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  1. Article ; Online: HEBP1 - An early trigger for neuronal cell death and circuit dysfunction in Alzheimer's disease.

    Chua, John Jia En

    Seminars in cell & developmental biology

    2022  Volume 139, Page(s) 102–110

    Abstract: Alzheimer's Disease (AD) is a progressive neurodegenerative disorder that gradually impairs memory, cognition and the ability to perform simple daily tasks. It is the most prevalent form of dementia in the elderly and its incidence increases ... ...

    Abstract Alzheimer's Disease (AD) is a progressive neurodegenerative disorder that gradually impairs memory, cognition and the ability to perform simple daily tasks. It is the most prevalent form of dementia in the elderly and its incidence increases exponentially with age. Neuronal and synapse loss, key hallmarks of the disorder, are widely regarded to occur early during the onset of AD, and the extent of this loss closely correlates with the progression of cognitive decline and dysfunction of the underlying neuronal circuity. Nevertheless, the mechanisms driving neuronal and synapse loss during early AD remains poorly understood. This review focuses on Heme-binding protein 1 (HEBP1), a mitochondrial-associated protein that has recently emerged as an important mediator of neuronal cell death during early AD pathogenesis. Acting downstream of Aβ and heme, HEBP1-mediated apoptosis contributes to neuronal loss and neuronal circuit dysfunction. Deleting HEBP1 expression in neurons protects them from heme- and Aβ-induced apoptosis, both of which are mechanisms implicated in neurodegeneration. HEBP1 participates in heme metabolism and binds to heme to modulate mitochondrial dynamics vital to the maintenance of neural circuitry that is affected in AD. HEBP1 elevation is also associated with AGE/RAGE-related neuronal damage, further implicating its involvement in neuronal loss during early AD. Moreover, F2L, a cleavage product of HEBP1 modulates inflammation. Collectively, these findings highlight the importance of HEBP1 in the disruption of neural circuits during early AD.
    MeSH term(s) Humans ; Aged ; Alzheimer Disease/metabolism ; Cognition ; Apoptosis ; Heme
    Chemical Substances Heme (42VZT0U6YR)
    Language English
    Publishing date 2022-07-14
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 1312473-0
    ISSN 1096-3634 ; 1084-9521
    ISSN (online) 1096-3634
    ISSN 1084-9521
    DOI 10.1016/j.semcdb.2022.07.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2918: 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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  2. Article ; Online: Redox changes and cellular senescence in Alzheimer's disease.

    Yu, Nicole / Pasha, Mazhar / Chua, John Jia En

    Redox biology

    2024  Volume 70, Page(s) 103048

    Abstract: The redox process and cellular senescence are involved in a range of essential physiological functions. However, they are also implicated in pathological processes underlying age-related neurodegenerative disorders, including Alzheimer's disease (AD). ... ...

    Abstract The redox process and cellular senescence are involved in a range of essential physiological functions. However, they are also implicated in pathological processes underlying age-related neurodegenerative disorders, including Alzheimer's disease (AD). Elevated levels of reactive oxygen species (ROS) are generated as a result of abnormal accumulation of beta-amyloid peptide (Aβ), tau protein, and heme dyshomeostasis and is further aggravated by mitochondria dysfunction and endoplasmic reticulum (ER) stress. Excessive ROS damages vital cellular components such as proteins, DNA and lipids. Such damage eventually leads to impaired neuronal function and cell death. Heightened oxidative stress can also induce cellular senescence via activation of the senescence-associated secretory phenotype to further exacerbate inflammation and tissue dysfunction. In this review, we focus on how changes in the redox system and cellular senescence contribute to AD and how they are affected by perturbations in heme metabolism and mitochondrial function. While potential therapeutic strategies targeting such changes have received some attention, more research is necessary to bring them into clinical application.
    MeSH term(s) Humans ; Alzheimer Disease/metabolism ; Reactive Oxygen Species/metabolism ; Amyloid beta-Peptides/metabolism ; Oxidative Stress/physiology ; Cellular Senescence ; Oxidation-Reduction ; Heme/metabolism
    Chemical Substances Reactive Oxygen Species ; Amyloid beta-Peptides ; Heme (42VZT0U6YR)
    Language English
    Publishing date 2024-01-17
    Publishing country Netherlands
    Document type Review ; Journal Article
    ZDB-ID 2701011-9
    ISSN 2213-2317 ; 2213-2317
    ISSN (online) 2213-2317
    ISSN 2213-2317
    DOI 10.1016/j.redox.2024.103048
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Retraction Note: Pharmacological perturbation of CXCL1 signaling alleviates neuropathogenesis in a model of HEVA71 infection.

    Gunaseelan, Saravanan / Ariffin, Mohammed Zacky / Khanna, Sanjay / Ooi, Mong How / Perera, David / Chu, Justin Jang Hann / Chua, John Jia En

    Nature communications

    2023  Volume 14, Issue 1, Page(s) 1053

    Language English
    Publishing date 2023-02-24
    Publishing country England
    Document type Retraction of Publication
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-36751-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: FEZ1 participates in human embryonic brain development by modulating neuronal progenitor subpopulation specification and migrations.

    Qu, Yinghua / Lim, Jonathan Jun-Yong / An, Omer / Yang, Henry / Toh, Yi-Chin / Chua, John Jia En

    iScience

    2023  Volume 26, Issue 12, Page(s) 108497

    Abstract: Mutations in the human fasciculation and elongation protein zeta 1 ( ...

    Abstract Mutations in the human fasciculation and elongation protein zeta 1 (
    Language English
    Publishing date 2023-11-20
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2023.108497
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Role of formyl peptide receptor 2 (FPR2) in the normal brain and in neurological conditions.

    Ong, Wei-Yi / Chua, John Jia En

    Neural regeneration research

    2019  Volume 14, Issue 12, Page(s) 2071–2072

    Language English
    Publishing date 2019-08-09
    Publishing country India
    Document type Journal Article
    ZDB-ID 2388460-5
    ISSN 1876-7958 ; 1673-5374
    ISSN (online) 1876-7958
    ISSN 1673-5374
    DOI 10.4103/1673-5374.262575
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Macromolecular complexes at active zones: integrated nano-machineries for neurotransmitter release.

    Chua, John Jia En

    Cellular and molecular life sciences : CMLS

    2014  Volume 71, Issue 20, Page(s) 3903–3916

    Abstract: The release of neurotransmitters from synaptic vesicles exocytosing at presynaptic nerve terminals is a critical event in the initiation of synaptic transmission. This event occurs at specialized sites known as active zones. The task of faithfully ... ...

    Abstract The release of neurotransmitters from synaptic vesicles exocytosing at presynaptic nerve terminals is a critical event in the initiation of synaptic transmission. This event occurs at specialized sites known as active zones. The task of faithfully executing various steps in the process is undertaken by careful orchestration of overlapping sets of molecular nano-machineries upon a core macromolecular scaffold situated at active zones. However, their composition remains incompletely elucidated. This review provides an overview of the role of the active zone in mediating neurotransmitter release and summarizes the recent progress using neuroproteomic approaches to decipher their composition. Key proteins of these nano-machineries are highlighted.
    MeSH term(s) Calcium Signaling ; Exocytosis ; Humans ; Neurotransmitter Agents/metabolism ; SNARE Proteins/metabolism ; Synaptic Transmission/physiology ; Synaptic Vesicles/metabolism
    Chemical Substances Neurotransmitter Agents ; SNARE Proteins
    Language English
    Publishing date 2014-06-10
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1358415-7
    ISSN 1420-9071 ; 1420-682X
    ISSN (online) 1420-9071
    ISSN 1420-682X
    DOI 10.1007/s00018-014-1657-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 195: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  7. Article ; Online: FEZ1 Forms Complexes with CRMP1 and DCC to Regulate Axon and Dendrite Development.

    Chua, Jie Yin / Ng, Shi Jun / Yagensky, Oleksandr / Wanker, Erich E / Chua, John Jia En

    eNeuro

    2021  Volume 8, Issue 2

    Abstract: Elaboration of neuronal processes is an early step in neuronal development. Guidance cues must work closely with intracellular trafficking pathways to direct expanding axons and dendrites to their target neurons during the formation of neuronal networks. ...

    Abstract Elaboration of neuronal processes is an early step in neuronal development. Guidance cues must work closely with intracellular trafficking pathways to direct expanding axons and dendrites to their target neurons during the formation of neuronal networks. However, how such coordination is achieved remains incompletely understood. Here, we characterize an interaction between fasciculation and elongation protein zeta 1 (FEZ1), an adapter involved in synaptic protein transport, and collapsin response mediator protein (CRMP)1, a protein that functions in growth cone guidance, at neuronal growth cones. We show that similar to CRMP1 loss-of-function mutants, FEZ1 deficiency in rat hippocampal neurons causes growth cone collapse and impairs axonal development. Strikingly, FEZ1-deficient neurons also exhibited a reduction in dendritic complexity stronger than that observed in CRMP1-deficient neurons, suggesting that the former could partake in additional developmental signaling pathways. Supporting this, FEZ1 colocalizes with VAMP2 in developing hippocampal neurons and forms a separate complex with deleted in colorectal cancer (DCC) and Syntaxin-1 (Stx1), components of the Netrin-1 signaling pathway that are also involved in regulating axon and dendrite development. Significantly, developing axons and dendrites of FEZ1-deficient neurons fail to respond to Netrin-1 or Netrin-1 and Sema3A treatment, respectively. Taken together, these findings highlight the importance of FEZ1 as a common effector to integrate guidance signaling pathways with intracellular trafficking to mediate axo-dendrite development during neuronal network formation.
    MeSH term(s) Adaptor Proteins, Signal Transducing ; Animals ; Axons/metabolism ; DCC Receptor ; Growth Cones/metabolism ; Nerve Tissue Proteins ; Neurons/metabolism ; Rats ; Receptors, Cell Surface/metabolism
    Chemical Substances Adaptor Proteins, Signal Transducing ; DCC Receptor ; Dcc protein, rat ; Fez1 protein, rat ; Nerve Tissue Proteins ; Receptors, Cell Surface
    Language English
    Publishing date 2021-04-16
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2800598-3
    ISSN 2373-2822 ; 2373-2822
    ISSN (online) 2373-2822
    ISSN 2373-2822
    DOI 10.1523/ENEURO.0193-20.2021
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: The importance of fasciculation and elongation protein zeta-1 in neural circuit establishment and neurological disorders.

    Razar, Rafhanah Banu Bte Abdul / Qu, Yinghua / Gunaseelan, Saravanan / Chua, John Jia En

    Neural regeneration research

    2021  Volume 17, Issue 6, Page(s) 1165–1171

    Abstract: The human brain contains an estimated 100 billion neurons that must be systematically organized into functional neural circuits for it to function properly. These circuits range from short-range local signaling networks between neighboring neurons to ... ...

    Abstract The human brain contains an estimated 100 billion neurons that must be systematically organized into functional neural circuits for it to function properly. These circuits range from short-range local signaling networks between neighboring neurons to long-range networks formed between various brain regions. Compelling converging evidence indicates that alterations in neural circuits arising from abnormalities during early neuronal development or neurodegeneration contribute significantly to the etiology of neurological disorders. Supporting this notion, efforts to identify genetic causes of these disorders have uncovered an over-representation of genes encoding proteins involved in the processes of neuronal differentiation, maturation, synaptogenesis and synaptic function. Fasciculation and elongation protein zeta-1, a Kinesin-1 adapter, has emerged as a key central player involved in many of these processes. Fasciculation and elongation protein zeta-1-dependent transport of synaptic cargoes and mitochondria is essential for neuronal development and synapse establishment. Furthermore, it acts downstream of guidance cue pathways to regulate axo-dendritic development. Significantly, perturbing its function causes abnormalities in neuronal development and synapse formation both in the brain as well as the peripheral nervous system. Mutations and deletions of the fasciculation and elongation protein zeta-1 gene are linked to neurodevelopmental disorders. Moreover, altered phosphorylation of the protein contributes to neurodegenerative disorders. Together, these findings strongly implicate the importance of fasciculation and elongation protein zeta-1 in the establishment of neuronal circuits and its maintenance.
    Language English
    Publishing date 2021-11-15
    Publishing country India
    Document type Journal Article ; Review
    ZDB-ID 2388460-5
    ISSN 1876-7958 ; 1673-5374
    ISSN (online) 1876-7958
    ISSN 1673-5374
    DOI 10.4103/1673-5374.327327
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Pharmacological perturbation of CXCL1 signaling alleviates neuropathogenesis in a model of HEVA71 infection.

    Gunaseelan, Saravanan / Ariffin, Mohammed Zacky / Khanna, Sanjay / Ooi, Mong How / Perera, David / Chu, Justin Jang Hann / Chua, John Jia En

    publication RETRACTED

    Nature communications

    2022  Volume 13, Issue 1, Page(s) 890

    Abstract: Hand, foot and mouth disease (HFMD) caused by Human Enterovirus A71 (HEVA71) infection is typically a benign infection. However, in minority of cases, children can develop severe neuropathology that culminate in fatality. Approximately 36.9% of HEVA71- ... ...

    Abstract Hand, foot and mouth disease (HFMD) caused by Human Enterovirus A71 (HEVA71) infection is typically a benign infection. However, in minority of cases, children can develop severe neuropathology that culminate in fatality. Approximately 36.9% of HEVA71-related hospitalizations develop neurological complications, of which 10.5% are fatal. Yet, the mechanism by which HEVA71 induces these neurological deficits remain unclear. Here, we show that HEVA71-infected astrocytes release CXCL1 which supports viral replication in neurons by activating the CXCR2 receptor-associated ERK1/2 signaling pathway. Elevated CXCL1 levels correlates with disease severity in a HEVA71-infected mice model. In humans infected with HEVA71, high CXCL1 levels are only present in patients presenting neurological complications. CXCL1 release is specifically triggered by VP4 synthesis in HEVA71-infected astrocytes, which then acts via its receptor CXCR2 to enhance viral replication in neurons. Perturbing CXCL1 signaling or VP4 myristylation strongly attenuates viral replication. Treatment with AZD5069, a CXCL1-specific competitor, improves survival and lessens disease severity in infected animals. Collectively, these results highlight the CXCL1-CXCR2 signaling pathway as a potential target against HFMD neuropathogenesis.
    MeSH term(s) Animals ; Astrocytes/metabolism ; Astrocytes/virology ; Cell Line ; Central Nervous System Diseases/pathology ; Central Nervous System Diseases/virology ; Chemokine CXCL1/metabolism ; Disease Models, Animal ; Enterovirus A, Human/metabolism ; Female ; HEK293 Cells ; Hand, Foot and Mouth Disease/pathology ; Hand, Foot and Mouth Disease/virology ; Humans ; MAP Kinase Signaling System/physiology ; Mice ; Mice, Inbred BALB C ; Pyrimidines/pharmacology ; Rats ; Receptors, Interleukin-8B/metabolism ; Severity of Illness Index ; Sulfonamides/pharmacology
    Chemical Substances CXCL1 protein, human ; CXCR2 protein, human ; Chemokine CXCL1 ; N-(2-(2,3-difluoro-6-benzylthio)-6-(3,4-dihydroxybutan-2-yloxy)pyrimidin-4-yl)azetidine-1-sulfonamide ; Pyrimidines ; Receptors, Interleukin-8B ; Sulfonamides
    Language English
    Publishing date 2022-02-16
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Retracted Publication
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-022-28533-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Author Correction: Pharmacological perturbation of CXCL1 signaling alleviates neuropathogenesis in a model of HEVA71 infection.

    Gunaseelan, Saravanan / Ariffin, Mohammed Zacky / Khanna, Sanjay / Ooi, Mong How / Perera, David / Chu, Justin Jang Hann / Chua, John Jia En

    Nature communications

    2022  Volume 13, Issue 1, Page(s) 1693

    Language English
    Publishing date 2022-03-24
    Publishing country England
    Document type Published Erratum
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-022-29362-w
    Database MEDical Literature Analysis and Retrieval System OnLINE

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