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Article ; Online: Sirtuins transduce STACs signals through steroid hormone receptors.

Bayele, Henry K

2020 Volume 10, Issue 1, Page(s) 5338

Abstract: SIRT1 protects against several complex metabolic and ageing-related diseases (MARDs), and is therefore considered a polypill target to improve healthy ageing. Although dietary sirtuin-activating compounds (dSTACs) including resveratrol are promising drug ...

Abstract	SIRT1 protects against several complex metabolic and ageing-related diseases (MARDs), and is therefore considered a polypill target to improve healthy ageing. Although dietary sirtuin-activating compounds (dSTACs) including resveratrol are promising drug candidates, their clinical application has been frustrated by an imprecise understanding of how their signals are transduced into increased healthspan. Recent work indicates that SIRT1 and orthologous sirtuins coactivate the oestrogen receptor/ER and the worm steroid receptor DAF-12. Here they are further shown to ligand-independently transduce dSTACs signals through these receptors. While some dSTACs elicit ER subtype-selectivity in the presence of hormone, most synergize with 17β-oestradiol and dafachronic acid respectively to increase ER and DAF-12 coactivation by the sirtuins. These data suggest that dSTACs functionally mimic gonadal steroid hormones, enabling sirtuins to transduce the cognate signals through a conserved endocrine pathway. Interestingly, resveratrol non-monotonically modulates sirtuin signalling, suggesting that it may induce hormesis, i.e. "less is more". Together, the findings suggest that dSTACs may be informational molecules that use exploitative mimicry to modulate sirtuin signalling through steroid receptors. Hence dSTACs' intrinsic oestrogenicity may underlie their proven ability to impart the health benefits of oestradiol, and also provides a mechanistic insight into how they extend healthspan or protect against MARDs.
MeSH term(s)	Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/metabolism ; Cell Line, Tumor ; Diet ; Estradiol/pharmacology ; Estrogen Receptor alpha/metabolism ; Estrogen Receptor beta/metabolism ; Gonadal Steroid Hormones/metabolism ; Gonadal Steroid Hormones/pharmacology ; Humans ; Isoflavones/pharmacology ; Receptors, Cytoplasmic and Nuclear/genetics ; Receptors, Cytoplasmic and Nuclear/metabolism ; Receptors, Estrogen/metabolism ; Resveratrol/pharmacology ; Signal Transduction/drug effects ; Sirtuin 1/genetics ; Sirtuin 1/metabolism ; Sirtuins/metabolism
Chemical Substances	Caenorhabditis elegans Proteins ; DAF-12 protein, C elegans ; ESR1 protein, human ; Estrogen Receptor alpha ; Estrogen Receptor beta ; Gonadal Steroid Hormones ; Isoflavones ; Receptors, Cytoplasmic and Nuclear ; Receptors, Estrogen ; Estradiol (4TI98Z838E) ; daidzein (6287WC5J2L) ; SIRT1 protein, human (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-) ; Sirtuins (EC 3.5.1.-) ; Resveratrol (Q369O8926L)
Language	English
Publishing date	2020-03-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-62162-0
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Article ; Online: A conserved mechanism of sirtuin signalling through steroid hormone receptors.

Bayele, Henry K

Bioscience reports

2019 Volume 39, Issue 12

Abstract: SIRT1 and orthologous sirtuins regulate a universal mechanism of ageing and thus determine lifespan across taxa; however, the precise mechanism remains vexingly polemical. They also protect against many metabolic and ageing-related diseases by ... ...

Abstract	SIRT1 and orthologous sirtuins regulate a universal mechanism of ageing and thus determine lifespan across taxa; however, the precise mechanism remains vexingly polemical. They also protect against many metabolic and ageing-related diseases by dynamically integrating several processes including autophagy, proteostasis, calorie restriction, circadian rhythmicity and metabolism. These sirtuins are therefore important drug targets particularly because they also transduce allosteric signals from sirtuin-activating compounds such as resveratrol into increased healthspan in evolutionarily diverse organisms. While many of these functions are apparently regulated by deacetylation, that mechanism may not be all-encompassing. Since gonadal signals have been shown to regulate ageing/lifespan in worms and flies, the present study hypothesized that these sirtuins may act as intermediary factors for steroid hormone signal transduction. Accordingly, SIRT1 and its orthologues, Sir2 and Sir-2.1, are shown to be veritable nuclear receptor coregulators that classically coactivate the oestrogen receptor in the absence of ligand; coactivation was further increased by 17β-oestradiol. Remarkably in response to the worm steroid hormone dafachronic acid, SIRT1 reciprocally coactivates DAF-12, the steroid receptor that regulates nematode lifespan. These results suggest that steroid hormones may co-opt and modulate a phyletically conserved mechanism of sirtuin signalling through steroid receptors. Hence, it is interesting to speculate that certain sirtuin functions including prolongevity and metabolic regulation may be mechanistically linked to this endocrine signalling pathway; this may also have implications for understanding the determinative role of gonadal steroids such as oestradiol in human ageing. At its simplest, this report shows evidence for a hitherto unknown deacetylation-independent mechanism of sirtuin signalling.
MeSH term(s)	Animals ; HEK293 Cells ; Humans ; Receptors, Steroid/genetics ; Receptors, Steroid/metabolism ; Signal Transduction ; Sirtuins/genetics ; Sirtuins/metabolism
Chemical Substances	Receptors, Steroid ; Sirtuins (EC 3.5.1.-)
Language	English
Publishing date	2019-11-17
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	764946-0
ISSN	1573-4935 ; 0144-8463
ISSN (online)	1573-4935
ISSN	0144-8463
DOI	10.1042/BSR20193535
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Article ; Online: A disease-causing mutation K240E disrupts ferroportin trafficking by SUMO (ferroportin SUMOylation).

Bayele, Henry K / Srai, Surjit Kaila S

Biochemistry and biophysics reports

2021 Volume 25, Page(s) 100873

Abstract: Ferroportin (Fpn/IREG1/MTP1) is the only known transporter mediating iron efflux from epithelial cells and macrophages, and thus regulates how much iron is released into the circulation. Consequently, Fpn mutations are associated with haemochromatosis. ... ...

Abstract	Ferroportin (Fpn/IREG1/MTP1) is the only known transporter mediating iron efflux from epithelial cells and macrophages, and thus regulates how much iron is released into the circulation. Consequently, Fpn mutations are associated with haemochromatosis. Fpn itself is post-translationally regulated by hepcidin (Hepc) which induces its redistribution and degradation in a ubiquitin-dependent process. Together, the two proteins appear to be the nexus for iron homeostasis. Here we show that a rare gain-of-function mutation (K240E) that is associated with iron overload, impedes Fpn binding and subcellular trafficking by the small ubiquitin-like modifier (SUMO). Whereas wild-type Fpn is ensconced within vesicular bodies, the FpnK240E mutant appeared diffused within the cell when co-expressed with SUMO. Furthermore, compared with wild type Fpn, the sumoylation-defective mutant was constitutively-active, resulting in a lower intracellular labile iron pool than the former. These findings suggest that SUMO may regulate iron homeostasis by controlling Fpn trafficking.
Language	English
Publishing date	2021-01-08
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2831046-9
ISSN	2405-5808 ; 2405-5808
ISSN (online)	2405-5808
ISSN	2405-5808
DOI	10.1016/j.bbrep.2020.100873
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Article ; Online: Trypanosoma brucei: a putative RNA polymerase II promoter.

Bayele, Henry K

Experimental parasitology

2009 Volume 123, Issue 4, Page(s) 313–318

Abstract: RNA polymerase II (pol II) promoters are rare in the African trypanosome Trypanosoma brucei because gene regulation in the parasite is complex and polycistronic. Here, we describe a putative pol II promoter and its structure-function relationship. The ... ...

Abstract	RNA polymerase II (pol II) promoters are rare in the African trypanosome Trypanosoma brucei because gene regulation in the parasite is complex and polycistronic. Here, we describe a putative pol II promoter and its structure-function relationship. The promoter has features of an archetypal eukaryotic pol II promoter including putative canonical CCAAT and TATA boxes, and an initiator element. However, the spatial arrangement of these elements is only similar to yeast pol II promoters. Deletion mapping and transcription assays enabled delineation of a minimal promoter that could drive orientation-independent reporter gene expression suggesting that it may be a bidirectional promoter. In vitro transcription in a heterologous nuclear extract revealed that the promoter can be recognized by the basal eukaryotic transcription complex. This suggests that the transcription machinery in the parasite may be very similar to those of other eukaryotes.
MeSH term(s)	Animals ; Base Sequence ; COS Cells ; Cercopithecus aethiops ; Cloning, Molecular ; Microscopy, Fluorescence ; Molecular Sequence Data ; Promoter Regions, Genetic/genetics ; RNA Polymerase II/genetics ; Restriction Mapping ; Structure-Activity Relationship ; Transcription Initiation Site ; Transcription, Genetic ; Transfection ; Trypanosoma brucei brucei/enzymology ; Trypanosoma brucei brucei/genetics
Chemical Substances	RNA Polymerase II (EC 2.7.7.-)
Language	English
Publishing date	2009-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	391089-1
ISSN	1090-2449 ; 0014-4894
ISSN (online)	1090-2449
ISSN	0014-4894
DOI	10.1016/j.exppara.2009.08.007
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Article ; Online: Nrf2 transcriptional derepression from Keap1 by dietary polyphenols.

Bayele, Henry K / Debnam, Edward S / Srai, Kaila S

Biochemical and biophysical research communications

2015 Volume 469, Issue 3, Page(s) 521–528

Abstract: The liver expresses batteries of cytoprotective genes that confer cellular resistance to oxidative stress and xenobiotic toxins, and protection against cancer and other stress-related diseases. These genes are mainly regulated by Nrf2, making this ... ...

Abstract	The liver expresses batteries of cytoprotective genes that confer cellular resistance to oxidative stress and xenobiotic toxins, and protection against cancer and other stress-related diseases. These genes are mainly regulated by Nrf2, making this transcription factor a target for small molecule discovery to treat such diseases. In this report, we identified dietary polyphenolic antioxidants that not only activated these genes but also relieved Nrf2 repression by Keap1, a Cul3-dependent ubiquitin ligase adaptor protein that mediates its degradation. Analysis of postprandial liver RNA revealed a marked activation of both genes by all test polyphenols compared with controls. Nrf2 inhibition by RNA interference reduced polyphenol effects on its target gene expression. Our data suggest that polyphenols may induce cellular defense genes by derepressing Nrf2 inhibition by Keap1. We posit that this ability to derepress Nrf2 and reactivate its target genes may underlie the protection conferred by polyphenols against oxidative stress-related diseases.
MeSH term(s)	Administration, Oral ; Animals ; Dietary Supplements ; Gene Expression Regulation/physiology ; Hepatocytes/drug effects ; Hepatocytes/physiology ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Kelch-Like ECH-Associated Protein 1 ; Male ; NF-E2-Related Factor 2/genetics ; NF-E2-Related Factor 2/metabolism ; Oxidative Stress/drug effects ; Oxidative Stress/physiology ; Polyphenols/administration & dosage ; Rats ; Rats, Sprague-Dawley ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; Transcription, Genetic/drug effects ; Transcription, Genetic/physiology
Chemical Substances	Intracellular Signaling Peptides and Proteins ; KEAP1 protein, rat ; Kelch-Like ECH-Associated Protein 1 ; NF-E2-Related Factor 2 ; Polyphenols ; Repressor Proteins
Language	English
Publishing date	2015-12-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2015.11.103
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Article ; Online: Phytoestrogens modulate hepcidin expression by Nrf2: Implications for dietary control of iron absorption.

Bayele, Henry K / Balesaria, Sara / Srai, Surjit K S

Free radical biology & medicine

2015 Volume 89, Page(s) 1192–1202

Abstract: Hepcidin is a liver-derived antimicrobial peptide that regulates iron absorption and is also an integral part of the acute phase response. In a previous report, we found evidence that this peptide could also be induced by toxic heavy metals and ... ...

Abstract	Hepcidin is a liver-derived antimicrobial peptide that regulates iron absorption and is also an integral part of the acute phase response. In a previous report, we found evidence that this peptide could also be induced by toxic heavy metals and xenobiotics, thus broadening its teleological role as a defensin. However it remained unclear how its sensing of disparate biotic and abiotic stressors might be integrated at the transcriptional level. We hypothesized that its function in cytoprotection may be regulated by NFE2-related factor 2 (Nrf2), the master transcriptional controller of cellular stress defenses. In this report, we show that hepcidin regulation is inextricably linked to the acute stress response through Nrf2 signaling. Nrf2 regulates hepcidin expression from a prototypical antioxidant response element in its promoter, and by synergizing with other basic leucine-zipper transcription factors. We also show that polyphenolic small molecules or phytoestrogens commonly found in fruits and vegetables including the red wine constituent resveratrol can induce hepcidin expression in vitro and post-prandially, with concomitant reductions in circulating iron levels and transferrin saturation by one such polyphenol quercetin. Furthermore, these molecules derepress hepcidin promoter activity when its transcription by Nrf2 is repressed by Keap1. Taken together, the data show that hepcidin is a prototypical antioxidant response or cytoprotective gene within the Nrf2 transcriptional circuitry. The ability of phytoestrogens to modulate hepcidin expression in vivo suggests a novel mechanism by which diet may impact iron homeostasis.
MeSH term(s)	Animals ; Antioxidant Response Elements/genetics ; Blotting, Western ; Chromatin Immunoprecipitation ; Electrophoretic Mobility Shift Assay ; Flow Cytometry ; Gene Expression Regulation/drug effects ; Hepcidins/genetics ; Hepcidins/metabolism ; Humans ; Iron/metabolism ; Male ; NF-E2-Related Factor 2/genetics ; NF-E2-Related Factor 2/metabolism ; Phytoestrogens/pharmacology ; RNA, Messenger/genetics ; Rats ; Rats, Sprague-Dawley ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; Tumor Cells, Cultured
Chemical Substances	HAMP protein, human ; Hepcidins ; NF-E2-Related Factor 2 ; NFE2L2 protein, human ; Phytoestrogens ; RNA, Messenger ; Iron (E1UOL152H7)
Language	English
Publishing date	2015-11-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2015.11.001
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Article ; Online: Tumour necrosis factor alpha downregulates human hemojuvelin expression via a novel response element within its promoter

Salama Mohamed / Bayele Henry K / Srai Surjit SK

Journal of Biomedical Science, Vol 19, Iss 1, p

2012 Volume 83

Abstract: Abstract Background Iron homeostasis is chiefly regulated by hepcidin whose expression is tightly controlled by inflammation, iron stores, and hypoxia. Hemojuvelin (HJV) is a bone morphogenetic protein co-receptor that has been identified as a main ... ...

Abstract	Abstract Background Iron homeostasis is chiefly regulated by hepcidin whose expression is tightly controlled by inflammation, iron stores, and hypoxia. Hemojuvelin (HJV) is a bone morphogenetic protein co-receptor that has been identified as a main upstream regulator of hepcidin expression; HJV mutations are associated with a severe form of iron overload (Juvenile haemochromatosis). Currently however, there is no information on how HJV is regulated by inflammation. Methods To study the regulation of Hjv expression by inflammation and whether Hfe has a role in that regulation, control and LPS-injected wild type and Hfe KO mice were used. Moreover, human hepatoma cells (HuH7) were used to study the effect of IL-6 and TNF-α on HJV mRNA expression. Results Here we show that LPS repressed hepatic Hjv and BMPs , while it induced hepcidin 1 expression in wild-type and Hfe KO mice with no effect on hepatic pSMAD 1, 5, 8 protein levels. In addition, exogenous TNF-α (20 ng/mL) decreased HJV mRNA and protein expression to 40% of control with no effect on hepcidin mRNA expression in 24 hours. On the other hand, IL-6 induced hepcidin mRNA and protein expression with no effect on HJV mRNA expression levels. Moreover, using the HJV promoter-luciferase reporter fusion construct (HJVP1.2-luc) , we showed that the basal luciferase activity of HJVP1.2-luc was inhibited by 33% following TNF-α treatment of HuH7 transfected cells suggesting that the TNF-α down-regulation is exerted at the transcriptional level. Additionally, mutation of a canonical TNF- alpha responsive element (TNFRE) within HJVP1.2-luc abolished TNF-α response suggesting that this TNFRE is functional. Conclusions From these results, we conclude that TNF-α suppresses HJV transcription possibly via a novel TNFRE within the HJV promoter. In addition, the results suggest that the proposed link between inflammation and BMP-SMAD signalling is independent of HJV and BMP ligands.
Keywords	Inflammation ; Hemojuvelin ; TNF-α ; Medicine ; R
Subject code	570
Language	English
Publishing date	2012-09-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
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Article: Nrf2 transcriptional derepression from Keap1 by dietary polyphenols

Bayele, Henry K / Edward S. Debnam / Kaila S. Srai

Biochemical and biophysical research communications. 2016 Jan. 15, v. 469

2016

Abstract	The liver expresses batteries of cytoprotective genes that confer cellular resistance to oxidative stress and xenobiotic toxins, and protection against cancer and other stress-related diseases. These genes are mainly regulated by Nrf2, making this transcription factor a target for small molecule discovery to treat such diseases. In this report, we identified dietary polyphenolic antioxidants that not only activated these genes but also relieved Nrf2 repression by Keap1, a Cul3-dependent ubiquitin ligase adaptor protein that mediates its degradation. Analysis of postprandial liver RNA revealed a marked activation of both genes by all test polyphenols compared with controls. Nrf2 inhibition by RNA interference reduced polyphenol effects on its target gene expression. Our data suggest that polyphenols may induce cellular defense genes by derepressing Nrf2 inhibition by Keap1. We posit that this ability to derepress Nrf2 and reactivate its target genes may underlie the protection conferred by polyphenols against oxidative stress-related diseases.
Keywords	RNA ; RNA interference ; antioxidants ; gene expression ; genes ; liver ; neoplasms ; oxidative stress ; polyphenols ; toxins ; transcription (genetics) ; transcription factors ; ubiquitin-protein ligase ; Antioxidant ; Antioxidant response element ; Detoxification ; Dietary polyphenols ; Cytoprotection ; ARE ; hQR1 ; GST-Ya ; Nrf2 ; Keap1 ; t-BHQ ; DMSO
Language	English
Dates of publication	2016-0115
Size	p. 521-528.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2015.11.103
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Article ; Online: Tumour necrosis factor alpha downregulates human hemojuvelin expression via a novel response element within its promoter.

Salama, Mohamed Fouda / Bayele, Henry K / Srai, Surjit S K

Journal of biomedical science

2012 Volume 19, Page(s) 83

Abstract: Background: Iron homeostasis is chiefly regulated by hepcidin whose expression is tightly controlled by inflammation, iron stores, and hypoxia. Hemojuvelin (HJV) is a bone morphogenetic protein co-receptor that has been identified as a main upstream ... ...

Abstract	Background: Iron homeostasis is chiefly regulated by hepcidin whose expression is tightly controlled by inflammation, iron stores, and hypoxia. Hemojuvelin (HJV) is a bone morphogenetic protein co-receptor that has been identified as a main upstream regulator of hepcidin expression; HJV mutations are associated with a severe form of iron overload (Juvenile haemochromatosis). Currently however, there is no information on how HJV is regulated by inflammation. Methods: To study the regulation of Hjv expression by inflammation and whether Hfe has a role in that regulation, control and LPS-injected wild type and Hfe KO mice were used. Moreover, human hepatoma cells (HuH7) were used to study the effect of IL-6 and TNF-α on HJV mRNA expression. Results: Here we show that LPS repressed hepatic Hjv and BMPs, while it induced hepcidin 1 expression in wild-type and Hfe KO mice with no effect on hepatic pSMAD 1, 5, 8 protein levels. In addition, exogenous TNF-α (20 ng/mL) decreased HJV mRNA and protein expression to 40% of control with no effect on hepcidin mRNA expression in 24 hours. On the other hand, IL-6 induced hepcidin mRNA and protein expression with no effect on HJV mRNA expression levels. Moreover, using the HJV promoter-luciferase reporter fusion construct (HJVP1.2-luc), we showed that the basal luciferase activity of HJVP1.2-luc was inhibited by 33% following TNF-α treatment of HuH7 transfected cells suggesting that the TNF-α down-regulation is exerted at the transcriptional level. Additionally, mutation of a canonical TNF- alpha responsive element (TNFRE) within HJVP1.2-luc abolished TNF-α response suggesting that this TNFRE is functional. Conclusions: From these results, we conclude that TNF-α suppresses HJV transcription possibly via a novel TNFRE within the HJV promoter. In addition, the results suggest that the proposed link between inflammation and BMP-SMAD signalling is independent of HJV and BMP ligands.
MeSH term(s)	Animals ; Antimicrobial Cationic Peptides/genetics ; Antimicrobial Cationic Peptides/metabolism ; Cell Line, Tumor ; GPI-Linked Proteins ; Gene Expression Regulation/drug effects ; Hemochromatosis/chemically induced ; Hemochromatosis/genetics ; Hemochromatosis/metabolism ; Hemochromatosis Protein ; Hepcidins ; Humans ; Inflammation/chemically induced ; Inflammation/genetics ; Inflammation/metabolism ; Interleukin-6/metabolism ; Interleukin-6/pharmacology ; Iron/metabolism ; Ligands ; Lipopolysaccharides/toxicity ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Mice, Knockout ; Phosphorylation ; Promoter Regions, Genetic ; Response Elements/genetics ; Smad Proteins/metabolism ; Tumor Necrosis Factor-alpha/genetics ; Tumor Necrosis Factor-alpha/metabolism ; Tumor Necrosis Factor-alpha/pharmacology
Chemical Substances	Antimicrobial Cationic Peptides ; GPI-Linked Proteins ; HAMP protein, human ; HJV protein, mouse ; Hamp protein, mouse ; Hemochromatosis Protein ; Hepcidins ; Interleukin-6 ; Ligands ; Lipopolysaccharides ; Membrane Proteins ; Smad Proteins ; Tumor Necrosis Factor-alpha ; Iron (E1UOL152H7)
Language	English
Publishing date	2012-09-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1193378-1
ISSN	1423-0127 ; 1021-7770
ISSN (online)	1423-0127
ISSN	1021-7770
DOI	10.1186/1423-0127-19-83
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Article: Delineation of epitopes on the Py235 rhoptry antigen of Plasmodium yoelii YM.

Bayele, Henry K / Brown, K Neil

FEMS immunology and medical microbiology

2007 Volume 50, Issue 3, Page(s) 389–395

Abstract: The 235-kDa antigenic rhoptry protein Py235 of Plasmodium yoelii is encoded by a large, highly polymorphic gene family. Monoclonal antibodies to some of these antigens have been shown to attenuate the virulence of the lethal YM strain of the parasite, ... ...

Abstract	The 235-kDa antigenic rhoptry protein Py235 of Plasmodium yoelii is encoded by a large, highly polymorphic gene family. Monoclonal antibodies to some of these antigens have been shown to attenuate the virulence of the lethal YM strain of the parasite, converting a potentially fatal YM infection to a fulminating one typical of the nonlethal 17X strain, by inducing a switch in target cell preference from mature red blood cells to reticulocytes. The reason for this is not known but would suggest that antigenic determinants of Py235 may be useful in or as subunit vaccines. To identify such determinants, we constructed an epitope expression library of one Py235 variant and screened the library with the antibodies. Thus, we mapped 5- and 12-amino acid epitopes to the C-terminus of the antigen. Both epitopes were more reactive with protective than with nonprotective monoclonal antibodies. This may explain the differential protection conferred by these antibodies upon their passive transfer into mice.
MeSH term(s)	Amino Acid Sequence ; Animals ; Antibodies, Monoclonal/immunology ; Antigens, Protozoan/chemistry ; Antigens, Protozoan/genetics ; Antigens, Protozoan/immunology ; Epitope Mapping ; Epitopes/chemistry ; Epitopes/genetics ; Epitopes/immunology ; Gene Library ; Molecular Sequence Data ; Plasmodium yoelii/immunology ; Protozoan Proteins/chemistry ; Protozoan Proteins/genetics ; Protozoan Proteins/immunology ; Sequence Analysis, Protein
Chemical Substances	Antibodies, Monoclonal ; Antigens, Protozoan ; Epitopes ; Protozoan Proteins ; rhoptry associated protein, Plasmodium
Language	English
Publishing date	2007-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1143208-1
ISSN	1574-695X ; 0928-8244
ISSN (online)	1574-695X
ISSN	0928-8244
DOI	10.1111/j.1574-695X.2007.00269.x
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