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  1. Article: Selenoprotein P Regulates Synaptic Zinc and Reduces Tau Phosphorylation.

    Kiyohara, Arlene C P / Torres, Daniel J / Hagiwara, Ayaka / Pak, Jenna / Rueli, Rachel H L H / Shuttleworth, C William R / Bellinger, Frederick P

    Frontiers in nutrition

    2021  Volume 8, Page(s) 683154

    Abstract: Selenoprotein P (SELENOP1) is a selenium-rich antioxidant protein involved in extracellular transport of selenium (Se). SELENOP1 also has metal binding properties. The trace element Zinc ( ... ...

    Abstract Selenoprotein P (SELENOP1) is a selenium-rich antioxidant protein involved in extracellular transport of selenium (Se). SELENOP1 also has metal binding properties. The trace element Zinc (Zn
    Language English
    Publishing date 2021-07-01
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2776676-7
    ISSN 2296-861X
    ISSN 2296-861X
    DOI 10.3389/fnut.2021.683154
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Methamphetamine acutely inhibits voltage-gated calcium channels but chronically up-regulates L-type channels.

    Andres, Marilou A / Cooke, Ian M / Bellinger, Frederick P / Berry, Marla J / Zaporteza, Maribel M / Rueli, Rachel H / Barayuga, Stephanie M / Chang, Linda

    Journal of neurochemistry

    2015  Volume 134, Issue 1, Page(s) 56–65

    Abstract: ... channels. Longer exposure to METH (20 min or 48 h) selectively up-regulates the expression of only ... the CACNA1C gene, thus increasing the number of L-type Ca(2+) channels. This up-regulation of CACNA1C is ... Chronically, neurons compensate by up-regulating the L-type Ca(2+) channel gene, CACNA1C. This compensatory ...

    Abstract In neurons, calcium (Ca(2+) ) channels regulate a wide variety of functions ranging from synaptic transmission to gene expression. They also induce neuroplastic changes that alter gene expression following psychostimulant administration. Ca(2+) channel blockers have been considered as potential therapeutic agents for the treatment of methamphetamine (METH) dependence because of their ability to reduce drug craving among METH users. Here, we studied the effects of METH exposure on voltage-gated Ca(2+) channels using SH-SY5Y cells as a model of dopaminergic neurons. We found that METH has different short- and long-term effects. A short-term effect involves immediate (< 5 min) direct inhibition of Ca(2+) ion movements through Ca(2+) channels. Longer exposure to METH (20 min or 48 h) selectively up-regulates the expression of only the CACNA1C gene, thus increasing the number of L-type Ca(2+) channels. This up-regulation of CACNA1C is associated with the expression of the cAMP-responsive element-binding protein (CREB), a known regulator of CACNA1C gene expression, and the MYC gene, which encodes a transcription factor that putatively binds to a site proximal to the CACNA1C gene transcription initiation site. The short-term inhibition of Ca(2+) ion movement and later, the up-regulation of Ca(2+) channel gene expression together suggest the operation of cAMP-responsive element-binding protein- and C-MYC-mediated mechanisms to compensate for Ca(2+) channel inhibition by METH. Increased Ca(2+) current density and subsequent increased intracellular Ca(2+) may contribute to the neurodegeneration accompanying chronic METH abuse. Methamphetamine (METH) exposure has both short- and long-term effects. Acutely, methamphetamine directly inhibits voltage-gated calcium channels. Chronically, neurons compensate by up-regulating the L-type Ca(2+) channel gene, CACNA1C. This compensatory mechanism is mediated by transcription factors C-MYC and CREB, in which CREB is linked to the dopamine D1 receptor signaling pathway. These findings suggest Ca(2+) -mediated neurotoxicity owing to over-expression of calcium channels.
    MeSH term(s) Calcium Channel Blockers/pharmacology ; Calcium Channels, L-Type/biosynthesis ; Cell Line, Tumor ; Humans ; Methamphetamine/pharmacology ; Time Factors ; Up-Regulation/drug effects ; Up-Regulation/physiology
    Chemical Substances CACNA1C protein, human ; Calcium Channel Blockers ; Calcium Channels, L-Type ; Methamphetamine (44RAL3456C)
    Language English
    Publishing date 2015-07
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 80158-6
    ISSN 1471-4159 ; 0022-3042 ; 1474-1644
    ISSN (online) 1471-4159
    ISSN 0022-3042 ; 1474-1644
    DOI 10.1111/jnc.13104
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Selenoprotein S Reduces Endoplasmic Reticulum Stress-Induced Phosphorylation of Tau: Potential Role in Selenate Mitigation of Tau Pathology.

    Rueli, Rachel H L H / Torres, Daniel J / Dewing, Andrea S T / Kiyohara, Arlene C / Barayuga, Stephanie M / Bellinger, Miyoko T / Uyehara-Lock, Jane H / White, Lon R / Moreira, Paula I / Berry, Marla J / Perry, George / Bellinger, Frederick P

    Journal of Alzheimer's disease : JAD

    2016  Volume 55, Issue 2, Page(s) 749–762

    Abstract: Previous studies demonstrated that selenium in the form of sodium selenate reduces neurofibrillary tangle formation in Alzheimer's disease models. Hyperphosphorylation of tau, which leads to formation of neurofibrillary tangles in Alzheimer's disease, is ...

    Abstract Previous studies demonstrated that selenium in the form of sodium selenate reduces neurofibrillary tangle formation in Alzheimer's disease models. Hyperphosphorylation of tau, which leads to formation of neurofibrillary tangles in Alzheimer's disease, is increased by endoplasmic reticulum (ER) stress. Selenoprotein S (SelS) is part of an ER membrane complex that removes misfolded proteins from the ER as a means to reduce ER stress. Selenate, as with other forms of selenium, will increase selenoprotein expression. We therefore proposed that increased SelS expression by selenate would contribute to the beneficial actions of selenate in Alzheimer's disease. SelS expression increased with ER stress and decreased under conditions of elevated glucose concentrations in the SH-SY5Y neuronal cell line. Reducing expression of SelS with siRNA promoted cell death in response to ER stress. Selenate increased SelS expression, which significantly correlated with decreased tau phosphorylation. Restricting SelS expression during ER stress conditions increased tau phosphorylation, and also promoted aggregation of phosphorylated tau in neurites and soma. In human postmortem brain, SelS expression coincided with neurofibrillary tangles, but not with amyloid-β plaques. These results indicate that selenate can alter phosphorylation of tau by increasing expression of SelS in Alzheimer's disease and potentially other neurodegenerative disorders.
    MeSH term(s) Aged ; Aged, 80 and over ; Analysis of Variance ; Brain/metabolism ; Cell Line, Tumor ; Endoplasmic Reticulum Stress/drug effects ; Endoplasmic Reticulum Stress/physiology ; Gene Expression Regulation/genetics ; Glucose/pharmacology ; Humans ; Leucine/genetics ; Membrane Proteins/genetics ; Membrane Proteins/pharmacology ; Mutation/genetics ; Neuroblastoma/pathology ; Phosphorylation/drug effects ; Proline/genetics ; RNA, Messenger/metabolism ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; Selenoproteins/genetics ; Selenoproteins/pharmacology ; Transfection ; tau Proteins/metabolism
    Chemical Substances Membrane Proteins ; RNA, Messenger ; RNA, Small Interfering ; SELENOS protein, human ; Selenoproteins ; tau Proteins ; Proline (9DLQ4CIU6V) ; Leucine (GMW67QNF9C) ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2016-11-02
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 1440127-7
    ISSN 1875-8908 ; 1387-2877
    ISSN (online) 1875-8908
    ISSN 1387-2877
    DOI 10.3233/JAD-151208
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  4. Article ; Online: Increased selenoprotein P in choroid plexus and cerebrospinal fluid in Alzheimer's disease brain.

    Rueli, Rachel H L H / Parubrub, Arlene C / Dewing, Andrea S T / Hashimoto, Ann C / Bellinger, Miyoko T / Weeber, Edwin J / Uyehara-Lock, Jane H / White, Lon R / Berry, Marla J / Bellinger, Frederick P

    Journal of Alzheimer's disease : JAD

    2014  Volume 44, Issue 2, Page(s) 379–383

    Abstract: Subjects with Alzheimer's disease (AD) have elevated brain levels of the selenium transporter selenoprotein P (Sepp1). We investigated if this elevation results from increased release of Sepp1 from the choroid plexus (CP). Sepp1 is significantly ... ...

    Abstract Subjects with Alzheimer's disease (AD) have elevated brain levels of the selenium transporter selenoprotein P (Sepp1). We investigated if this elevation results from increased release of Sepp1 from the choroid plexus (CP). Sepp1 is significantly increased in CP from AD brains in comparison to non-AD brains. Sepp1 localizes to the trans-Golgi network within CP epithelia, where it is processed for secretion. The cerebrospinal fluid from AD subjects also contains increased levels Sepp1 in comparison to non-AD subjects. These findings suggest that AD pathology induces increased levels of Sepp1 within CP epithelia for release into the cerebrospinal fluid to ultimately increase brain selenium.
    MeSH term(s) Aged, 80 and over ; Alzheimer Disease/metabolism ; Blotting, Western ; Brain/metabolism ; Choroid Plexus/metabolism ; Humans ; Immunohistochemistry ; Male ; Selenoprotein P/metabolism
    Chemical Substances Selenoprotein P
    Language English
    Publishing date 2014-10-08
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1440127-7
    ISSN 1875-8908 ; 1387-2877
    ISSN (online) 1875-8908
    ISSN 1387-2877
    DOI 10.3233/JAD-141755
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6084: Show issues Location:
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