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  1. Article ; Online: Synaptic dysregulation in autism spectrum disorders.

    Zhang, Huaye

    Journal of neuroscience research

    2020  Volume 98, Issue 11, Page(s) 2111–2114

    MeSH term(s) Adolescent ; Adult ; Animals ; Autism Spectrum Disorder/pathology ; Autism Spectrum Disorder/psychology ; Brain/growth & development ; Brain/pathology ; Child ; Child, Preschool ; Humans ; Synapses/pathology
    Language English
    Publishing date 2020-08-11
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 195324-2
    ISSN 1097-4547 ; 0360-4012
    ISSN (online) 1097-4547
    ISSN 0360-4012
    DOI 10.1002/jnr.24711
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1232: 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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  2. Article ; Online: Polarity proteins: Shaping dendritic spines and memory.

    Voglewede, Mikayla M / Zhang, Huaye

    Developmental biology

    2022  Volume 488, Page(s) 68–73

    Abstract: The morphogenesis and plasticity of dendritic spines are associated with synaptic strength, learning, and memory. Dendritic spines are highly compartmentalized structures, which makes proteins involved in cellular polarization and membrane ... ...

    Abstract The morphogenesis and plasticity of dendritic spines are associated with synaptic strength, learning, and memory. Dendritic spines are highly compartmentalized structures, which makes proteins involved in cellular polarization and membrane compartmentalization likely candidates regulating their formation and maintenance. Indeed, recent studies suggest polarity proteins help form and maintain dendritic spines by compartmentalizing the spine neck and head. Here, we review emerging evidence that polarity proteins regulate dendritic spine plasticity and stability through the cytoskeleton, scaffolding molecules, and signaling molecules. We specifically analyze various polarity complexes known to contribute to different forms of cell polarization processes and examine the essential conceptual context linking these groups of polarity proteins to dendritic spine morphogenesis, plasticity, and cognitive functions.
    MeSH term(s) Cytoskeleton ; Dendritic Spines/metabolism ; Morphogenesis ; Neuronal Plasticity/physiology ; Signal Transduction ; Synapses/metabolism
    Language English
    Publishing date 2022-05-14
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 1114-9
    ISSN 1095-564X ; 0012-1606
    ISSN (online) 1095-564X
    ISSN 0012-1606
    DOI 10.1016/j.ydbio.2022.05.007
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    Zs.B 508: Show issues Location:
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  3. Article: Polarity proteins: Shaping dendritic spines and memory

    Voglewede, Mikayla M. / Zhang, Huaye

    Developmental biology. 2022 Aug., v. 488

    2022  

    Abstract: The morphogenesis and plasticity of dendritic spines are associated with synaptic strength, learning, and memory. Dendritic spines are highly compartmentalized structures, which makes proteins involved in cellular polarization and membrane ... ...

    Abstract The morphogenesis and plasticity of dendritic spines are associated with synaptic strength, learning, and memory. Dendritic spines are highly compartmentalized structures, which makes proteins involved in cellular polarization and membrane compartmentalization likely candidates regulating their formation and maintenance. Indeed, recent studies suggest polarity proteins help form and maintain dendritic spines by compartmentalizing the spine neck and head. Here, we review emerging evidence that polarity proteins regulate dendritic spine plasticity and stability through the cytoskeleton, scaffolding molecules, and signaling molecules. We specifically analyze various polarity complexes known to contribute to different forms of cell polarization processes and examine the essential conceptual context linking these groups of polarity proteins to dendritic spine morphogenesis, plasticity, and cognitive functions.
    Keywords cognition ; cytoskeleton ; dendrites ; morphogenesis ; neck
    Language English
    Dates of publication 2022-08
    Size p. 68-73.
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 1114-9
    ISSN 1095-564X ; 0012-1606
    ISSN (online) 1095-564X
    ISSN 0012-1606
    DOI 10.1016/j.ydbio.2022.05.007
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Bonn / Germany

    Z 76/715: Show issues

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  4. Article ; Online: Polarity Determinants in Dendritic Spine Development and Plasticity.

    Zhang, Huaye

    Neural plasticity

    2016  Volume 2016, Page(s) 3145019

    Abstract: The asymmetric distribution of various proteins and RNAs is essential for all stages of animal development, and establishment and maintenance of this cellular polarity are regulated by a group of conserved polarity determinants. Studies over the last 10 ... ...

    Abstract The asymmetric distribution of various proteins and RNAs is essential for all stages of animal development, and establishment and maintenance of this cellular polarity are regulated by a group of conserved polarity determinants. Studies over the last 10 years highlight important functions for polarity proteins, including apical-basal polarity and planar cell polarity regulators, in dendritic spine development and plasticity. Remarkably, many of the conserved polarity machineries function in similar manners in the context of spine development as they do in epithelial morphogenesis. Interestingly, some polarity proteins also utilize neuronal-specific mechanisms. Although many questions remain unanswered in our understanding of how polarity proteins regulate spine development and plasticity, current and future research will undoubtedly shed more light on how this conserved group of proteins orchestrates different pathways to shape the neuronal circuitry.
    MeSH term(s) Animals ; Cell Polarity/physiology ; Dendritic Spines/physiology ; Humans ; Neurogenesis/physiology ; Neuronal Plasticity/physiology ; Neurons/cytology ; Neurons/physiology
    Language English
    Publishing date 2016
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1454938-4
    ISSN 1687-5443 ; 2090-5904 ; 0792-8483
    ISSN (online) 1687-5443
    ISSN 2090-5904 ; 0792-8483
    DOI 10.1155/2016/3145019
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3305: 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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  5. Article ; Online: MARK1 regulates dendritic spine morphogenesis and cognitive functions in vivo.

    Kelly-Castro, Emily C / Shear, Rebecca / Dindigal, Ankitha H / Bhagwat, Maitreyee / Zhang, Huaye

    Experimental neurology

    2024  Volume 376, Page(s) 114752

    Abstract: Dendritic spines play a pivotal role in synaptic communication and are crucial for learning and memory processes. Abnormalities in spine morphology and plasticity are observed in neurodevelopmental and neuropsychiatric disorders, yet the underlying ... ...

    Abstract Dendritic spines play a pivotal role in synaptic communication and are crucial for learning and memory processes. Abnormalities in spine morphology and plasticity are observed in neurodevelopmental and neuropsychiatric disorders, yet the underlying signaling mechanisms remain poorly understood. The microtubule affinity regulating kinase 1 (MARK1) has been implicated in neurodevelopmental disorders, and the MARK1 gene shows accelerated evolution in the human lineage suggesting a role in cognition. However, the in vivo role of MARK1 in synaptogenesis and cognitive functions remains unknown. Here we show that forebrain-specific conditional knockout (cKO) of Mark1 in mice causes defects in dendritic spine morphogenesis in hippocampal CA1 pyramidal neurons with a significant reduction in spine density. In addition, we found loss of MARK1 causes synaptic accumulation of GKAP and GluA2. Furthermore, we found that MARK1 cKO mice show defects in spatial learning in the Morris water maze and reduced anxiety-like behaviors in the elevated plus maze. Taken together, our data show a novel role for MARK1 in regulating dendritic spine morphogenesis and cognitive functions in vivo.
    MeSH term(s) Animals ; Dendritic Spines ; Mice ; Mice, Knockout ; Protein Serine-Threonine Kinases/genetics ; Cognition/physiology ; Maze Learning/physiology ; Morphogenesis/physiology ; Morphogenesis/genetics ; Pyramidal Cells/metabolism ; CA1 Region, Hippocampal/growth & development ; CA1 Region, Hippocampal/metabolism ; Male ; Mice, Inbred C57BL
    Chemical Substances Protein Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2024-03-12
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 207148-4
    ISSN 1090-2430 ; 0014-4886
    ISSN (online) 1090-2430
    ISSN 0014-4886
    DOI 10.1016/j.expneurol.2024.114752
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 184: 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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  6. Article ; Online: Corrigendum "Oxidation of KCNB1 potassium channels in the murine brain during aging is associated with cognitive impairment" [Biochem. Biophys. Res. Commun. 512(4) (2019) 665-669].

    Yu, Wei / Zhang, Huaye / Shin, Mi Ryung / Sesti, Federico

    Biochemical and biophysical research communications

    2022  Volume 632, Page(s) 206–207

    Language English
    Publishing date 2022-10-08
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 205723-2
    ISSN 1090-2104 ; 0006-291X ; 0006-291X
    ISSN (online) 1090-2104 ; 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2022.10.012
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 116: 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: SHANK3 Mutations Associated with Autism and Schizophrenia Lead to Shared and Distinct Changes in Dendritic Spine Dynamics in the Developing Mouse Brain.

    Huang, Chengyu / Voglewede, Mikayla M / Ozsen, Elif Naz / Wang, Hui / Zhang, Huaye

    Neuroscience

    2023  Volume 528, Page(s) 1–11

    Abstract: Autism Spectrum Disorders (ASD) and schizophrenia are distinct neurodevelopmental disorders that share certain symptoms and genetic components. Both disorders show abnormalities in dendritic spines, which are the main sites of excitatory synaptic inputs. ...

    Abstract Autism Spectrum Disorders (ASD) and schizophrenia are distinct neurodevelopmental disorders that share certain symptoms and genetic components. Both disorders show abnormalities in dendritic spines, which are the main sites of excitatory synaptic inputs. Recent studies have identified the synaptic scaffolding protein Shank3 as a leading candidate gene for both disorders. Mutations in the SHANK3 gene have been linked to both ASD and schizophrenia; however, how patient-derived mutations affect the structural plasticity of dendritic spines during brain development is unknown. Here we use live two photon in vivo imaging to examine dendritic spine structural plasticity in mice with SHANK3 mutations associated with ASD and schizophrenia. We identified shared and distinct phenotypes in dendritic spine morphogenesis and plasticity in the ASD-associated InsG3680 mutant mice and the schizophrenia-associated R1117X mutant mice. No significant changes in dendritic arborization were observed in either mutant, raising the possibility that synaptic dysregulation may be a key contributor to the behavioral defects previously reported in these mice. These findings shed light on how patient-linked mutations in SHANK3 affect dendritic spine dynamics in the developing brain, which provides insight into the synaptic basis for the distinct phenotypes observed in ASD and schizophrenia.
    MeSH term(s) Mice ; Animals ; Autistic Disorder/genetics ; Dendritic Spines/metabolism ; Schizophrenia/genetics ; Schizophrenia/metabolism ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Autism Spectrum Disorder/genetics ; Autism Spectrum Disorder/metabolism ; Brain/metabolism ; Mutation/genetics ; Microfilament Proteins/metabolism
    Chemical Substances Nerve Tissue Proteins ; Shank3 protein, mouse ; Microfilament Proteins
    Language English
    Publishing date 2023-07-31
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 196739-3
    ISSN 1873-7544 ; 0306-4522
    ISSN (online) 1873-7544
    ISSN 0306-4522
    DOI 10.1016/j.neuroscience.2023.07.024
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    Zs.A 1215: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  8. Article: MARK1 regulates dendritic spine morphogenesis and cognitive functions

    Kelly-Castro, Emily C / Shear, Rebecca / Dindigal, Ankitha H / Bhagwat, Maitreyee / Zhang, Huaye

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Dendritic spines play a pivotal role in synaptic communication and are crucial for learning and memory processes. Abnormalities in spine morphology and plasticity are observed in neurodevelopmental and neuropsychiatric disorders, yet the underlying ... ...

    Abstract Dendritic spines play a pivotal role in synaptic communication and are crucial for learning and memory processes. Abnormalities in spine morphology and plasticity are observed in neurodevelopmental and neuropsychiatric disorders, yet the underlying signaling mechanisms remain poorly understood. The microtubule affinity regulating kinase 1 (MARK1) has been implicated in neurodevelopmental disorders, and the
    Language English
    Publishing date 2023-12-04
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.12.03.569757
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  9. Article ; Online: Par3 and aPKC regulate BACE1 endosome-to-TGN trafficking through PACS1.

    Sun, Miao / Zhang, Huaye

    Neurobiology of aging

    2017  Volume 60, Page(s) 129–140

    Abstract: The cleavage of amyloid precursor protein (APP) by β-site APP cleaving enzyme 1 (BACE1) is the rate-limiting step in beta amyloid generation during Alzheimer's disease (AD) pathogenesis. In AD brains, BACE1 is abnormally accumulated in endocytic ... ...

    Abstract The cleavage of amyloid precursor protein (APP) by β-site APP cleaving enzyme 1 (BACE1) is the rate-limiting step in beta amyloid generation during Alzheimer's disease (AD) pathogenesis. In AD brains, BACE1 is abnormally accumulated in endocytic compartments, where the acidic pH is optimal for its activity. However, mechanisms regulating the endosome-to-trans-Golgi network (TGN) retrieval of BACE1 remain unclear. Here, we show that partitioning defective 3 (Par3) facilitates BACE1 retrograde trafficking from endosomes to the TGN. Par3 functions through aPKC-mediated phosphorylation of BACE1 on Ser498, which in turn promotes the interaction between BACE1 and phosphofurin acidic cluster sorting protein 1 and facilitates the retrograde trafficking of BACE1 to the TGN. In human AD brains, there is a significant decrease in Ser498 phosphorylation of BACE1 suggesting that defective phosphorylation-dependent retrograde transport of BACE1 is important in AD pathogenesis. Together, our studies provide mechanistic insight into a novel role for Par3 and aPKC in regulating the retrograde endosome-to-TGN trafficking of BACE1 and shed light on the mechanisms of AD pathogenesis.
    MeSH term(s) Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Amyloid Precursor Protein Secretases/metabolism ; Amyloid Precursor Protein Secretases/physiology ; Amyloid beta-Protein Precursor/metabolism ; Animals ; Aspartic Acid Endopeptidases/metabolism ; Aspartic Acid Endopeptidases/physiology ; Brain/metabolism ; Carrier Proteins/physiology ; Cells, Cultured ; Endosomes/metabolism ; Golgi Apparatus/metabolism ; Humans ; Nerve Tissue Proteins ; Phosphorylation ; Protein Kinase C/physiology ; Rats ; Vesicular Transport Proteins/physiology
    Chemical Substances Amyloid beta-Protein Precursor ; Carrier Proteins ; Nerve Tissue Proteins ; PACS1 protein, human ; Pard3 protein, rat ; Vesicular Transport Proteins ; PKC-3 protein (EC 2.7.11.13) ; Protein Kinase C (EC 2.7.11.13) ; Amyloid Precursor Protein Secretases (EC 3.4.-) ; Aspartic Acid Endopeptidases (EC 3.4.23.-) ; BACE1 protein, human (EC 3.4.23.46)
    Language English
    Publishing date 2017-09-21
    Publishing country United States
    Document type Journal Article
    ZDB-ID 604505-4
    ISSN 1558-1497 ; 0197-4580
    ISSN (online) 1558-1497
    ISSN 0197-4580
    DOI 10.1016/j.neurobiolaging.2017.08.024
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1685: 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)
    Zs.MG 10: Show issues

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  10. Article: Neuronal connectivity, behavioral, and transcriptional alterations associated with the loss of MARK2.

    Caiola, Hanna O / Wu, Qian / Soni, Shaili / Wang, Xue-Feng / Monahan, Kevin / Pang, Zhiping P / Wagner, George C / Zhang, Huaye

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Neuronal connectivity is essential for adaptive brain responses and can be modulated by dendritic spine plasticity and the intrinsic excitability of individual neurons. Dysregulation of these processes can lead to aberrant neuronal activity, which has ... ...

    Abstract Neuronal connectivity is essential for adaptive brain responses and can be modulated by dendritic spine plasticity and the intrinsic excitability of individual neurons. Dysregulation of these processes can lead to aberrant neuronal activity, which has been associated with numerous neurological disorders including autism, epilepsy, and Alzheimer's disease. Nonetheless, the molecular mechanisms underlying aberrant neuronal connectivity remains unclear. We previously found that the serine/threonine kinase Microtubule Affinity Regulating Kinase 2 (MARK2), also known as Partitioning Defective 1b (Par1b), is important for the formation of dendritic spines
    Language English
    Publishing date 2023-12-07
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.12.05.569759
    Database MEDical Literature Analysis and Retrieval System OnLINE

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