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  1. Book ; Thesis: Thyroid hormone control over beta-adrenergic signalling system in rat atria

    Kaasik, Allen

    (Dissertationes medicinae Universitatis Tartuensis ; 38)

    1998  

    Author's details Allen Kaasik
    Series title Dissertationes medicinae Universitatis Tartuensis ; 38
    Collection
    Language English
    Size 91 S. : graph. Darst.
    Publisher Tartu Univ. Press
    Publishing place Tartu
    Publishing country Estonia
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Tartu, Univ., Diss., 1998
    Note Zsfassung in estn. Sprache
    HBZ-ID HT009009724
    ISBN 9985-56-325-5 ; 978-9985-56-325-0
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    98 E 2059 order for loan Magazin

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  2. Article ; Online: Mitochondrial Mobility and Neuronal Recovery.

    Kaasik, Allen

    The New England journal of medicine

    2016  Volume 375, Issue 13, Page(s) 1295–1296

    MeSH term(s) Adenosine Triphosphate/metabolism ; Animals ; Axons/physiology ; Humans ; Mice ; Mice, Knockout ; Microtubule-Associated Proteins/deficiency ; Microtubule-Associated Proteins/genetics ; Mitochondria/physiology ; Mitochondrial Proteins/metabolism ; Molecular Motor Proteins/physiology ; Regeneration/physiology
    Chemical Substances Microtubule-Associated Proteins ; Mitochondrial Proteins ; Molecular Motor Proteins ; Snph protein, mouse ; Adenosine Triphosphate (8L70Q75FXE)
    Language English
    Publishing date 2016-09-29
    Publishing country United States
    Document type Journal Article
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMcibr1607955
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Principles of mitochondrial fusion and fission cycle in neurons.

    Kaasik, Allen

    SpringerPlus

    2015  Volume 4, Issue Suppl 1, Page(s) L34

    Language English
    Publishing date 2015-06-12
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2661116-8
    ISSN 2193-1801
    ISSN 2193-1801
    DOI 10.1186/2193-1801-4-S1-L34
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Negative feedback system to maintain cell ROS homeostasis: KEAP1-PGAM5 complex senses mitochondrially generated ROS to induce mitophagy.

    Zeb, Akbar / Choubey, Vinay / Gupta, Ruby / Veksler, Vladimir / Kaasik, Allen

    Autophagy

    2022  Volume 18, Issue 9, Page(s) 2249–2251

    Abstract: If cellular reactive oxygen species (ROS) production surpasses the intracellular antioxidant capacity, thus altering the ROS homeostasis, the cell needs to eradicate faulty mitochondria responsible for these excessive ROS. We have shown that even ... ...

    Abstract If cellular reactive oxygen species (ROS) production surpasses the intracellular antioxidant capacity, thus altering the ROS homeostasis, the cell needs to eradicate faulty mitochondria responsible for these excessive ROS. We have shown that even moderate ROS production breaks the KEAP1-PGAM5 complex, inhibiting the proteasomal removal of PGAM5. This leads to an accumulation of PGAM5 interfering with PINK1 processing that sensitizes mitochondria to autophagic removal. We propose that such a negative feedback system maintains cell ROS homeostasis.
    MeSH term(s) Autophagy ; Feedback ; Homeostasis ; Kelch-Like ECH-Associated Protein 1 ; Mitochondrial Proteins/metabolism ; Mitophagy ; NF-E2-Related Factor 2 ; Phosphoprotein Phosphatases/metabolism ; Reactive Oxygen Species/metabolism
    Chemical Substances Kelch-Like ECH-Associated Protein 1 ; Mitochondrial Proteins ; NF-E2-Related Factor 2 ; Reactive Oxygen Species ; Phosphoprotein Phosphatases (EC 3.1.3.16)
    Language English
    Publishing date 2022-01-28
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2021.2024702
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Molecular Mechanisms and Regulation of Mammalian Mitophagy.

    Choubey, Vinay / Zeb, Akbar / Kaasik, Allen

    Cells

    2021  Volume 11, Issue 1

    Abstract: Mitochondria in the cell are the center for energy production, essential biomolecule synthesis, and cell fate determination. Moreover, the mitochondrial functional versatility enables cells to adapt to the changes in cellular environment and various ... ...

    Abstract Mitochondria in the cell are the center for energy production, essential biomolecule synthesis, and cell fate determination. Moreover, the mitochondrial functional versatility enables cells to adapt to the changes in cellular environment and various stresses. In the process of discharging its cellular duties, mitochondria face multiple types of challenges, such as oxidative stress, protein-related challenges (import, folding, and degradation) and mitochondrial DNA damage. They mitigate all these challenges with robust quality control mechanisms which include antioxidant defenses, proteostasis systems (chaperones and proteases) and mitochondrial biogenesis. Failure of these quality control mechanisms leaves mitochondria as terminally damaged, which then have to be promptly cleared from the cells before they become a threat to cell survival. Such damaged mitochondria are degraded by a selective form of autophagy called mitophagy. Rigorous research in the field has identified multiple types of mitophagy processes based on targeting signals on damaged or superfluous mitochondria. In this review, we provide an in-depth overview of mammalian mitophagy and its importance in human health and diseases. We also attempted to highlight the future area of investigation in the field of mitophagy.
    MeSH term(s) Animals ; Humans ; Mammals/metabolism ; Mitophagy/genetics ; Models, Biological ; Organelle Biogenesis ; Receptors, Cell Surface/metabolism ; Ubiquitin/metabolism
    Chemical Substances Receptors, Cell Surface ; Ubiquitin
    Language English
    Publishing date 2021-12-23
    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/cells11010038
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  6. Article: Treatment with the dual-incretin agonist DA-CH5 demonstrates potent therapeutic effect in a rat model of Wolfram Syndrome.

    Jagomäe, Toomas / Gaur, Nayana / Seppa, Kadri / Reimets, Riin / Pastak, Marko / Plaas, Mihkel / Kaasik, Allen / Vasar, Eero / Plaas, Mario

    Frontiers in endocrinology

    2023  Volume 14, Page(s) 1234925

    Abstract: Aim: Wolfram Syndrome (WS) is a rare condition caused by mutations in : Methods: Eight-month-old : Results: DA-CH5 therapy reversed glucose intolerance in KO rats and provided lasting anti-diabetogenic protection. Treatment also reversed intra- ... ...

    Abstract Aim: Wolfram Syndrome (WS) is a rare condition caused by mutations in
    Methods: Eight-month-old
    Results: DA-CH5 therapy reversed glucose intolerance in KO rats and provided lasting anti-diabetogenic protection. Treatment also reversed intra-islet alterations, including reduced endocrine islet area and β-cell density, indicating its regenerative potential. Although no rescue effect was noted for hearing loss, visual acuity and retinal ganglion cell density were better preserved in DA-CH5-treated rats.
    Conclusion: We present preclinical evidence for the pleiotropic therapeutic effects of long-term dual incretin agonist treatment; effects were seen despite treatment beginning after symptom-onset, indicating reversal of disease progression. Dual incretins represent a promising therapeutic avenue for WS patients.
    MeSH term(s) Humans ; Rats ; Animals ; Infant ; Incretins/pharmacology ; Wolfram Syndrome/drug therapy ; Glucagon-Like Peptide 1/pharmacology ; Gastric Inhibitory Polypeptide ; Insulin-Secreting Cells
    Chemical Substances Incretins ; Glucagon-Like Peptide 1 (89750-14-1) ; Gastric Inhibitory Polypeptide (59392-49-3)
    Language English
    Publishing date 2023-10-13
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2592084-4
    ISSN 1664-2392
    ISSN 1664-2392
    DOI 10.3389/fendo.2023.1234925
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  7. Article ; Online: Uniting the divergent Wolfram syndrome-linked proteins WFS1 and CISD2 as modulators of Ca

    Loncke, Jens / Vervliet, Tim / Parys, Jan B / Kaasik, Allen / Bultynck, Geert

    Science signaling

    2021  Volume 14, Issue 702, Page(s) eabc6165

    Abstract: Mutations ... ...

    Abstract Mutations in
    MeSH term(s) Humans ; Membrane Proteins/genetics ; Signal Transduction ; Wolfram Syndrome/genetics
    Chemical Substances Membrane Proteins
    Language English
    Publishing date 2021-09-28
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2417226-1
    ISSN 1937-9145 ; 1945-0877
    ISSN (online) 1937-9145
    ISSN 1945-0877
    DOI 10.1126/scisignal.abc6165
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Balancing ER-Mitochondrial Ca

    Loncke, Jens / Kaasik, Allen / Bezprozvanny, Ilya / Parys, Jan B / Kerkhofs, Martijn / Bultynck, Geert

    Trends in cell biology

    2021  Volume 31, Issue 7, Page(s) 598–612

    Abstract: Organelles cooperate with each other to control cellular homeostasis and cell functions by forming close connections through membrane contact sites. Important contacts are present between the endoplasmic reticulum (ER), the main intracellular ... ...

    Abstract Organelles cooperate with each other to control cellular homeostasis and cell functions by forming close connections through membrane contact sites. Important contacts are present between the endoplasmic reticulum (ER), the main intracellular Ca
    MeSH term(s) Calcium/metabolism ; Calcium Signaling ; Endoplasmic Reticulum/metabolism ; Mitochondria/metabolism ; Mitochondrial Membranes/metabolism
    Chemical Substances Calcium (SY7Q814VUP)
    Language English
    Publishing date 2021-03-04
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 30122-x
    ISSN 1879-3088 ; 0962-8924
    ISSN (online) 1879-3088
    ISSN 0962-8924
    DOI 10.1016/j.tcb.2021.02.003
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    Zs.A 3410: Show issues Location:
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  9. Article ; Online: Parvalbumin alters mitochondrial dynamics and affects cell morphology.

    Lichvarova, Lucia / Henzi, Thomas / Safiulina, Dzhamilja / Kaasik, Allen / Schwaller, Beat

    Cellular and molecular life sciences : CMLS

    2018  Volume 75, Issue 24, Page(s) 4643–4666

    Abstract: ... The ... ...

    Abstract The Ca
    MeSH term(s) Animals ; Calcium Signaling ; Cell Size ; Dogs ; Epithelial Cells/cytology ; Epithelial Cells/metabolism ; Epithelial Cells/ultrastructure ; Madin Darby Canine Kidney Cells ; Mitochondria/metabolism ; Mitochondria/ultrastructure ; Mitochondrial Degradation ; Mitochondrial Dynamics ; Parvalbumins/metabolism
    Chemical Substances Parvalbumins
    Language English
    Publishing date 2018-09-25
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 1358415-7
    ISSN 1420-9071 ; 1420-682X
    ISSN (online) 1420-9071
    ISSN 1420-682X
    DOI 10.1007/s00018-018-2921-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 195: Show issues Location:
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  10. Article ; Online: Energetic and dynamic: how mitochondria meet neuronal energy demands.

    Safiulina, Dzhamilja / Kaasik, Allen

    PLoS biology

    2013  Volume 11, Issue 12, Page(s) e1001755

    Abstract: Mitochondria are the power houses of the cell, but unlike the static structures portrayed in textbooks, they are dynamic organelles that move about the cell to deliver energy to locations in need. These organelles fuse with each other then split apart; ... ...

    Abstract Mitochondria are the power houses of the cell, but unlike the static structures portrayed in textbooks, they are dynamic organelles that move about the cell to deliver energy to locations in need. These organelles fuse with each other then split apart; some appear anchored and others more free to move around, and when damaged they are engulfed by autophagosomes. Together, these processes-mitochondrial trafficking, fusion and fission, and mitophagy-are best described by the term "mitochondrial dynamics". The molecular machineries behind these events are relatively well known yet the precise dynamics in neurons remains under debate. Neurons pose a peculiar logistical challenge to mitochondria; how do these energy suppliers manage to traffic down long axons to deliver the requisite energy supply to distant parts of the cell? To date, the majority of neuronal mitochondrial dynamics studies have used cultured neurons, Drosophila larvae, zebrafish embryos, with occasional experiments in resting mouse nerves. However, a new study in this issue of PLOS Biology from Marija Sajic and colleagues provides an in vivo look at mitochondrial dynamics along resting and electrically active neurons of live anaesthetized mice.
    MeSH term(s) Animals ; Male ; Mitochondria/physiology ; Neural Conduction/physiology ; Peripheral Nerves/physiology
    Language English
    Publishing date 2013-12-31
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 2126776-5
    ISSN 1545-7885 ; 1544-9173
    ISSN (online) 1545-7885
    ISSN 1544-9173
    DOI 10.1371/journal.pbio.1001755
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