Reversal of hyperactive Wnt signaling-dependent adipocyte defects by peptide boronic acids

Deregulated Wnt signaling and altered lipid metabolism have been linked to obesity, diabetes, and various cancers, highlighting the importance of identifying inhibitors that can modulate Wnt signaling and aberrant lipid metabolism. We have established a Drosophila model with hyperactivated Wnt signa...
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Autor*in:	Zhang, Tianyi [verfasserIn] Hsu, Fu-Ning Xie, Xiao-Jun Li, Xiao Liu, Mengmeng Gao, Xinsheng Pei, Xun Liao, Yang Du, Wei Ji, Jun-Yuan

Format:	Artikel
Sprache:	Englisch

Erschienen:	2017

Schlagwörter:	Peptides Wnt proteins Chemical properties Fat cells Physiological aspects β-catenin Mitigation Wnt protein Deregulation Pharmacology Lipids Mutants Defects Aberration α-catenin Adipocytes Bortezomib Larvae Transcription Studies Lipid metabolism Diabetes Diabetes mellitus Gene regulation Acids Drosophila Metabolism Hyperactivity Signal transduction

Übergeordnetes Werk:	Enthalten in: Proceedings of the National Academy of Sciences of the United States of America - Washington, DC : NAS, 1877, 114(2017), 36, Seite E7469
Übergeordnetes Werk:	volume:114 ; year:2017 ; number:36 ; pages:E7469

Links:	Volltext Link aufrufen

DOI / URN:	10.1073/pnas.1621048114

Katalog-ID:	OLC1998536351

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520			\|a Deregulated Wnt signaling and altered lipid metabolism have been linked to obesity, diabetes, and various cancers, highlighting the importance of identifying inhibitors that can modulate Wnt signaling and aberrant lipid metabolism. We have established a Drosophila model with hyperactivated Wnt signaling caused by partial loss of axin, a key component of the Wnt cascade. The Axin mutant larvae are transparent and have severe adipocyte defects caused by up-regulation of β-catenin transcriptional activities. We demonstrate pharmacologic mitigation of these phenotypes in Axin mutants by identifying bortezomib and additional peptide boronic acids. We show that the suppressive effect of peptide boronic acids on hyperactive Wnt signaling is dependent on a-catenin; the rescue effect is completely abolished with the depletion of a-catenin in adipocytes. These results indicate that rather than targeting the canonical Wnt signaling pathway directly, pharmacologic modulation of β-catenin activity through a-catenin is a potentially attractive approach to attenuating Wnt signaling in vivo.
650		4	\|a Peptides
650		4	\|a Wnt proteins
650		4	\|a Chemical properties
650		4	\|a Fat cells
650		4	\|a Physiological aspects
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650		4	\|a Mitigation
650		4	\|a Wnt protein
650		4	\|a Deregulation
650		4	\|a Pharmacology
650		4	\|a Lipids
650		4	\|a Mutants
650		4	\|a Defects
650		4	\|a Aberration
650		4	\|a α-catenin
650		4	\|a Adipocytes
650		4	\|a Bortezomib
650		4	\|a Larvae
650		4	\|a Transcription
650		4	\|a Studies
650		4	\|a Lipid metabolism
650		4	\|a Diabetes
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650		4	\|a Gene regulation
650		4	\|a Acids
650		4	\|a Drosophila
650		4	\|a Metabolism
650		4	\|a Hyperactivity
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700	1		\|a Hsu, Fu-Ning \|4 oth
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700	1		\|a Gao, Xinsheng \|4 oth
700	1		\|a Pei, Xun \|4 oth
700	1		\|a Liao, Yang \|4 oth
700	1		\|a Du, Wei \|4 oth
700	1		\|a Ji, Jun-Yuan \|4 oth
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allfields	10.1073/pnas.1621048114 doi PQ20171228 (DE-627)OLC1998536351 (DE-599)GBVOLC1998536351 (PRQ)g1168-71f1d30f2dfe7e9987af1bab49e312e3dab5af006091f3f83e107ab2996d747d0 (KEY)0583363920170000114003607469reversalofhyperactivewntsignalingdependentadipocyt DE-627 ger DE-627 rakwb eng 500 DE-101 570 AVZ LING fid BIODIV fid Zhang, Tianyi verfasserin aut Reversal of hyperactive Wnt signaling-dependent adipocyte defects by peptide boronic acids 2017 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Deregulated Wnt signaling and altered lipid metabolism have been linked to obesity, diabetes, and various cancers, highlighting the importance of identifying inhibitors that can modulate Wnt signaling and aberrant lipid metabolism. We have established a Drosophila model with hyperactivated Wnt signaling caused by partial loss of axin, a key component of the Wnt cascade. The Axin mutant larvae are transparent and have severe adipocyte defects caused by up-regulation of β-catenin transcriptional activities. We demonstrate pharmacologic mitigation of these phenotypes in Axin mutants by identifying bortezomib and additional peptide boronic acids. We show that the suppressive effect of peptide boronic acids on hyperactive Wnt signaling is dependent on a-catenin; the rescue effect is completely abolished with the depletion of a-catenin in adipocytes. These results indicate that rather than targeting the canonical Wnt signaling pathway directly, pharmacologic modulation of β-catenin activity through a-catenin is a potentially attractive approach to attenuating Wnt signaling in vivo. Peptides Wnt proteins Chemical properties Fat cells Physiological aspects β-catenin Mitigation Wnt protein Deregulation Pharmacology Lipids Mutants Defects Aberration α-catenin Adipocytes Bortezomib Larvae Transcription Studies Lipid metabolism Diabetes Diabetes mellitus Gene regulation Acids Drosophila Metabolism Hyperactivity Signal transduction Hsu, Fu-Ning oth Xie, Xiao-Jun oth Li, Xiao oth Liu, Mengmeng oth Gao, Xinsheng oth Pei, Xun oth Liao, Yang oth Du, Wei oth Ji, Jun-Yuan oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 114(2017), 36, Seite E7469 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:114 year:2017 number:36 pages:E7469 http://dx.doi.org/10.1073/pnas.1621048114 Volltext https://search.proquest.com/docview/1946431246 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 114 2017 36 E7469
spelling	10.1073/pnas.1621048114 doi PQ20171228 (DE-627)OLC1998536351 (DE-599)GBVOLC1998536351 (PRQ)g1168-71f1d30f2dfe7e9987af1bab49e312e3dab5af006091f3f83e107ab2996d747d0 (KEY)0583363920170000114003607469reversalofhyperactivewntsignalingdependentadipocyt DE-627 ger DE-627 rakwb eng 500 DE-101 570 AVZ LING fid BIODIV fid Zhang, Tianyi verfasserin aut Reversal of hyperactive Wnt signaling-dependent adipocyte defects by peptide boronic acids 2017 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Deregulated Wnt signaling and altered lipid metabolism have been linked to obesity, diabetes, and various cancers, highlighting the importance of identifying inhibitors that can modulate Wnt signaling and aberrant lipid metabolism. We have established a Drosophila model with hyperactivated Wnt signaling caused by partial loss of axin, a key component of the Wnt cascade. The Axin mutant larvae are transparent and have severe adipocyte defects caused by up-regulation of β-catenin transcriptional activities. We demonstrate pharmacologic mitigation of these phenotypes in Axin mutants by identifying bortezomib and additional peptide boronic acids. We show that the suppressive effect of peptide boronic acids on hyperactive Wnt signaling is dependent on a-catenin; the rescue effect is completely abolished with the depletion of a-catenin in adipocytes. These results indicate that rather than targeting the canonical Wnt signaling pathway directly, pharmacologic modulation of β-catenin activity through a-catenin is a potentially attractive approach to attenuating Wnt signaling in vivo. Peptides Wnt proteins Chemical properties Fat cells Physiological aspects β-catenin Mitigation Wnt protein Deregulation Pharmacology Lipids Mutants Defects Aberration α-catenin Adipocytes Bortezomib Larvae Transcription Studies Lipid metabolism Diabetes Diabetes mellitus Gene regulation Acids Drosophila Metabolism Hyperactivity Signal transduction Hsu, Fu-Ning oth Xie, Xiao-Jun oth Li, Xiao oth Liu, Mengmeng oth Gao, Xinsheng oth Pei, Xun oth Liao, Yang oth Du, Wei oth Ji, Jun-Yuan oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 114(2017), 36, Seite E7469 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:114 year:2017 number:36 pages:E7469 http://dx.doi.org/10.1073/pnas.1621048114 Volltext https://search.proquest.com/docview/1946431246 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 114 2017 36 E7469
allfields_unstemmed	10.1073/pnas.1621048114 doi PQ20171228 (DE-627)OLC1998536351 (DE-599)GBVOLC1998536351 (PRQ)g1168-71f1d30f2dfe7e9987af1bab49e312e3dab5af006091f3f83e107ab2996d747d0 (KEY)0583363920170000114003607469reversalofhyperactivewntsignalingdependentadipocyt DE-627 ger DE-627 rakwb eng 500 DE-101 570 AVZ LING fid BIODIV fid Zhang, Tianyi verfasserin aut Reversal of hyperactive Wnt signaling-dependent adipocyte defects by peptide boronic acids 2017 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Deregulated Wnt signaling and altered lipid metabolism have been linked to obesity, diabetes, and various cancers, highlighting the importance of identifying inhibitors that can modulate Wnt signaling and aberrant lipid metabolism. We have established a Drosophila model with hyperactivated Wnt signaling caused by partial loss of axin, a key component of the Wnt cascade. The Axin mutant larvae are transparent and have severe adipocyte defects caused by up-regulation of β-catenin transcriptional activities. We demonstrate pharmacologic mitigation of these phenotypes in Axin mutants by identifying bortezomib and additional peptide boronic acids. We show that the suppressive effect of peptide boronic acids on hyperactive Wnt signaling is dependent on a-catenin; the rescue effect is completely abolished with the depletion of a-catenin in adipocytes. These results indicate that rather than targeting the canonical Wnt signaling pathway directly, pharmacologic modulation of β-catenin activity through a-catenin is a potentially attractive approach to attenuating Wnt signaling in vivo. Peptides Wnt proteins Chemical properties Fat cells Physiological aspects β-catenin Mitigation Wnt protein Deregulation Pharmacology Lipids Mutants Defects Aberration α-catenin Adipocytes Bortezomib Larvae Transcription Studies Lipid metabolism Diabetes Diabetes mellitus Gene regulation Acids Drosophila Metabolism Hyperactivity Signal transduction Hsu, Fu-Ning oth Xie, Xiao-Jun oth Li, Xiao oth Liu, Mengmeng oth Gao, Xinsheng oth Pei, Xun oth Liao, Yang oth Du, Wei oth Ji, Jun-Yuan oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 114(2017), 36, Seite E7469 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:114 year:2017 number:36 pages:E7469 http://dx.doi.org/10.1073/pnas.1621048114 Volltext https://search.proquest.com/docview/1946431246 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 114 2017 36 E7469
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language	English
source	Enthalten in Proceedings of the National Academy of Sciences of the United States of America 114(2017), 36, Seite E7469 volume:114 year:2017 number:36 pages:E7469
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topic_facet	Peptides Wnt proteins Chemical properties Fat cells Physiological aspects β-catenin Mitigation Wnt protein Deregulation Pharmacology Lipids Mutants Defects Aberration α-catenin Adipocytes Bortezomib Larvae Transcription Studies Lipid metabolism Diabetes Diabetes mellitus Gene regulation Acids Drosophila Metabolism Hyperactivity Signal transduction
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author	Zhang, Tianyi
spellingShingle	Zhang, Tianyi ddc 500 ddc 570 fid LING fid BIODIV misc Peptides misc Wnt proteins misc Chemical properties misc Fat cells misc Physiological aspects misc β-catenin misc Mitigation misc Wnt protein misc Deregulation misc Pharmacology misc Lipids misc Mutants misc Defects misc Aberration misc α-catenin misc Adipocytes misc Bortezomib misc Larvae misc Transcription misc Studies misc Lipid metabolism misc Diabetes misc Diabetes mellitus misc Gene regulation misc Acids misc Drosophila misc Metabolism misc Hyperactivity misc Signal transduction Reversal of hyperactive Wnt signaling-dependent adipocyte defects by peptide boronic acids
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topic_title	500 DE-101 570 AVZ LING fid BIODIV fid Reversal of hyperactive Wnt signaling-dependent adipocyte defects by peptide boronic acids Peptides Wnt proteins Chemical properties Fat cells Physiological aspects β-catenin Mitigation Wnt protein Deregulation Pharmacology Lipids Mutants Defects Aberration α-catenin Adipocytes Bortezomib Larvae Transcription Studies Lipid metabolism Diabetes Diabetes mellitus Gene regulation Acids Drosophila Metabolism Hyperactivity Signal transduction
topic	ddc 500 ddc 570 fid LING fid BIODIV misc Peptides misc Wnt proteins misc Chemical properties misc Fat cells misc Physiological aspects misc β-catenin misc Mitigation misc Wnt protein misc Deregulation misc Pharmacology misc Lipids misc Mutants misc Defects misc Aberration misc α-catenin misc Adipocytes misc Bortezomib misc Larvae misc Transcription misc Studies misc Lipid metabolism misc Diabetes misc Diabetes mellitus misc Gene regulation misc Acids misc Drosophila misc Metabolism misc Hyperactivity misc Signal transduction
topic_unstemmed	ddc 500 ddc 570 fid LING fid BIODIV misc Peptides misc Wnt proteins misc Chemical properties misc Fat cells misc Physiological aspects misc β-catenin misc Mitigation misc Wnt protein misc Deregulation misc Pharmacology misc Lipids misc Mutants misc Defects misc Aberration misc α-catenin misc Adipocytes misc Bortezomib misc Larvae misc Transcription misc Studies misc Lipid metabolism misc Diabetes misc Diabetes mellitus misc Gene regulation misc Acids misc Drosophila misc Metabolism misc Hyperactivity misc Signal transduction
topic_browse	ddc 500 ddc 570 fid LING fid BIODIV misc Peptides misc Wnt proteins misc Chemical properties misc Fat cells misc Physiological aspects misc β-catenin misc Mitigation misc Wnt protein misc Deregulation misc Pharmacology misc Lipids misc Mutants misc Defects misc Aberration misc α-catenin misc Adipocytes misc Bortezomib misc Larvae misc Transcription misc Studies misc Lipid metabolism misc Diabetes misc Diabetes mellitus misc Gene regulation misc Acids misc Drosophila misc Metabolism misc Hyperactivity misc Signal transduction
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title	Reversal of hyperactive Wnt signaling-dependent adipocyte defects by peptide boronic acids
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title_full	Reversal of hyperactive Wnt signaling-dependent adipocyte defects by peptide boronic acids
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title_sort	reversal of hyperactive wnt signaling-dependent adipocyte defects by peptide boronic acids
title_auth	Reversal of hyperactive Wnt signaling-dependent adipocyte defects by peptide boronic acids
abstract	Deregulated Wnt signaling and altered lipid metabolism have been linked to obesity, diabetes, and various cancers, highlighting the importance of identifying inhibitors that can modulate Wnt signaling and aberrant lipid metabolism. We have established a Drosophila model with hyperactivated Wnt signaling caused by partial loss of axin, a key component of the Wnt cascade. The Axin mutant larvae are transparent and have severe adipocyte defects caused by up-regulation of β-catenin transcriptional activities. We demonstrate pharmacologic mitigation of these phenotypes in Axin mutants by identifying bortezomib and additional peptide boronic acids. We show that the suppressive effect of peptide boronic acids on hyperactive Wnt signaling is dependent on a-catenin; the rescue effect is completely abolished with the depletion of a-catenin in adipocytes. These results indicate that rather than targeting the canonical Wnt signaling pathway directly, pharmacologic modulation of β-catenin activity through a-catenin is a potentially attractive approach to attenuating Wnt signaling in vivo.
abstractGer	Deregulated Wnt signaling and altered lipid metabolism have been linked to obesity, diabetes, and various cancers, highlighting the importance of identifying inhibitors that can modulate Wnt signaling and aberrant lipid metabolism. We have established a Drosophila model with hyperactivated Wnt signaling caused by partial loss of axin, a key component of the Wnt cascade. The Axin mutant larvae are transparent and have severe adipocyte defects caused by up-regulation of β-catenin transcriptional activities. We demonstrate pharmacologic mitigation of these phenotypes in Axin mutants by identifying bortezomib and additional peptide boronic acids. We show that the suppressive effect of peptide boronic acids on hyperactive Wnt signaling is dependent on a-catenin; the rescue effect is completely abolished with the depletion of a-catenin in adipocytes. These results indicate that rather than targeting the canonical Wnt signaling pathway directly, pharmacologic modulation of β-catenin activity through a-catenin is a potentially attractive approach to attenuating Wnt signaling in vivo.
abstract_unstemmed	Deregulated Wnt signaling and altered lipid metabolism have been linked to obesity, diabetes, and various cancers, highlighting the importance of identifying inhibitors that can modulate Wnt signaling and aberrant lipid metabolism. We have established a Drosophila model with hyperactivated Wnt signaling caused by partial loss of axin, a key component of the Wnt cascade. The Axin mutant larvae are transparent and have severe adipocyte defects caused by up-regulation of β-catenin transcriptional activities. We demonstrate pharmacologic mitigation of these phenotypes in Axin mutants by identifying bortezomib and additional peptide boronic acids. We show that the suppressive effect of peptide boronic acids on hyperactive Wnt signaling is dependent on a-catenin; the rescue effect is completely abolished with the depletion of a-catenin in adipocytes. These results indicate that rather than targeting the canonical Wnt signaling pathway directly, pharmacologic modulation of β-catenin activity through a-catenin is a potentially attractive approach to attenuating Wnt signaling in vivo.
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container_issue	36
title_short	Reversal of hyperactive Wnt signaling-dependent adipocyte defects by peptide boronic acids
url	http://dx.doi.org/10.1073/pnas.1621048114 https://search.proquest.com/docview/1946431246
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author2	Hsu, Fu-Ning Xie, Xiao-Jun Li, Xiao Liu, Mengmeng Gao, Xinsheng Pei, Xun Liao, Yang Du, Wei Ji, Jun-Yuan
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up_date	2024-07-04T05:11:47.079Z
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Reversal of hyperactive Wnt signaling-dependent adipocyte defects by peptide boronic acids

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Zugang & Verfügbarkeit

Vorhandene Bände

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