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Development of an improved inhibitor of Lats kinases to promote regeneration of mammalian organs
The Hippo signaling pathway acts as a brake on regeneration in many tissues. This cascade of kinases culminates in the phosphorylation of the transcriptional cofactors Yap and Taz, whose concentration in the nucleus consequently remains low. Various types of cellular signals can reduce phosphorylati...
Autores principales: | , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
National Academy of Sciences
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9282237/ https://www.ncbi.nlm.nih.gov/pubmed/35867764 http://dx.doi.org/10.1073/pnas.2206113119 |
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author | Kastan, Nathaniel R. Oak, Sanyukta Liang, Rui Baxt, Leigh Myers, Robert W. Ginn, John Liverton, Nigel Huggins, David J. Pichardo, John Paul, Matthew Carroll, Thomas S. Nagiel, Aaron Gnedeva, Ksenia Hudspeth, A. J. |
author_facet | Kastan, Nathaniel R. Oak, Sanyukta Liang, Rui Baxt, Leigh Myers, Robert W. Ginn, John Liverton, Nigel Huggins, David J. Pichardo, John Paul, Matthew Carroll, Thomas S. Nagiel, Aaron Gnedeva, Ksenia Hudspeth, A. J. |
author_sort | Kastan, Nathaniel R. |
collection | PubMed |
description | The Hippo signaling pathway acts as a brake on regeneration in many tissues. This cascade of kinases culminates in the phosphorylation of the transcriptional cofactors Yap and Taz, whose concentration in the nucleus consequently remains low. Various types of cellular signals can reduce phosphorylation, however, resulting in the accumulation of Yap and Taz in the nucleus and subsequently in mitosis. We earlier identified a small molecule, TRULI, that blocks the final kinases in the pathway, Lats1 and Lats2, and thus elicits proliferation of several cell types that are ordinarily postmitotic and aids regeneration in mammals. In the present study, we present the results of chemical modification of the original compound and demonstrate that a derivative, TDI-011536, is an effective blocker of Lats kinases in vitro at nanomolar concentrations. The compound fosters extensive proliferation in retinal organoids derived from human induced pluripotent stem cells. Intraperitoneal administration of the substance to mice suppresses Yap phosphorylation for several hours and induces transcriptional activation of Yap target genes in the heart, liver, and skin. Moreover, the compound initiates the proliferation of cardiomyocytes in adult mice following cardiac cryolesions. After further chemical refinement, related compounds might prove useful in protective and regenerative therapies. |
format | Online Article Text |
id | pubmed-9282237 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | National Academy of Sciences |
record_format | MEDLINE/PubMed |
spelling | pubmed-92822372022-07-15 Development of an improved inhibitor of Lats kinases to promote regeneration of mammalian organs Kastan, Nathaniel R. Oak, Sanyukta Liang, Rui Baxt, Leigh Myers, Robert W. Ginn, John Liverton, Nigel Huggins, David J. Pichardo, John Paul, Matthew Carroll, Thomas S. Nagiel, Aaron Gnedeva, Ksenia Hudspeth, A. J. Proc Natl Acad Sci U S A Biological Sciences The Hippo signaling pathway acts as a brake on regeneration in many tissues. This cascade of kinases culminates in the phosphorylation of the transcriptional cofactors Yap and Taz, whose concentration in the nucleus consequently remains low. Various types of cellular signals can reduce phosphorylation, however, resulting in the accumulation of Yap and Taz in the nucleus and subsequently in mitosis. We earlier identified a small molecule, TRULI, that blocks the final kinases in the pathway, Lats1 and Lats2, and thus elicits proliferation of several cell types that are ordinarily postmitotic and aids regeneration in mammals. In the present study, we present the results of chemical modification of the original compound and demonstrate that a derivative, TDI-011536, is an effective blocker of Lats kinases in vitro at nanomolar concentrations. The compound fosters extensive proliferation in retinal organoids derived from human induced pluripotent stem cells. Intraperitoneal administration of the substance to mice suppresses Yap phosphorylation for several hours and induces transcriptional activation of Yap target genes in the heart, liver, and skin. Moreover, the compound initiates the proliferation of cardiomyocytes in adult mice following cardiac cryolesions. After further chemical refinement, related compounds might prove useful in protective and regenerative therapies. National Academy of Sciences 2022-07-08 2022-07-12 /pmc/articles/PMC9282237/ /pubmed/35867764 http://dx.doi.org/10.1073/pnas.2206113119 Text en Copyright © 2022 the Author(s). Published by PNAS. https://creativecommons.org/licenses/by/4.0/This open access article is distributed under Creative Commons Attribution License 4.0 (CC BY) (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Biological Sciences Kastan, Nathaniel R. Oak, Sanyukta Liang, Rui Baxt, Leigh Myers, Robert W. Ginn, John Liverton, Nigel Huggins, David J. Pichardo, John Paul, Matthew Carroll, Thomas S. Nagiel, Aaron Gnedeva, Ksenia Hudspeth, A. J. Development of an improved inhibitor of Lats kinases to promote regeneration of mammalian organs |
title | Development of an improved inhibitor of Lats kinases to promote regeneration of mammalian organs |
title_full | Development of an improved inhibitor of Lats kinases to promote regeneration of mammalian organs |
title_fullStr | Development of an improved inhibitor of Lats kinases to promote regeneration of mammalian organs |
title_full_unstemmed | Development of an improved inhibitor of Lats kinases to promote regeneration of mammalian organs |
title_short | Development of an improved inhibitor of Lats kinases to promote regeneration of mammalian organs |
title_sort | development of an improved inhibitor of lats kinases to promote regeneration of mammalian organs |
topic | Biological Sciences |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9282237/ https://www.ncbi.nlm.nih.gov/pubmed/35867764 http://dx.doi.org/10.1073/pnas.2206113119 |
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