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  1. Article ; Online: Mitochondrial hitch-hiking of

    Harbauer, Angelika B / Schwarz, Thomas L

    Autophagy

    2022  Volume 18, Issue 12, Page(s) 3048–3049

    Abstract: Mitostasis, the process of mitochondrial maintenance by biogenesis and degradative mechanisms, is challenged by the extreme length of axons. PINK1 (PTEN induced putative kinase 1) is a mitochondrial protein that targets damaged mitochondria for mitophagy. ...

    Abstract Mitostasis, the process of mitochondrial maintenance by biogenesis and degradative mechanisms, is challenged by the extreme length of axons. PINK1 (PTEN induced putative kinase 1) is a mitochondrial protein that targets damaged mitochondria for mitophagy. In reconciling the short half-life of PINK1 with the need for mitophagy of damaged axonal mitochondria, we found that axonal mitophagy depends on local translation of the
    MeSH term(s) Mitophagy/genetics ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Protein Kinases/genetics ; Protein Kinases/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Autophagy/physiology ; Mitochondria/metabolism ; Axons/metabolism ; Mitochondrial Proteins/metabolism
    Chemical Substances RNA, Messenger ; Protein Kinases (EC 2.7.-) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Mitochondrial Proteins
    Language English
    Publishing date 2022-05-03
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2022.2070332
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6741: Show issues Location:
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  2. Article ; Online: Live-Cell Imaging of RNA Transport in Axons of Cultured Primary Neurons.

    Hees, J Tabitha / Harbauer, Angelika B

    Methods in molecular biology (Clifton, N.J.)

    2022  Volume 2431, Page(s) 225–237

    Abstract: The use of fluorescent proteins has revolutionized the study of protein localization and transport. However, the visualization of other molecules and specifically RNA during live-cell imaging remains challenging. In this chapter, we provide guidance to ... ...

    Abstract The use of fluorescent proteins has revolutionized the study of protein localization and transport. However, the visualization of other molecules and specifically RNA during live-cell imaging remains challenging. In this chapter, we provide guidance to the available methods, their advantages and drawbacks as well as provide a detailed protocol for the detection of RNA transport using the MS2/PP7-split-Venus system for background-free RNA imaging.
    MeSH term(s) Axons/metabolism ; Neurons/metabolism ; RNA/metabolism ; RNA Transport ; RNA, Messenger/genetics
    Chemical Substances RNA, Messenger ; RNA (63231-63-0)
    Language English
    Publishing date 2022-04-12
    Publishing country United States
    Document type Journal Article
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-1990-2_11
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  3. Article ; Online: Insulin signalling regulates Pink1 mRNA localization via modulation of AMPK activity to support PINK1 function in neurons.

    Hees, J Tabitha / Wanderoy, Simone / Lindner, Jana / Helms, Marlena / Murali Mahadevan, Hariharan / Harbauer, Angelika B

    Nature metabolism

    2024  Volume 6, Issue 3, Page(s) 514–530

    Abstract: Mitochondrial quality control failure is frequently observed in neurodegenerative diseases. The detection of damaged mitochondria by stabilization of PTEN-induced kinase 1 (PINK1) requires transport of Pink1 messenger RNA (mRNA) by tethering it to the ... ...

    Abstract Mitochondrial quality control failure is frequently observed in neurodegenerative diseases. The detection of damaged mitochondria by stabilization of PTEN-induced kinase 1 (PINK1) requires transport of Pink1 messenger RNA (mRNA) by tethering it to the mitochondrial surface. Here, we report that inhibition of AMP-activated protein kinase (AMPK) by activation of the insulin signalling cascade prevents Pink1 mRNA binding to mitochondria. Mechanistically, AMPK phosphorylates the RNA anchor complex subunit SYNJ2BP within its PDZ domain, a phosphorylation site that is necessary for its interaction with the RNA-binding protein SYNJ2. Notably, loss of mitochondrial Pink1 mRNA association upon insulin addition is required for PINK1 protein activation and its function as a ubiquitin kinase in the mitophagy pathway, thus placing PINK1 function under metabolic control. Induction of insulin resistance in vitro by the key genetic Alzheimer risk factor apolipoprotein E4 retains Pink1 mRNA at the mitochondria and prevents proper PINK1 activity, especially in neurites. Our results thus identify a metabolic switch controlling Pink1 mRNA localization and PINK1 activity via insulin and AMPK signalling in neurons and propose a mechanistic connection between insulin resistance and mitochondrial dysfunction.
    MeSH term(s) Humans ; AMP-Activated Protein Kinases/metabolism ; Insulin/metabolism ; Insulin Resistance ; Neurons/metabolism ; Phosphorylation ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Ubiquitin-Protein Ligases/genetics ; Animals ; Mice ; Protein Kinases/genetics ; Protein Kinases/metabolism
    Chemical Substances AMP-Activated Protein Kinases (EC 2.7.11.31) ; Insulin ; RNA, Messenger ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; PTEN-induced putative kinase (EC 2.7.11.1) ; Protein Kinases (EC 2.7.-)
    Language English
    Publishing date 2024-03-19
    Publishing country Germany
    Document type Journal Article
    ISSN 2522-5812
    ISSN (online) 2522-5812
    DOI 10.1038/s42255-024-01007-w
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Mitochondrial health maintenance in axons.

    Harbauer, Angelika B

    Biochemical Society transactions

    2017  Volume 45, Issue 5, Page(s) 1045–1052

    Abstract: Neurons are post-mitotic cells that must function throughout the life of an organism. The high energetic requirements and ... ...

    Abstract Neurons are post-mitotic cells that must function throughout the life of an organism. The high energetic requirements and Ca
    Language English
    Publishing date 2017-10-15
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 184237-7
    ISSN 1470-8752 ; 0300-5127
    ISSN (online) 1470-8752
    ISSN 0300-5127
    DOI 10.1042/BST20170023
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  5. Article ; Online: Microfluidics-Assisted Selective Depolarization of Axonal Mitochondria.

    Wanderoy, Simone / Rühmkorf, Alina / Harbauer, Angelika B

    Journal of visualized experiments : JoVE

    2022  , Issue 186

    Abstract: Mitochondria are the primary suppliers of ATP (adenosine triphosphate) in neurons. Mitochondrial dysfunction is a common phenotype in many neurodegenerative diseases. Given some axons' elaborate architecture and extreme length, it is not surprising that ... ...

    Abstract Mitochondria are the primary suppliers of ATP (adenosine triphosphate) in neurons. Mitochondrial dysfunction is a common phenotype in many neurodegenerative diseases. Given some axons' elaborate architecture and extreme length, it is not surprising that mitochondria in axons can experience different environments compared to their cell body counterparts. Interestingly, dysfunction of axonal mitochondria often precedes effects on the cell body. To model axonal mitochondrial dysfunction in vitro, microfluidic devices allow treatment of axonal mitochondria without affecting the somal mitochondria. The fluidic pressure gradient in these chambers prevents diffusion of molecules against the gradient, thus allowing for analysis of mitochondrial properties in response to local pharmacological challenges within axons. The current protocol describes the seeding of dissociated hippocampal neurons in microfluidic devices, staining with a membrane-potential sensitive dye, treatment with a mitochondrial toxin, and the subsequent microscopic analysis. This versatile method to study axonal biology can be applied to many pharmacological perturbations and imaging readouts, and is suitable for several neuronal subtypes.
    MeSH term(s) Adenosine Triphosphate/metabolism ; Axonal Transport/physiology ; Axons/physiology ; Microfluidics ; Mitochondria/metabolism ; Neurons/physiology
    Chemical Substances Adenosine Triphosphate (8L70Q75FXE)
    Language English
    Publishing date 2022-08-04
    Publishing country United States
    Document type Journal Article ; Video-Audio Media ; Research Support, Non-U.S. Gov't
    ZDB-ID 2259946-0
    ISSN 1940-087X ; 1940-087X
    ISSN (online) 1940-087X
    ISSN 1940-087X
    DOI 10.3791/64196
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Analysis of Mitochondria by Single-Organelle Resolution.

    Harbauer, Angelika B / Schneider, Annika / Wohlleber, Dirk

    Annual review of analytical chemistry (Palo Alto, Calif.)

    2022  Volume 15, Issue 1, Page(s) 1–16

    Abstract: Cellular organelles are highly specialized compartments with distinct functions. With the increasing resolution of detection methods, it is becoming clearer that same organelles may have different functions or properties not only within different cell ... ...

    Abstract Cellular organelles are highly specialized compartments with distinct functions. With the increasing resolution of detection methods, it is becoming clearer that same organelles may have different functions or properties not only within different cell populations of a tissue but also within the same cell. Dysfunction or altered function affects the organelle itself and may also lead to malignancies or undesirable cell death. To understand cellular function or dysfunction, it is therefore necessary to analyze cellular components at the single-organelle level. Here, we review the recent advances in analyzing cellular function at single-organelle resolution using high-parameter flow cytometry or multicolor confocal microscopy. We focus on the analysis of mitochondria, as they are organelles at the crossroads of various cellular signaling pathways and functions. However, most of the applied methods/technologies are transferable to any other organelle, such as the endoplasmic reticulum, lysosomes, or peroxisomes.
    MeSH term(s) Endoplasmic Reticulum/metabolism ; Endoplasmic Reticulum/pathology ; Lysosomes/metabolism ; Lysosomes/pathology ; Microscopy, Confocal ; Mitochondria/metabolism ; Mitochondria/pathology ; Peroxisomes/metabolism ; Peroxisomes/pathology
    Language English
    Publishing date 2022-03-18
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2398707-8
    ISSN 1936-1335 ; 1936-1327
    ISSN (online) 1936-1335
    ISSN 1936-1327
    DOI 10.1146/annurev-anchem-061020-111722
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Mitochondrial Phenotypes in Parkinson's Diseases-A Focus on Human iPSC-Derived Dopaminergic Neurons.

    Heger, Leonie M / Wise, Rachel M / Hees, J Tabitha / Harbauer, Angelika B / Burbulla, Lena F

    Cells

    2021  Volume 10, Issue 12

    Abstract: Established disease models have helped unravel the mechanistic underpinnings of pathological phenotypes in Parkinson's disease (PD), the second most common neurodegenerative disorder. However, these discoveries have been limited to relatively simple ... ...

    Abstract Established disease models have helped unravel the mechanistic underpinnings of pathological phenotypes in Parkinson's disease (PD), the second most common neurodegenerative disorder. However, these discoveries have been limited to relatively simple cellular systems and animal models, which typically manifest with incomplete or imperfect recapitulation of disease phenotypes. The advent of induced pluripotent stem cells (iPSCs) has provided a powerful scientific tool for investigating the underlying molecular mechanisms of both familial and sporadic PD within disease-relevant cell types and patient-specific genetic backgrounds. Overwhelming evidence supports mitochondrial dysfunction as a central feature in PD pathophysiology, and iPSC-based neuronal models have expanded our understanding of mitochondrial dynamics in the development and progression of this devastating disorder. The present review provides a comprehensive assessment of mitochondrial phenotypes reported in iPSC-derived neurons generated from PD patients' somatic cells, with an emphasis on the role of mitochondrial respiration, morphology, and trafficking, as well as mitophagy and calcium handling in health and disease. Furthermore, we summarize the distinguishing characteristics of vulnerable midbrain dopaminergic neurons in PD and report the unique advantages and challenges of iPSC disease modeling at present, and for future mechanistic and therapeutic applications.
    MeSH term(s) Dopaminergic Neurons/metabolism ; Dopaminergic Neurons/pathology ; Humans ; Induced Pluripotent Stem Cells/metabolism ; Induced Pluripotent Stem Cells/pathology ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitophagy/genetics ; Parkinson Disease/genetics ; Parkinson Disease/metabolism ; Parkinson Disease/pathology ; Phenotype
    Language English
    Publishing date 2021-12-07
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells10123436
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  8. Article ; Online: Fluorogenic Chemical Probes for Wash-free Imaging of Cell Membrane Damage in Ferroptosis, Necrosis, and Axon Injury.

    Mauker, Philipp / Beckmann, Daniela / Kitowski, Annabel / Heise, Constanze / Wientjens, Chantal / Davidson, Andrew J / Wanderoy, Simone / Fabre, Gabin / Harbauer, Angelika B / Wood, Will / Wilhelm, Christoph / Thorn-Seshold, Julia / Misgeld, Thomas / Kerschensteiner, Martin / Thorn-Seshold, Oliver

    Journal of the American Chemical Society

    2024  

    Abstract: Selectively labeling cells with damaged membranes is needed not only for identifying dead cells in culture, but also for imaging membrane barrier dysfunction in ... ...

    Abstract Selectively labeling cells with damaged membranes is needed not only for identifying dead cells in culture, but also for imaging membrane barrier dysfunction in pathologies
    Language English
    Publishing date 2024-04-09
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3155-0
    ISSN 1520-5126 ; 0002-7863
    ISSN (online) 1520-5126
    ISSN 0002-7863
    DOI 10.1021/jacs.3c07662
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  9. Article ; Online: Kill one or kill the many: interplay between mitophagy and apoptosis.

    Wanderoy, Simone / Hees, J Tabitha / Klesse, Ramona / Edlich, Frank / Harbauer, Angelika B

    Biological chemistry

    2020  Volume 402, Issue 1, Page(s) 73–88

    Abstract: Mitochondria are key players of cellular metabolism, ... ...

    Abstract Mitochondria are key players of cellular metabolism, Ca
    MeSH term(s) Apoptosis ; Humans ; Mitochondria/metabolism ; Mitophagy ; Proto-Oncogene Proteins c-bcl-2/metabolism
    Chemical Substances BCL2 protein, human ; Proto-Oncogene Proteins c-bcl-2
    Language English
    Publishing date 2020-10-12
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1334659-3
    ISSN 1437-4315 ; 1431-6730 ; 1432-0355
    ISSN (online) 1437-4315
    ISSN 1431-6730 ; 1432-0355
    DOI 10.1515/hsz-2020-0231
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  10. Article ; Online: Neuronal mitochondria transport Pink1 mRNA via synaptojanin 2 to support local mitophagy.

    Harbauer, Angelika B / Hees, J Tabitha / Wanderoy, Simone / Segura, Inmaculada / Gibbs, Whitney / Cheng, Yiming / Ordonez, Martha / Cai, Zerong / Cartoni, Romain / Ashrafi, Ghazaleh / Wang, Chen / Perocchi, Fabiana / He, Zhigang / Schwarz, Thomas L

    Neuron

    2022  Volume 110, Issue 9, Page(s) 1516–1531.e9

    Abstract: PTEN-induced kinase 1 (PINK1) is a short-lived protein required for the removal of damaged mitochondria through Parkin translocation and mitophagy. Because the short half-life of PINK1 limits its ability to be trafficked into neurites, local translation ... ...

    Abstract PTEN-induced kinase 1 (PINK1) is a short-lived protein required for the removal of damaged mitochondria through Parkin translocation and mitophagy. Because the short half-life of PINK1 limits its ability to be trafficked into neurites, local translation is required for this mitophagy pathway to be active far from the soma. The Pink1 transcript is associated and cotransported with neuronal mitochondria. In concert with translation, the mitochondrial outer membrane proteins synaptojanin 2 binding protein (SYNJ2BP) and synaptojanin 2 (SYNJ2) are required for tethering Pink1 mRNA to mitochondria via an RNA-binding domain in SYNJ2. This neuron-specific adaptation for the local translation of PINK1 provides distal mitochondria with a continuous supply of PINK1 for the activation of mitophagy.
    MeSH term(s) Mitochondria/metabolism ; Mitophagy/genetics ; Nerve Tissue Proteins ; Neurons/metabolism ; Phosphoric Monoester Hydrolases ; Protein Kinases/genetics ; RNA, Messenger/metabolism ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism
    Chemical Substances Nerve Tissue Proteins ; RNA, Messenger ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Protein Kinases (EC 2.7.-) ; synaptojanin (EC 3.1.3.-) ; Phosphoric Monoester Hydrolases (EC 3.1.3.2)
    Language English
    Publishing date 2022-02-24
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 808167-0
    ISSN 1097-4199 ; 0896-6273
    ISSN (online) 1097-4199
    ISSN 0896-6273
    DOI 10.1016/j.neuron.2022.01.035
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