shukla, Publisher: ELSEVIER ACADEMIC PRESS INC, Pages: 55-72, ISBN: 978-0-12-803595-5

BOOK CHAPTER

Jonas KC, Fanelli F, Huhtaniemi IT, Hanyaloglu ACet al., 2015, Single Molecule Analysis of Functionally Asymmetric G Protein-coupled Receptor (GPCR) Oligomers Reveals Diverse Spatial and Structural Assemblies, JOURNAL OF BIOLOGICAL CHEMISTRY, Vol: 290, Pages: 3875-3892, ISSN: 0021-9258

JOURNAL ARTICLE

Psichas A, Sleeth ML, Murphy KG, Brooks L, Bewick GA, Hanyaloglu AC, Ghatei MA, Bloom SR, Frost Get al., 2015, The short chain fatty acid propionate stimulates GLP-1 and PYY secretion via free fatty acid receptor 2 in rodents, INTERNATIONAL JOURNAL OF OBESITY, Vol: 39, Pages: 424-429, ISSN: 0307-0565

JOURNAL ARTICLE

Sposini S, Caltabiano G, Hanyaloglu AC, Miele Ret al., 2015, Identification of transmembrane domains that regulate spatial arrangements and activity of prokineticin receptor 2 dimers., Mol Cell Endocrinol, Vol: 399, Pages: 362-372

The chemokine prokineticin 2 (PK2) activates its cognate G protein-coupled receptor (GPCR) PKR2 to elicit various downstream signaling pathways involved in diverse biological processes. Many GPCRs undergo dimerization that can modulate a number of functions including membrane delivery and signal transduction. The aim of this study was to elucidate the interface of PKR2 protomers within dimers by analyzing the ability of PKR2 transmembrane (TM) deletion mutants to associate with wild type (WT) PKR2 in yeast using co-immunoprecipitation and mammalian cells using bioluminescence resonance energy transfer. Deletion of TMs 5-7 resulted in a lack of detectable association with WT PKR2, but could associate with a truncated mutant lacking TMs 6-7 (TM1-5). Interestingly, TM1-5 modulated the distance, or organization, between protomers and positively regulated Gαs signaling and surface expression of WT PKR2. We propose that PKR2 protomers form type II dimers involving TMs 4 and 5, with a role for TM5 in modulation of PKR2 function.

JOURNAL ARTICLE

West C, Hanyaloglu AC, 2015, Minireview: Spatial Programming of G Protein-Coupled Receptor Activity: Decoding Signaling in Health and Disease., Mol Endocrinol, Vol: 29, Pages: 1095-1106

Probing the multiplicity of hormone signaling via G protein-coupled receptors (GPCRs) has demonstrated the complex signal pathways that underlie the multiple functions these receptors play in vivo. This is highly pertinent for the GPCRs key in reproduction and pregnancy that are exposed to cyclical and dynamic changes in their extracellular milieu. How such functional pleiotropy in GPCR signaling is translated to specific downstream cellular responses, however, is largely unknown. Emerging data strongly support mechanisms for a central role of receptor location in signal regulation via membrane trafficking. In this review, we discuss current progress in our understanding of the role membrane trafficking plays in location control of GPCR signaling, from organized plasma membrane signaling microdomains, potentially provided by both distinct endocytic and exocytic pathways, to more recent evidence for spatial control within the endomembrane system. Application of these emerging mechanisms in their relevance to GPCR activity in physiological and pathophysiological conditions will also be discussed, and in improving therapeutic strategies that exploits these mechanisms in order to program highly regulated and distinct signaling profiles.

JOURNAL ARTICLE

Jean-Alphonse F, Bowersox S, Chen S, Beard G, Puthenveedu MA, Hanyaloglu ACet al., 2014, Spatially Restricted G Protein-coupled Receptor Activity via Divergent Endocytic Compartments, JOURNAL OF BIOLOGICAL CHEMISTRY, Vol: 289, Pages: 3960-3977, ISSN: 0021-9258

JOURNAL ARTICLE

Kandola MK, Sykes L, Lee YS, Johnson MR, Hanyaloglu AC, Bennett PRet al., 2014, EP2 Receptor Activates Dual G Protein Signaling Pathways that Mediate Contrasting Proinflammatory and Relaxatory Responses in Term Pregnant Human Myometrium, ENDOCRINOLOGY, Vol: 155, Pages: 605-617, ISSN: 0013-7227

JOURNAL ARTICLE

Kim SH, Blanks A, Thornton S, Bennett PR, Terzidou Vet al., 2014, Oxytocin Receptor Antagonist, Atosiban, Drives Proinflammatory Effects in Human Amnion Via G(ai) Signaling., REPRODUCTIVE SCIENCES, Vol: 21, Pages: 111A-111A, ISSN: 1933-7191

JOURNAL ARTICLE

Nikolopoulou E, Papacleovoulou G, Jean-Alphonse F, Grimaldi G, Parker MG, Hanyaloglu AC, Christian Met al., 2014, Arachidonic acid-dependent gene regulation during preadipocyte differentiation controls adipocyte potential, JOURNAL OF LIPID RESEARCH, Vol: 55, Pages: 2479-2490, ISSN: 0022-2275

JOURNAL ARTICLE

Jonas KC, Rivero-Mueller A, Huhtaniemi IT, Hanyaloglu ACet al., 2013, G Protein-Coupled Receptor Transactivation: From Molecules to Mice, RECEPTOR-RECEPTOR INTERACTIONS, Vol: 117, Pages: 433-450, ISSN: 0091-679X

JOURNAL ARTICLE

Arulkumaran S, Kandola MK, Hoffman B, Hanyaloglu AC, Johnson MR, Bennett PRet al., 2012, The Roles of Prostaglandin EP 1 and 3 Receptors in the Control of Human Myometrial Contractility, JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, Vol: 97, Pages: 489-498, ISSN: 0021-972X

JOURNAL ARTICLE

Al-Sabbagh M, Fusi L, Higham J, Lee Y, Lei K, Hanyaloglu AC, Lam EW-F, Christian M, Brosens JJet al., 2011, NADPH Oxidase-Derived Reactive Oxygen Species Mediate Decidualization of Human Endometrial Stromal Cells in Response to Cyclic AMP Signaling, ENDOCRINOLOGY, Vol: 152, Pages: 730-740, ISSN: 0013-7227

JOURNAL ARTICLE

Jean-Alphonse F, Hanyaloglu AC, 2011, Regulation of GPCR signal networks via membrane trafficking, MOLECULAR AND CELLULAR ENDOCRINOLOGY, Vol: 331, Pages: 205-214, ISSN: 0303-7207

JOURNAL ARTICLE

Rivero-Muller A, Chou Y-Y, Ji I, Lajic S, Hanyaloglu AC, Jonas K, Rahman N, Ji TH, Huhtaniemi Iet al., 2010, Rescue of defective G protein-coupled receptor function in vivo by intermolecular cooperation, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol: 107, Pages: 2319-2324, ISSN: 0027-8424

JOURNAL ARTICLE

Hanyaloglu AC, von Zastrow M, 2008, Regulation of GPCRs by Endocytic membrane trafficking and its potential implications, ANNUAL REVIEW OF PHARMACOLOGY AND TOXICOLOGY, Vol: 48, Pages: 537-568, ISSN: 0362-1642

JOURNAL ARTICLE

N'Diaye E-N, Hanyaloglu AC, Kajihara KK, Puthenveedu MA, Wu P, von Zastrow M, Brown EJet al., 2008, The ubiquitin-like protein PLIC-2 is a negative regulator of G protein-coupled receptor endocytosis, MOLECULAR BIOLOGY OF THE CELL, Vol: 19, Pages: 1252-1260, ISSN: 1059-1524

JOURNAL ARTICLE

Hanyaloglu AC, von Zastrow M, 2007, A novel sorting sequence in the beta(2)-adrenergic receptor switches recycling from default to the Hrs-dependent mechanism, JOURNAL OF BIOLOGICAL CHEMISTRY, Vol: 282, Pages: 3095-3104, ISSN: 0021-9258

JOURNAL ARTICLE

Hanyaloglu AC, McCullagh E, von Zastrow M, 2005, Essential role of Hrs in a recycling mechanism mediating functional resensitization of cell signaling, EMBO JOURNAL, Vol: 24, Pages: 2265-2283, ISSN: 0261-4189

JOURNAL ARTICLE

Miles LEC, Hanyaloglu AC, Dromey JR, Pfleger KDG, Eidne KAet al., 2004, Gonadotropin-releasing hormone receptor-mediated growth suppression of immortalized L beta T2 gonadotrope and stable HEK293 cell lines, ENDOCRINOLOGY, Vol: 145, Pages: 194-204, ISSN: 0013-7227

JOURNAL ARTICLE

Ward BK, Magno AL, Davis EA, Hanyaloglu AC, Stuckey BGA, Burrows M, Eidne KA, Charles AK, Ratajczak Tet al., 2004, Functional deletion of the calcium-sensing receptor in a case of neonatal severe hyperparathyroidism, JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, Vol: 89, Pages: 3721-3730, ISSN: 0021-972X

JOURNAL ARTICLE

Eidne KA, Kroeger KM, Hanyaloglu AC, 2002, Applications of novel resonance energy transfer techniques to study dynamic hormone receptor interactions in living cells, TRENDS IN ENDOCRINOLOGY AND METABOLISM, Vol: 13, Pages: 415-421, ISSN: 1043-2760

JOURNAL ARTICLE

Hanyaloglu AC, Seeber RM, Kohout TA, Lefkowitz RJ, Eidne KAet al., 2002, Homo- and hetero-oligomerization of thyrotropin-releasing hormone (TRH) receptor subtypes - Differential regulation of beta-arrestins 1 and 2, JOURNAL OF BIOLOGICAL CHEMISTRY, Vol: 277, Pages: 50422-50430, ISSN: 0021-9258

JOURNAL ARTICLE

Hanyaloglu AC, Vrecl M, Kroeger KM, Miles LEC, Qian HW, Thomas WG, Eidne KAet al., 2001, Casein kinase II sites in the intracellular C-terminal domain of the thyrotropin-releasing hormone receptor and chimeric gonadotropin-releasing hormone receptors contribute to beta-arrestin-dependent internalization, JOURNAL OF BIOLOGICAL CHEMISTRY, Vol: 276, Pages: 18066-18074, ISSN: 0021-9258

JOURNAL ARTICLE

Kroeger KM, Hanyaloglu AC, Eidne KA, 2001, Applications of BRET to study dynamic G-protein coupled receptor interactions in living cells, 4th International Australian Peptide Conference, Publisher: KLUWER ACADEMIC PUBL, Pages: 155-162, ISSN: 0929-5666

CONFERENCE PAPER

Kroeger KM, Hanyaloglu AC, Seeber RM, Miles LEC, Eidne KAet al., 2001, Constitutive and agonist-dependent homo-oligomerization of the thyrotropin-releasing hormone receptor - Detection in living cells using bioluminescence resonance energy transfer, JOURNAL OF BIOLOGICAL CHEMISTRY, Vol: 276, Pages: 12736-12743, ISSN: 0021-9258

JOURNAL ARTICLE

Heding A, Vrecl M, Hanyaloglu AC, Sellar R, Taylor PL, Eidne KAet al., 2000, The rat gonadotropin-releasing hormone receptor internalizes via a beta-arrestin-independent, but dynamin-dependent, pathway: Addition of a carboxyl-terminal tail confers beta-arrestin dependency, ENDOCRINOLOGY, Vol: 141, Pages: 299-306, ISSN: 0013-7227

JOURNAL ARTICLE

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