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Article ; Online: Preclinical and translational pharmacology of afucosylated anti-CCR8 antibody for depletion of tumour-infiltrating regulatory T cells.

Gampa, Gautham / Spinosa, Phillip / Getz, Jennifer / Zhong, Yu / Halpern, Wendy / Esen, Emel / Davies, John / Chou, Cassie / Kwong, Mandy / Wang, Yingyun / Arenzana, Teresita L / Shivva, Vittal / Huseni, Mahrukh / Hsieh, Robert / Schartner, Jill / Koerber, James T / Rutz, Sascha / Hosseini, Iraj

British journal of pharmacology

2024

Abstract: Background and purpose: RO7502175 is an afucosylated antibody designed to eliminate C-C motif chemokine receptor 8 (CCR8): Experimental approach: We report findings from preclinical studies characterizing pharmacology, pharmacokinetics (PK)/ ... ...

Abstract	Background and purpose: RO7502175 is an afucosylated antibody designed to eliminate C-C motif chemokine receptor 8 (CCR8) Experimental approach: We report findings from preclinical studies characterizing pharmacology, pharmacokinetics (PK)/pharmacodynamics (PD) and safety profile of RO7502175 and discuss the translational PK/PD approach used to inform first-in-human (FiH) dosing strategy and clinical development in solid tumour indications. Key results: RO7502175 demonstrated selective ADCC against human CCR8 Conclusion and implications: This work demonstrates a translational research strategy for collecting and utilizing relevant nonclinical data, developing a mechanistic PK/PD model and using a comprehensive approach to inform clinical study design for RO7502175.
Language	English
Publishing date	2024-03-14
Publishing country	England
Document type	Journal Article
ZDB-ID	80081-8
ISSN	1476-5381 ; 0007-1188
ISSN (online)	1476-5381
ISSN	0007-1188
DOI	10.1111/bph.16326
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Article ; Online: Aerobic glycolysis in osteoblasts.

Esen, Emel / Long, Fanxin

Current osteoporosis reports

2014 Volume 12, Issue 4, Page(s) 433–438

Abstract: Osteoblasts, the chief bone-making cells in the body, are a focus of osteoporosis research. Although teriparatide, a synthetic fragment of the human parathyroid hormone (PTH), has been an effective bone anabolic drug, there remains a clinical need for ... ...

Abstract	Osteoblasts, the chief bone-making cells in the body, are a focus of osteoporosis research. Although teriparatide, a synthetic fragment of the human parathyroid hormone (PTH), has been an effective bone anabolic drug, there remains a clinical need for additional therapeutics that safely stimulates osteoblast number and function. Work in the past several decades has provided unprecedented clarity about the roles of growth factors and transcription factors in regulating osteoblast differentiation and activity, but whether these factors may regulate cellular metabolism to influence cell fate and function has been largely unexplored. The past few years have witnessed a resurgence of interest in the cellular metabolism of osteoblasts, with the hope that elucidation of their metabolic profile may open new avenues for developing bone anabolic agents. Here we review the current understanding about glucose metabolism in osteoblasts.
MeSH term(s)	Animals ; Cell Differentiation/physiology ; Glucose/metabolism ; Humans ; Models, Animal ; Osteoblasts/cytology ; Osteoblasts/metabolism ; Osteogenesis/physiology ; Parathyroid Hormone/physiology
Chemical Substances	Parathyroid Hormone ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2014-09-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2186581-4
ISSN	1544-2241 ; 1544-1873
ISSN (online)	1544-2241
ISSN	1544-1873
DOI	10.1007/s11914-014-0235-y
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Article: Ethical dilemmas and decision making in accounting

Caliskan, Arzu Ozsozgun / Akbas, Halil Emre / Esen, Emel

Corporate governance : an international perspective , p. 241-252

2014 , Page(s) 241–252

Author's details	Arzu Ozsozgun Caliskan, Halil Emre Akbas, and Emel Esen
Keywords	Wirtschaftsprüfung ; Unternehmensethik ; Entscheidung
Language	English
Publisher	Springer
Publishing place	Berlin [u.a.]
Document type	Article
ISBN	978-3-642-45166-9 ; 3-642-45166-7
Database	ECONomics Information System

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Article: An empirical research about whistleblowing behavior in accounting context

Erkmen, Turhan / Çalışkan, Arzu Özsözgün / Esen, Emel

Journal of accounting & organizational change Vol. 10, No. 2 , p. 229-243

2014 Volume 10, Issue 2, Page(s) 229–243

Author's details	Turhan Erkmen, Arzu Özsözgün Çalışkan and Emel Esen
Keywords	Whistleblowing ; Accounting professionals
Language	English
Size	graph. Darst.
Publisher	Emerald
Publishing place	Bradford
Document type	Article
ZDB-ID	2248719-0
ISSN	1832-5912
Database	ECONomics Information System

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Article ; Online: PTH Promotes Bone Anabolism by Stimulating Aerobic Glycolysis via IGF Signaling.

Esen, Emel / Lee, Seung-Yon / Wice, Burton M / Long, Fanxin

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

2015 Volume 30, Issue 11, Page(s) 2137

Language	English
Publishing date	2015-11
Publishing country	United States
Document type	Published Erratum
ZDB-ID	632783-7
ISSN	1523-4681 ; 0884-0431
ISSN (online)	1523-4681
ISSN	0884-0431
DOI	10.1002/jbmr.2714
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Article ; Online: PTH Promotes Bone Anabolism by Stimulating Aerobic Glycolysis via IGF Signaling.

Esen, Emel / Lee, Seung-Yon / Wice, Burton M / Long, Fanxin

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

2015 Volume 30, Issue 11, Page(s) 1959–1968

Abstract: Teriparatide, a recombinant peptide corresponding to amino acids 1-34 of human parathyroid hormone (PTH), has been an effective bone anabolic drug for over a decade. However, the mechanism whereby PTH stimulates bone formation remains incompletely ... ...

Abstract	Teriparatide, a recombinant peptide corresponding to amino acids 1-34 of human parathyroid hormone (PTH), has been an effective bone anabolic drug for over a decade. However, the mechanism whereby PTH stimulates bone formation remains incompletely understood. Here we report that in cultures of osteoblast-lineage cells, PTH stimulates glucose consumption and lactate production in the presence of oxygen, a hallmark of aerobic glycolysis, also known as Warburg effect. Experiments with radioactively labeled glucose demonstrate that PTH suppresses glucose entry into the tricarboxylic acid cycle (TCA cycle). Mechanistically, the increase in aerobic glycolysis is secondary to insulin-like growth factor (Igf) signaling induced by PTH, whereas the metabolic effect of Igf is dependent on activation of mammalian target of rapamycin complex 2 (mTORC2). Importantly, pharmacological perturbation of glycolysis suppresses the bone anabolic effect of intermittent PTH in the mouse. Thus, stimulation of aerobic glycolysis via Igf signaling contributes to bone anabolism in response to PTH.
MeSH term(s)	Aerobiosis/drug effects ; Animals ; Animals, Newborn ; Bone and Bones/diagnostic imaging ; Bone and Bones/drug effects ; Bone and Bones/metabolism ; Carbon Dioxide/metabolism ; Carbon Isotopes ; Cell Differentiation/drug effects ; Cell Line ; Cell Lineage/drug effects ; Cyclic AMP/metabolism ; Glucose/metabolism ; Glycolysis/drug effects ; Immediate-Early Proteins/metabolism ; Insulin-Like Growth Factor I/metabolism ; Mechanistic Target of Rapamycin Complex 2 ; Mice, Inbred C57BL ; Multiprotein Complexes/metabolism ; Osteoblasts/cytology ; Osteoblasts/drug effects ; Parathyroid Hormone/pharmacology ; Protein-Serine-Threonine Kinases/metabolism ; Signal Transduction/drug effects ; TOR Serine-Threonine Kinases/metabolism ; Tibia/diagnostic imaging ; Tibia/drug effects ; X-Ray Microtomography
Chemical Substances	Carbon Isotopes ; Immediate-Early Proteins ; Multiprotein Complexes ; Parathyroid Hormone ; Carbon Dioxide (142M471B3J) ; Insulin-Like Growth Factor I (67763-96-6) ; Cyclic AMP (E0399OZS9N) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Mechanistic Target of Rapamycin Complex 2 (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; serum-glucocorticoid regulated kinase (EC 2.7.11.1) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2015-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	632783-7
ISSN	1523-4681 ; 0884-0431
ISSN (online)	1523-4681
ISSN	0884-0431
DOI	10.1002/jbmr.2556
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Article ; Online: Wnt Protein Signaling Reduces Nuclear Acetyl-CoA Levels to Suppress Gene Expression during Osteoblast Differentiation.

Karner, Courtney M / Esen, Emel / Chen, Jiakun / Hsu, Fong-Fu / Turk, John / Long, Fanxin

The Journal of biological chemistry

2016 Volume 291, Issue 25, Page(s) 13028–13039

Abstract: Developmental signals in metazoans play critical roles in inducing cell differentiation from multipotent progenitors. The existing paradigm posits that the signals operate directly through their downstream transcription factors to activate expression of ... ...

Abstract	Developmental signals in metazoans play critical roles in inducing cell differentiation from multipotent progenitors. The existing paradigm posits that the signals operate directly through their downstream transcription factors to activate expression of cell type-specific genes, which are the hallmark of cell identity. We have investigated the mechanism through which Wnt signaling induces osteoblast differentiation in an osteoblast-adipocyte bipotent progenitor cell line. Unexpectedly, Wnt3a acutely suppresses the expression of a large number of genes while inducing osteoblast differentiation. The suppressed genes include Pparg and Cebpa, which encode adipocyte-specifying transcription factors and suppression of which is sufficient to induce osteoblast differentiation. The large scale gene suppression induced by Wnt3a corresponds to a global decrease in histone acetylation, an epigenetic modification that is associated with gene activation. Mechanistically, Wnt3a does not alter histone acetyltransferase or deacetylase activities but, rather, decreases the level of acetyl-CoA in the nucleus. The Wnt-induced decrease in histone acetylation is independent of β-catenin signaling but, rather, correlates with suppression of glucose metabolism in the tricarboxylic acid cycle. Functionally, preventing histone deacetylation by increasing nucleocytoplasmic acetyl-CoA levels impairs Wnt3a-induced osteoblast differentiation. Thus, Wnt signaling induces osteoblast differentiation in part through histone deacetylation and epigenetic suppression of an alternative cell fate.
MeSH term(s)	Acetyl Coenzyme A/metabolism ; Acetylation ; Animals ; Cell Differentiation ; Cell Line ; Cell Nucleus/metabolism ; Citric Acid/metabolism ; Citric Acid Cycle ; Gene Expression ; Gene Silencing ; Glucose/metabolism ; Histones/metabolism ; Mice ; Osteoblasts/physiology ; Protein Processing, Post-Translational ; Wnt Signaling Pathway ; Wnt3A Protein/physiology
Chemical Substances	Histones ; Wnt3A Protein ; Wnt3a protein, mouse ; Citric Acid (2968PHW8QP) ; Acetyl Coenzyme A (72-89-9) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2016-04-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M115.708578
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Article ; Online: MAP4K4 negatively regulates CD8 T cell-mediated antitumor and antiviral immunity.

Esen, Emel / Sergin, Ismail / Jesudason, Rajiv / Himmels, Patricia / Webster, Joshua D / Zhang, Hua / Xu, Min / Piskol, Robert / McNamara, Erin / Gould, Stephen / Capietto, Aude-Hélène / Delamarre, Lélia / Walsh, Kevin / Ye, Weilan

Science immunology

2020 Volume 5, Issue 45

Abstract: During cytotoxic T cell activation, lymphocyte function-associated antigen-1 (LFA-1) engages its ligands on antigen-presenting cells (APCs) or target cells to enhance T cell priming or lytic activity. Inhibiting LFA-1 dampens T cell-dependent symptoms in ...

Abstract	During cytotoxic T cell activation, lymphocyte function-associated antigen-1 (LFA-1) engages its ligands on antigen-presenting cells (APCs) or target cells to enhance T cell priming or lytic activity. Inhibiting LFA-1 dampens T cell-dependent symptoms in inflammation, autoimmune diseases, and graft-versus-host disease. However, the therapeutic potential of augmenting LFA-1 function is less explored. Here, we show that genetic deletion or inhibition of mitogen-activated protein kinase kinase kinase kinase 4 (MAP4K4) enhances LFA-1 activation on CD8 T cells and improves their adherence to APCs or LFA-1 ligand. In addition, loss of
MeSH term(s)	Animals ; Antigen-Presenting Cells/immunology ; CD8-Positive T-Lymphocytes/immunology ; Disease Models, Animal ; Humans ; Intracellular Signaling Peptides and Proteins/deficiency ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/immunology ; Lymphocyte Function-Associated Antigen-1/immunology ; Mice ; Mice, Knockout ; Mice, Transgenic ; Neoplasms/immunology ; Protein-Serine-Threonine Kinases/deficiency ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/immunology ; Viruses/immunology
Chemical Substances	Intracellular Signaling Peptides and Proteins ; Lymphocyte Function-Associated Antigen-1 ; MAP4K4 protein, human (EC 2.7.1.11) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2020-03-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2470-9468
ISSN (online)	2470-9468
DOI	10.1126/sciimmunol.aay2245
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Article ; Online: Increased glutamine catabolism mediates bone anabolism in response to WNT signaling.

Karner, Courtney M / Esen, Emel / Okunade, Adewole L / Patterson, Bruce W / Long, Fanxin

The Journal of clinical investigation

2015 Volume 125, Issue 2, Page(s) 551–562

Abstract: WNT signaling stimulates bone formation by increasing both the number of osteoblasts and their protein-synthesis activity. It is not clear how WNT augments the capacity of osteoblast progenitors to meet the increased energetic and synthetic needs ... ...

Abstract	WNT signaling stimulates bone formation by increasing both the number of osteoblasts and their protein-synthesis activity. It is not clear how WNT augments the capacity of osteoblast progenitors to meet the increased energetic and synthetic needs associated with mature osteoblasts. Here, in cultured osteoblast progenitors, we determined that WNT stimulates glutamine catabolism through the tricarboxylic acid (TCA) cycle and consequently lowers intracellular glutamine levels. The WNT-induced reduction of glutamine concentration triggered a general control nonderepressible 2-mediated (GCN2-mediated) integrated stress response (ISR) that stimulated expression of genes responsible for amino acid supply, transfer RNA (tRNA) aminoacylation, and protein folding. WNT-induced glutamine catabolism and ISR were β-catenin independent, but required mammalian target of rapamycin complex 1 (mTORC1) activation. In a hyperactive WNT signaling mouse model of human osteosclerosis, inhibition of glutamine catabolism or Gcn2 deletion suppressed excessive bone formation. Together, our data indicate that glutamine is both an energy source and a protein-translation rheostat that is responsive to WNT and suggest that manipulation of the glutamine/GCN2 signaling axis may provide a valuable approach for normalizing deranged protein anabolism associated with human diseases.
MeSH term(s)	Animals ; Cell Line ; Citric Acid Cycle ; Gene Deletion ; Glutamine/genetics ; Glutamine/metabolism ; Humans ; Mechanistic Target of Rapamycin Complex 1 ; Mice ; Multiprotein Complexes/genetics ; Multiprotein Complexes/metabolism ; Osteoblasts/metabolism ; Osteoblasts/pathology ; Osteogenesis ; Osteosclerosis/genetics ; Osteosclerosis/metabolism ; Osteosclerosis/pathology ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/metabolism ; RNA, Transfer, Amino Acyl/genetics ; RNA, Transfer, Amino Acyl/metabolism ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/metabolism ; Wnt Signaling Pathway
Chemical Substances	Multiprotein Complexes ; RNA, Transfer, Amino Acyl ; Glutamine (0RH81L854J) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; EIF2AK4 protein, human (EC 2.7.11.1) ; Eif2ak4 protein, mouse (EC 2.7.11.1) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2015-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI78470
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Article ; Online: Inclusion bodies enriched for p62 and polyubiquitinated proteins in macrophages protect against atherosclerosis.

Sergin, Ismail / Bhattacharya, Somashubhra / Emanuel, Roy / Esen, Emel / Stokes, Carl J / Evans, Trent D / Arif, Batool / Curci, John A / Razani, Babak

Science signaling

2016 Volume 9, Issue 409, Page(s) ra2

Abstract: Autophagy is a catabolic cellular mechanism that degrades dysfunctional proteins and organelles. Atherosclerotic plaque formation is enhanced in mice with macrophages deficient for the critical autophagy protein ATG5. We showed that exposure of ... ...

Abstract	Autophagy is a catabolic cellular mechanism that degrades dysfunctional proteins and organelles. Atherosclerotic plaque formation is enhanced in mice with macrophages deficient for the critical autophagy protein ATG5. We showed that exposure of macrophages to lipids that promote atherosclerosis increased the abundance of the autophagy chaperone p62 and that p62 colocalized with polyubiquitinated proteins in cytoplasmic inclusions, which are characterized by insoluble protein aggregates. ATG5-null macrophages developed further p62 accumulation at the sites of large cytoplasmic ubiquitin-positive inclusion bodies. Aortas from atherosclerotic mice and plaques from human endarterectomy samples showed increased abundance of p62 and polyubiquitinated proteins that colocalized with plaque macrophages, suggesting that p62-enriched protein aggregates were characteristic of atherosclerosis. The formation of the cytoplasmic inclusions depended on p62 because lipid-loaded p62-null macrophages accumulated polyubiquitinated proteins in a diffuse cytoplasmic pattern. Lipid-loaded p62-null macrophages also exhibited increased secretion of interleukin-1β (IL-1β) and had an increased tendency to undergo apoptosis, which depended on the p62 ubiquitin-binding domain and at least partly involved p62-mediated clearance of NLRP3 inflammasomes. Consistent with our in vitro observations, p62-deficient mice formed greater numbers of more complex atherosclerotic plaques, and p62 deficiency further increased atherosclerotic plaque burden in mice with a macrophage-specific ablation of ATG5. Together, these data suggested that sequestration of cytotoxic ubiquitinated proteins by p62 protects against atherogenesis, a condition in which the clearance of protein aggregates is disrupted.
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Apolipoproteins E/genetics ; Apolipoproteins E/metabolism ; Apoptosis/genetics ; Atherosclerosis/genetics ; Atherosclerosis/metabolism ; Autophagy/genetics ; Autophagy-Related Protein 5 ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Cells, Cultured ; Cytoplasm/genetics ; Cytoplasm/metabolism ; Heat-Shock Proteins/genetics ; Heat-Shock Proteins/metabolism ; Humans ; Immunoblotting ; Inclusion Bodies/metabolism ; Inflammasomes/genetics ; Inflammasomes/metabolism ; Interleukin-1beta/metabolism ; Macrophages/metabolism ; Mice, Inbred C57BL ; Mice, Knockout ; Microscopy, Fluorescence ; Microtubule-Associated Proteins/genetics ; Microtubule-Associated Proteins/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein ; Polyubiquitin ; RNA Interference ; Sequestosome-1 Protein ; Ubiquitinated Proteins/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; Apolipoproteins E ; Atg5 protein, mouse ; Autophagy-Related Protein 5 ; Carrier Proteins ; Heat-Shock Proteins ; Inflammasomes ; Interleukin-1beta ; Microtubule-Associated Proteins ; NLR Family, Pyrin Domain-Containing 3 Protein ; Nlrp3 protein, mouse ; Sequestosome-1 Protein ; Sqstm1 protein, mouse ; Ubiquitinated Proteins ; Polyubiquitin (120904-94-1)
Language	English
Publishing date	2016-01-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2417226-1
ISSN	1937-9145 ; 1945-0877
ISSN (online)	1937-9145
ISSN	1945-0877
DOI	10.1126/scisignal.aad5614
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