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spak jnk  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc spak jnk
    Spak Jnk, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1126 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rabbit+anti+spak/JNK2+Rabbit+mAb/pm40748498-77-51-54
    Average 96 stars, based on 1126 article reviews
    spak jnk - by Bioz Stars, 2026-09
    96/100 stars

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    Related Articles

    Incubation:

    Article Title: Target inhibition of SPAK in choroid plexus attenuates T cell infiltration and demyelination in experimental autoimmune encephalomyelitis.
    Article Snippet: .. After PBS washes, cells were incubated overnight at 4 °C with the following primary antibodies: rabbit anti-ZO-1 (1:200, 21773-1-AP, Proteintech, Illinois, USA), rabbit anti-SPAK (1:200, 2281, Cell Signaling Technology, Massachusetts, USA), and rabbit anti-p-SPAK (1:200, 07-2273, Millipore, Massachusetts, USA). .. Following PBS washes containing Tween 20 detergent (1x PBST), cells were incubated with Alexa Fluor 568-conjugated secondary antibodies (1:500, Abcam, Cambridgeshire, England) for one hour at room temperature.

    other:

    Article Title: Carotid artery vascular stenosis causes the blood-CSF barrier damage and neuroinflammation.
    Article Snippet: Rabbit anti-pSPAK/pOSR1 (pSer383 SPAK/ pSer325 OSR1), rabbit anti-SPAK/OSR1 were developed by Dr. Yang at Taiwan National University [20, 21], rabbit anti-SPAK was from Cell Signaling Technology (Cat# 2281S, USA), and rabbit anti-pSPAK was from EMD Millipore (Cat# 07-2273, USA).

    Article Title: Carotid artery vascular stenosis causes the blood-CSF barrier damage and neuroinflammation
    Article Snippet: Rabbit anti-pSPAK/pOSR1 (pSer383 SPAK/pSer325 OSR1), rabbit anti-SPAK/OSR1 were developed by Dr. Yang at Taiwan National University [ , ], rabbit anti-SPAK was from Cell Signaling Technology (Cat# 2281S, USA), and rabbit anti-pSPAK was from EMD Millipore (Cat# 07-2273, USA).



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    Dynamic changes of <t>SPAK-NKCC1</t> complex phosphorylation in LVCP after ischemic stroke. (A) Representative confocal immunofluorescence staining images of phosphorylated SPAK and NKCC1 proteins in LVCP (IL: ipsilateral) at 5-day post-stroke or sham surgery. Arrow: high expression. Arrowhead: low expression. (B) Quantification of pSPAK and pNKCC1 fluorescence intensity. Data are mean ± SEM, n = 3. ** p < 0.01; *** p < 0.001.
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    Dynamic changes of <t>SPAK-NKCC1</t> complex phosphorylation in LVCP after ischemic stroke. (A) Representative confocal immunofluorescence staining images of phosphorylated SPAK and NKCC1 proteins in LVCP (IL: ipsilateral) at 5-day post-stroke or sham surgery. Arrow: high expression. Arrowhead: low expression. (B) Quantification of pSPAK and pNKCC1 fluorescence intensity. Data are mean ± SEM, n = 3. ** p < 0.01; *** p < 0.001.
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    Image Search Results


    Dynamic changes of SPAK-NKCC1 complex phosphorylation in LVCP after ischemic stroke. (A) Representative confocal immunofluorescence staining images of phosphorylated SPAK and NKCC1 proteins in LVCP (IL: ipsilateral) at 5-day post-stroke or sham surgery. Arrow: high expression. Arrowhead: low expression. (B) Quantification of pSPAK and pNKCC1 fluorescence intensity. Data are mean ± SEM, n = 3. ** p < 0.01; *** p < 0.001.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Transient ischemic stroke triggers sustained damage of the choroid plexus blood-CSF barrier

    doi: 10.3389/fncel.2023.1279385

    Figure Lengend Snippet: Dynamic changes of SPAK-NKCC1 complex phosphorylation in LVCP after ischemic stroke. (A) Representative confocal immunofluorescence staining images of phosphorylated SPAK and NKCC1 proteins in LVCP (IL: ipsilateral) at 5-day post-stroke or sham surgery. Arrow: high expression. Arrowhead: low expression. (B) Quantification of pSPAK and pNKCC1 fluorescence intensity. Data are mean ± SEM, n = 3. ** p < 0.01; *** p < 0.001.

    Article Snippet: Rabbit anti-SPAK/OSR1 (Cat# 2281S) and rabbit anti-NKCC1 antibody (Cat# 85403T) were purchased from Cell Signaling.

    Techniques: Phospho-proteomics, Immunofluorescence, Staining, Expressing, Fluorescence

    Dynamic changes of SPAK-NKCC1 complex expression in ChP after ischemic stroke. (A) Representative confocal immunofluorescence staining images of SPAK and NKCC1 protein in the LVCP (IL: ipsilateral) at 1-, 5-, or 7-day post-stroke or sham surgery. Arrow: high expression. Arrowhead: low expression. (B) Quantification for fluorescence intensity of apical SPAK and NKCC1 protein in ROI. Data are mean ± SEM, n = 3–6. * p < 0.05.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Transient ischemic stroke triggers sustained damage of the choroid plexus blood-CSF barrier

    doi: 10.3389/fncel.2023.1279385

    Figure Lengend Snippet: Dynamic changes of SPAK-NKCC1 complex expression in ChP after ischemic stroke. (A) Representative confocal immunofluorescence staining images of SPAK and NKCC1 protein in the LVCP (IL: ipsilateral) at 1-, 5-, or 7-day post-stroke or sham surgery. Arrow: high expression. Arrowhead: low expression. (B) Quantification for fluorescence intensity of apical SPAK and NKCC1 protein in ROI. Data are mean ± SEM, n = 3–6. * p < 0.05.

    Article Snippet: Rabbit anti-SPAK/OSR1 (Cat# 2281S) and rabbit anti-NKCC1 antibody (Cat# 85403T) were purchased from Cell Signaling.

    Techniques: Expressing, Immunofluorescence, Staining, Fluorescence

    Schematic illustration of ischemic stroke-induced changes of the ChP blood-CSF barrier integrity. Ischemic stroke triggers the damage of blood-CSF barrier and results in permeability increase which lasts at least 7 days post-stroke, which reflected by uptake of the albumin by CPECs, the breakdown of TJs and infiltration of circulating immune cells, etc. Ischemic stroke also causes upregulation of proinflammatory Lcn2 gene and LCN2 protein expression especially in the early acute post-stroke stage, accompanied with sustained reduction of choroidal SPAK-NKCC1 protein expression but activation of SPAK as well as NKCC1 phosphorylation. Ischemic stroke also induced infiltration of CD45 + /CD11b + myeloid cells into the ChP. Taken together, stroke-mediated damages of the ChP may lead to inflammation and dysregulation of CSF.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Transient ischemic stroke triggers sustained damage of the choroid plexus blood-CSF barrier

    doi: 10.3389/fncel.2023.1279385

    Figure Lengend Snippet: Schematic illustration of ischemic stroke-induced changes of the ChP blood-CSF barrier integrity. Ischemic stroke triggers the damage of blood-CSF barrier and results in permeability increase which lasts at least 7 days post-stroke, which reflected by uptake of the albumin by CPECs, the breakdown of TJs and infiltration of circulating immune cells, etc. Ischemic stroke also causes upregulation of proinflammatory Lcn2 gene and LCN2 protein expression especially in the early acute post-stroke stage, accompanied with sustained reduction of choroidal SPAK-NKCC1 protein expression but activation of SPAK as well as NKCC1 phosphorylation. Ischemic stroke also induced infiltration of CD45 + /CD11b + myeloid cells into the ChP. Taken together, stroke-mediated damages of the ChP may lead to inflammation and dysregulation of CSF.

    Article Snippet: Rabbit anti-SPAK/OSR1 (Cat# 2281S) and rabbit anti-NKCC1 antibody (Cat# 85403T) were purchased from Cell Signaling.

    Techniques: Permeability, Expressing, Activation Assay, Phospho-proteomics