Difference between revisions of "Torres-Quesada 2022 Abstract Bioblast"

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Torres-Quesada Omar, Strich S, Stefan E (2022) Kinase perturbations redirect mitochondrial function. Bioblast 2022: BEC Inaugural Conference. »MitoFit Preprint«

Link: Bioblast 2022: BEC Inaugural Conference

Torres-Quesada Omar, Strich Sophie, Stefan Eduardl (2022)

Event: Bioblast 2022

Protein kinases take the center stage in numerous signaling pathways by phosphorylating compartmentalized protein substrates for controlling cell proliferation, cell cycle and metabolism. Kinase dysfunctions have been linked to numerous human diseases such as cancer. This has led to the development of kinase inhibitors which aim to target oncogenic kinase activities. The specificity of the cancer blockers depends on the range of targeted kinases. Therefore, the question arises of how cell-type-specific off-target effects impair the specificities of cancer drugs. Blockade of kinase activities has been shown to converge on the energetic organelle, the mitochondria. In this review, we highlight examples of selected major kinases which impact mitochondrial signaling. Further, we discuss pharmacological strategies to target kinase activities which are linked to cancer progression and redirecting mitochondrial function. Finally, we propose that cell-based recordings of mitochondrial bioenergetic states might predict off-target or identify specific on-target effects of kinase inhibitors.

• Keywords: Kinases, signaling, mitochondria, kinase inhibitors, cancer, drug off-target effects

• O2k-Network Lab: AT Innsbruck Oroboros

Affiliations

Torres-Quesada O^1,2, Strich S¹, Stefan E^1,2

Tyrolean Cancer Research Institute, Innrain 66, 6020 Innsbruck, Austria - [email protected]
Institute of Biochemistry and Center for Molecular Biosciences, University of Innsbruck, Innrain 80/82, 6020 Innsbruck, Austria

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Labels: MiParea: Pharmacology;toxicology Pathology: Cancer

Organism: Human

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+[[File:Bioblast2022 banner.jpg|link=Bioblast_2022]]
 {{Abstract
 |title=[[File:Torres-QuesadaO.jpg|left|100px|Torres-Quesada Omar]] <u>Torres-Quesada Omar</u>, Strich S, Stefan E (2022) Kinase perturbations redirect mitochondrial function. Bioblast 2022: BEC Inaugural Conference. <br>[[Torres-Quesada 2022 MitoFit Kinase|»''MitoFit Preprint''«]]
 |info=[https://wiki.oroboros.at/index.php/Bioblast_2022#Submitted_abstracts Bioblast 2022: BEC Inaugural Conference]
 |authors=Torres-Quesada Omar, Strich Sophie, Stefan Eduardl
 |year=2022
 |event=[[Bioblast 2022]]
-|abstract=
+|abstract=Protein kinases take the center stage in numerous signaling pathways by phosphorylating compartmentalized protein substrates for controlling cell proliferation, cell cycle and metabolism. Kinase dysfunctions have been linked to numerous human diseases such as cancer. This has led to the development of kinase inhibitors which aim to target oncogenic kinase activities. The specificity of the cancer blockers depends on the range of targeted kinases. Therefore, the question arises of how cell-type-specific off-target effects impair the specificities of cancer drugs. Blockade of kinase activities has been shown to converge on the energetic organelle, the mitochondria. In this review, we highlight examples of selected major kinases which impact mitochondrial signaling. Further, we discuss pharmacological strategies to target kinase activities which are linked to cancer progression and redirecting mitochondrial function. Finally, we propose that cell-based recordings of mitochondrial bioenergetic states might predict off-target or identify specific on-target effects of kinase inhibitors.
-Protein kinases take the center stage in numerous signaling pathways by phosphorylating compartmentalized protein substrates for controlling cell proliferation, cell cycle and metabolism. Kinase dysfunctions have been linked to numerous human diseases such as cancer. This has led to the development of kinase inhibitors which aim to target oncogenic kinase activities. The specificity of the cancer blockers depends on the range of targeted kinases. Therefore, the question arises of how cell-type-specific off-target effects impair the specificities of cancer drugs. Blockade of kinase activities has been shown to converge on the energetic organelle, the mitochondria. In this review, we highlight examples of selected major kinases which impact mitochondrial signaling. Further, we discuss pharmacological strategies to target kinase activities which are linked to cancer progression and redirecting mitochondrial function. Finally, we propose that cell-based recordings of mitochondrial bioenergetic states might predict off-target or identify specific on-target effects of kinase inhibitors.<br><br>
 |keywords=Kinases, signaling, mitochondria, kinase inhibitors, cancer, drug off-target effects
 |mipnetlab=AT Innsbruck Oroboros
 }}
 == Affiliations ==
-:::: Torres-Quesada O(1,2), Strich S(1), Stefan E (1,2)
+:::: Torres-Quesada O<sup>1,2</sup>, Strich S<sup>1</sup>, Stefan E<sup>1,2</sup>
+::::# Tyrolean Cancer Research Institute, Innrain 66, 6020 Innsbruck, Austria - [email protected]
-::::#Tyrolean Cancer Research Institute, Innrain 66, 6020 Innsbruck, Austria - [email protected]
+::::# Institute of Biochemistry and Center for Molecular Biosciences, University of Innsbruck, Innrain 80/82, 6020 Innsbruck, Austria
-::::#Institute of Biochemistry and Center for Molecular Biosciences, University of Innsbruck, Innrain 80/82, 6020 Innsbruck, Austria
 == Help ==