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  1. Article ; Online: ER stress and UPR in Alzheimer's disease: mechanisms, pathogenesis, treatments.

    Ajoolabady, Amir / Lindholm, Dan / Ren, Jun / Pratico, Domenico

    Cell death & disease

    2022  Volume 13, Issue 8, Page(s) 706

    Abstract: Alzheimer's disease (AD) is a devastating neurodegenerative disorder characterized by gradual loss of memory and cognitive function, which constitutes a heavy burden on the healthcare system globally. Current therapeutics to interfere with the underlying ...

    Abstract Alzheimer's disease (AD) is a devastating neurodegenerative disorder characterized by gradual loss of memory and cognitive function, which constitutes a heavy burden on the healthcare system globally. Current therapeutics to interfere with the underlying disease process in AD is still under development. Although many efforts have centered on the toxic forms of Aβ to effectively tackle AD, considering the unsatisfactory results so far it is vital to examine other targets and therapeutic approaches as well. The endoplasmic reticulum (ER) stress refers to the build-up of unfolded or misfolded proteins within the ER, thus, perturbing the ER and cellular homeostasis. Emerging evidence indicates that ER stress contributes to the onset and development of AD. A thorough elucidation of ER stress machinery in AD pathology may help to open up new therapeutic avenues in the management of this devastating condition to relieve the cognitive dementia symptoms. Herein, we aim at deciphering the unique role of ER stress in AD pathogenesis, reviewing key findings, and existing controversy in an attempt to summarize plausible therapeutic interventions in the management of AD pathophysiology.
    MeSH term(s) Alzheimer Disease/metabolism ; Endoplasmic Reticulum Stress ; Humans ; Unfolded Protein Response
    Language English
    Publishing date 2022-08-15
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2541626-1
    ISSN 2041-4889 ; 2041-4889
    ISSN (online) 2041-4889
    ISSN 2041-4889
    DOI 10.1038/s41419-022-05153-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Unveiling the Function of the Mitochondrial Filament-Forming Protein LACTB in Lipid Metabolism and Cancer.

    Cascone, Annunziata / Lalowski, Maciej / Lindholm, Dan / Eriksson, Ove

    Cells

    2022  Volume 11, Issue 10

    Abstract: LACTB is a relatively unknown mitochondrial protein structurally related to the bacterial penicillin-binding and beta-lactamase superfamily of serine proteases. LACTB has recently gained an increased interest due to its potential role in lipid metabolism ...

    Abstract LACTB is a relatively unknown mitochondrial protein structurally related to the bacterial penicillin-binding and beta-lactamase superfamily of serine proteases. LACTB has recently gained an increased interest due to its potential role in lipid metabolism and tumorigenesis. To date, around ninety studies pertaining to LACTB have been published, but the exact biochemical and cell biological function of LACTB still remain elusive. In this review, we summarise the current knowledge about LACTB with particular attention to the implications of the recently published study on the cryo-electron microscopy structure of the filamentous form of LACTB. From this and other studies, several specific properties of LACTB emerge, suggesting that the protein has distinct functions in different physiological settings. Resolving these issues by further research may ultimately lead to a unified model of LACTB's function in cell and organismal physiology. LACTB is the only member of its protein family in higher animals and LACTB may, therefore, be of particular interest for future drug targeting initiatives.
    MeSH term(s) Animals ; Cryoelectron Microscopy ; Lipid Metabolism ; Membrane Proteins/metabolism ; Mitochondrial Proteins/metabolism ; Neoplasms
    Chemical Substances Membrane Proteins ; Mitochondrial Proteins
    Language English
    Publishing date 2022-05-20
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells11101703
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Proliferation and migration of ML1 follicular thyroid cancer cells are inhibited by IU1 targeting USP14: role of proteasome and autophagy flux.

    Srinivasan, Vignesh / Asghar, Muhammad Yasir / Zafar, Sadia / Törnquist, Kid / Lindholm, Dan

    Frontiers in cell and developmental biology

    2023  Volume 11, Page(s) 1234204

    Abstract: USP14 is a deubiquitinating enzyme involved in protein degradation by interacting with the proteasome and removal of poly-ubiquitin chains on target proteins. USP14 can influence cellular processes such as cell survival, DNA repair, ER stress, ... ...

    Abstract USP14 is a deubiquitinating enzyme involved in protein degradation by interacting with the proteasome and removal of poly-ubiquitin chains on target proteins. USP14 can influence cellular processes such as cell survival, DNA repair, ER stress, endocytosis, and the inflammatory response. USP14 further plays a role in tumor growth, and the inhibition of USP14 by compounds such as IU1 may affect cancer cell migration and invasion. Here we have studied the mechanisms for the action of IU1 in ML1 follicular thyroid cancer cells, comparing them with control, primary thyroid cells. Treatment with IU1 reduced proliferation of ML1 cells in a concentration-dependent manner, and more prominently than in control cells. IU1 decreased basal migration of ML1 cells, and after stimulation of cells with the bioactive compound, sphingosine-1-phosphate. The sphingosine-1-phosphate receptor 3 was increased in ML1 cells as compared with control thyroid cells, but this was not influenced by IU1. Further studies on the mechanism, revealed that IU1 enhanced the proteasome activity as well as LC3B-dependent autophagy flux in ML1 cells with an opposite effect on control thyroid cells. This indicates that IU1 elicits a cell-type dependent autophagy response, increasing it in ML1 cancer cells. The IU1-mediated stimulation of autophagy and proteasomes can likely contribute to the reduced cell proliferation and migration observed in ML1 cells. The precise set of proteins affected by IU1 in ML1 thyroid and other cancer cells warrant further investigations.
    Language English
    Publishing date 2023-08-30
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2023.1234204
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: The Unfolded Protein Response and Autophagy as Drug Targets in Neuropsychiatric Disorders.

    Srinivasan, Vignesh / Korhonen, Laura / Lindholm, Dan

    Frontiers in cellular neuroscience

    2020  Volume 14, Page(s) 554548

    Abstract: Neurons are polarized in structure with a cytoplasmic compartment extending into dendrites and a long axon that terminates at the synapse. The high level of compartmentalization imposes specific challenges for protein quality control in neurons making ... ...

    Abstract Neurons are polarized in structure with a cytoplasmic compartment extending into dendrites and a long axon that terminates at the synapse. The high level of compartmentalization imposes specific challenges for protein quality control in neurons making them vulnerable to disturbances that may lead to neurological dysfunctions including neuropsychiatric diseases. Synapse and dendrites undergo structural modulations regulated by neuronal activity involve key proteins requiring strict control of their turnover rates and degradation pathways. Recent advances in the study of the unfolded protein response (UPR) and autophagy processes have brought novel insights into the specific roles of these processes in neuronal physiology and synaptic signaling. In this review, we highlight recent data and concepts about UPR and autophagy in neuropsychiatric disorders and synaptic plasticity including a brief outline of possible therapeutic approaches to influence UPR and autophagy signaling in these diseases.
    Language English
    Publishing date 2020-09-29
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2452963-1
    ISSN 1662-5102
    ISSN 1662-5102
    DOI 10.3389/fncel.2020.554548
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Book ; Thesis: Thyroid hormones and regulation of neuronal protein synthesis in developing rat brain cortex

    Lindholm, Dan

    1984  

    Size 45 S.
    Publishing country Finland
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Helsinki, Univ., Diss., 1984
    HBZ-ID HT003069718
    ISBN 951-99593-0-0 ; 978-951-99593-0-6
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    88 E 329 order for loan Magazin

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  6. Article ; Online: Multivariate analyses of immune markers reveal increases in plasma EN-RAGE in first-episode psychosis patients.

    Korhonen, Laura / Paul, Elisabeth R / Wåhlén, Karin / Haring, Liina / Vasar, Eero / Vaheri, Antti / Lindholm, Dan

    Translational psychiatry

    2023  Volume 13, Issue 1, Page(s) 326

    Abstract: Immune cells and cytokines are largely recognized as significant factors in the pathophysiology of neuropsychiatric disorders. The possible role of other blood cells such as leukocytes in events of acute psychosis is in contrast only emerging. To study ... ...

    Abstract Immune cells and cytokines are largely recognized as significant factors in the pathophysiology of neuropsychiatric disorders. The possible role of other blood cells such as leukocytes in events of acute psychosis is in contrast only emerging. To study blood-born markers in acute psychosis we here evaluated plasma proteins in drug-naive first-episode psychosis (FEP) patients and healthy controls using a multiplex proximity extension assay technique. We analyzed a panel of 92 immune markers and plasma samples from 60 FEP patients and 50 controls and evaluated the changes obtained using multivariate statistical methods followed by protein pathway analyses. Data showed that 11 proteins are significantly different between FEP patients and healthy controls We observed increases in pro-inflammatory proteins such as interleukin-6, oncostatin-M, and transforming growth factor-alpha in FEP patients compared with controls. Likewise, the extracellular newly identified RAGE-binding protein (EN-RAGE) that regulates the expression of various cytokines was also elevated in the plasma of FEP patients. The results indicate that neutrophil-derived EN-RAGE could play an important role during the early phase of acute psychosis by stimulating cytokines and the immune response targeting thereby likely also the brain vasculature.
    MeSH term(s) Humans ; Biomarkers ; Interleukin-6 ; Multivariate Analysis ; Psychotic Disorders/metabolism
    Chemical Substances Biomarkers ; Interleukin-6 ; S100A12 protein, human
    Language English
    Publishing date 2023-10-20
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2609311-X
    ISSN 2158-3188 ; 2158-3188
    ISSN (online) 2158-3188
    ISSN 2158-3188
    DOI 10.1038/s41398-023-02627-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: The E3 ubiquitin ligase inducible degrader of the LDL receptor/myosin light chain interacting protein in health and disease.

    van Loon, Nienke M / Lindholm, Dan / Zelcer, Noam

    Current opinion in lipidology

    2019  Volume 30, Issue 3, Page(s) 192–197

    Abstract: Purpose of review: The RING E3 ubiquitin ligase inducible degrader of the LDL receptor (IDOL, also known as MYLIP) promotes ubiquitylation and subsequent lysosomal degradation of the LDL receptor (LDLR), thus acting to limit uptake of lipoprotein- ... ...

    Abstract Purpose of review: The RING E3 ubiquitin ligase inducible degrader of the LDL receptor (IDOL, also known as MYLIP) promotes ubiquitylation and subsequent lysosomal degradation of the LDL receptor (LDLR), thus acting to limit uptake of lipoprotein-derived cholesterol into cells. Next to the LDLR, IDOL also promotes degradation of two related receptors, the very LDL receptor (VLDLR) and apolipoprotein E receptor 2 (APOER2), which have important signaling functions in the brain. We review here the emerging role of IDOL in lipoprotein and energy metabolism, neurodegenerative diseases, and the potential for therapeutic targeting of IDOL.
    Recent findings: Genetic studies suggest an association between IDOL and lipoprotein metabolism in humans. Studies in rodents and nonhuman primates support an in-vivo role for IDOL in lipoprotein metabolism, and also uncovered an unexpected role in whole-body energy metabolism. Recent evaluation of IDOL function in the brain revealed a role in memory formation and progression of Alzheimer's disease. The report of the first IDOL inhibitor may facilitate further investigations on therapeutic strategies to target IDOL.
    Summary: IDOL is emerging as an important determinant of lipid and energy metabolism in metabolic disease as well as in Alzheimer's disease. IDOL targeting may be beneficial in treating these conditions.
    MeSH term(s) Animals ; Disease ; Health ; Humans ; Proteolysis ; Receptors, LDL/metabolism ; Ubiquitin-Protein Ligases/metabolism
    Chemical Substances Receptors, LDL ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
    Language English
    Publishing date 2019-03-21
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1045394-5
    ISSN 1473-6535 ; 0957-9672
    ISSN (online) 1473-6535
    ISSN 0957-9672
    DOI 10.1097/MOL.0000000000000593
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3010: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  8. Article ; Online: Prolyl oligopeptidase inhibition reduces PolyQ aggregation and improves cell viability in cellular model of Huntington's disease.

    Norrbacka, Susanna / Lindholm, Dan / Myöhänen, Timo T

    Journal of cellular and molecular medicine

    2019  Volume 23, Issue 12, Page(s) 8511–8515

    MeSH term(s) Acetylcysteine/analogs & derivatives ; Acetylcysteine/pharmacology ; Biocatalysis/drug effects ; Cell Survival/drug effects ; Cell Survival/genetics ; Cysteine Proteinase Inhibitors/pharmacology ; HeLa Cells ; Humans ; Huntingtin Protein/chemistry ; Huntingtin Protein/genetics ; Huntingtin Protein/metabolism ; Huntington Disease/genetics ; Huntington Disease/metabolism ; Peptides/antagonists & inhibitors ; Peptides/genetics ; Proline/analogs & derivatives ; Proline/pharmacology ; Prolyl Oligopeptidases ; Proteasome Endopeptidase Complex/metabolism ; Protein Aggregates/drug effects ; Protein Aggregation, Pathological/prevention & control ; Serine Endopeptidases/metabolism ; Trinucleotide Repeats/genetics
    Chemical Substances 4-phenylbutanoyl-prolylcyanopyrrolidine ; Cysteine Proteinase Inhibitors ; Huntingtin Protein ; Peptides ; Protein Aggregates ; lactacystin (133343-34-7) ; polyglutamine (26700-71-0) ; Proline (9DLQ4CIU6V) ; Serine Endopeptidases (EC 3.4.21.-) ; PREPL protein, human (EC 3.4.21.26) ; Prolyl Oligopeptidases (EC 3.4.21.26) ; Proteasome Endopeptidase Complex (EC 3.4.25.1) ; Acetylcysteine (WYQ7N0BPYC)
    Language English
    Publishing date 2019-09-29
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2074559-X
    ISSN 1582-4934 ; 1582-4934 ; 1582-1838
    ISSN (online) 1582-4934
    ISSN 1582-4934 ; 1582-1838
    DOI 10.1111/jcmm.14675
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5752: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  9. Article: Sphingolipids as Modulators of SARS-CoV-2 Infection.

    Törnquist, Kid / Asghar, Muhammad Yasir / Srinivasan, Vignesh / Korhonen, Laura / Lindholm, Dan

    Frontiers in cell and developmental biology

    2021  Volume 9, Page(s) 689854

    Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of the COVID-19 pandemic with severe consequences for afflicted individuals and the society as a whole. The biology and infectivity of the virus has been intensively studied in ... ...

    Abstract Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of the COVID-19 pandemic with severe consequences for afflicted individuals and the society as a whole. The biology and infectivity of the virus has been intensively studied in order to gain a better understanding of the molecular basis of virus-host cell interactions during infection. It is known that SARS-CoV-2 binds to angiotensin-converting enzyme 2 (ACE2) via its spike protein. Priming of the virus by specific proteases leads to viral entry via endocytosis and to the subsequent steps in the life cycle of SARS-CoV-2. Sphingosine and ceramide belong to the sphingolipid family and are abundantly present in cell membranes. These lipids were recently shown to interfere with the uptake of virus particles of SARS-CoV-2 into epithelial cell lines and primary human nasal cells in culture. The mechanisms of action were partly different, as sphingosine blocked, whilst ceramide facilitated viral entry. Acid sphingomyelinase (ASM) is vital for the generation of ceramide and functional inhibition of ASM by drugs like amitriptyline reduced SARS-CoV-2 entry into the epithelial cells. Recent data indicates that serum level of sphingosine-1-phosphate (S1P) is a prognostic factor for COVID-2 severity. Further, stimulation of sphingosine-1-phosphate receptor 1 (S1PR1) might also constrain the hyper-inflammatory conditions linked to SARS-CoV-2. Here, we review recent exciting findings regarding sphingolipids in the uptake of SARS-CoV-2 and in the course of COVID-19 disease. More studies are required on the mechanisms of action and the potential use of antidepressant drugs and sphingolipid modifiers in SARS-CoV-2 infections and in the treatment of the more serious and fatal consequences of the disease.
    Language English
    Publishing date 2021-06-17
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2021.689854
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: Stem cell therapy: how to do it right.

    Cova, Lidia / Lindholm, Dan

    Frontiers in cell and developmental biology

    2014  Volume 2, Page(s) 66

    Language English
    Publishing date 2014-11-06
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2014.00066
    Database MEDical Literature Analysis and Retrieval System OnLINE

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