acc 005  (Alomone Labs)


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    Alomone Labs acc 005
    Acc 005, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/acc 005/product/Alomone Labs
    Average 94 stars, based on 4 article reviews
    Price from $9.99 to $1999.99
    acc 005 - by Bioz Stars, 2022-11
    94/100 stars

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    Alomone Labs anti cav1 3
    Graphic representation of the results. The activity-dependent signaling between the nerve terminals that are in competition through several metabotropic receptors can result in the modulation of the downstream effector kinases, specifically cPKCβI, nPKCε, and PKA. Changes in kinases activity can allow the coordinate phosphorylation of the L-type <t>CaV1.3</t> and P/Q-type VGCC. The high calcium entry through these operative channels present in immature nerve endings can result in their final loss. Also, muscle CaV1.1 and contractile activity can contribute to the synapse elimination. A component of this mechanism may be mediated by a retrograde influence from the postsynaptic site, via the BDNF-TrkB pathway, on the presynaptic calcium channels
    Anti Cav1 3, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti cav1 3/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti cav1 3 - by Bioz Stars, 2022-11
    94/100 stars
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    Graphic representation of the results. The activity-dependent signaling between the nerve terminals that are in competition through several metabotropic receptors can result in the modulation of the downstream effector kinases, specifically cPKCβI, nPKCε, and PKA. Changes in kinases activity can allow the coordinate phosphorylation of the L-type CaV1.3 and P/Q-type VGCC. The high calcium entry through these operative channels present in immature nerve endings can result in their final loss. Also, muscle CaV1.1 and contractile activity can contribute to the synapse elimination. A component of this mechanism may be mediated by a retrograde influence from the postsynaptic site, via the BDNF-TrkB pathway, on the presynaptic calcium channels

    Journal: Molecular Neurobiology

    Article Title: Involvement of the Voltage-Gated Calcium Channels L- P/Q- and N-Types in Synapse Elimination During Neuromuscular Junction Development

    doi: 10.1007/s12035-022-02818-2

    Figure Lengend Snippet: Graphic representation of the results. The activity-dependent signaling between the nerve terminals that are in competition through several metabotropic receptors can result in the modulation of the downstream effector kinases, specifically cPKCβI, nPKCε, and PKA. Changes in kinases activity can allow the coordinate phosphorylation of the L-type CaV1.3 and P/Q-type VGCC. The high calcium entry through these operative channels present in immature nerve endings can result in their final loss. Also, muscle CaV1.1 and contractile activity can contribute to the synapse elimination. A component of this mechanism may be mediated by a retrograde influence from the postsynaptic site, via the BDNF-TrkB pathway, on the presynaptic calcium channels

    Article Snippet: Primary antibodies were incubated at 4 °C overnight (rabbit anti-P/Q-type calcium channel (1:1000; ACC-001, Alomone; Jerusalem, Israel); rabbit anti-α1D L-type calcium channel (CaV1.3, 1:500; ACC-005, Alomone, Jerusalem, Israel); rabbit anti-N-type calcium channel (1:500; ACC-002, Alomone); rabbit anti-Munc18-1 (1:1000; ≠ 13414, Cell Signalling Technology; Massachusetts, USA), and rabbit anti-PKCε (1:1000; ≠ 2683, Cell Signalling Technology; Massachusetts, USA)).

    Techniques: Activity Assay