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p dna  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p dna
    P Dna, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 70 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/p+pkc/Phospho-DNA-PKcs+(Ser2056)+Rabbit+mAb/pmc12918168-92-9-11
    Average 95 stars, based on 70 article reviews
    p dna - by Bioz Stars, 2026-09
    95/100 stars

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    Related Articles

    other:

    Article Title: BET inhibition induces vulnerability to MCL1 targeting through upregulation of fatty acid synthesis pathway in breast cancer
    Article Snippet: p-PKC , Cell Signaling Technology , Cat 9375, RRID:AB_2284224.

    Article Title: Piezo1 activates nitric oxide synthase in red blood cells via protein kinase C with increased activity in diabetes
    Article Snippet: p-PKC , HUVEC , 1:1000 , 9371S; Cell Signaling Technology , Rabbit; 1:2000 (W4011; Promega).

    Article Title: Bmal1 haploinsufficiency impairs fear memory and modulates neuroinflammation via the 5-HT2C receptor
    Article Snippet: p-PKC , Cell Signaling Technology , #9379 , 1:1000.

    Incubation:

    Article Title: Tussilagone inhibits MRGPRX2-mediated mast cell degranulation and suppresses pseudo-allergic reactions.
    Article Snippet: Mas-related G protein-coupled receptor X2 (MRGPRX2) is a crucial target in pseudo-allergic reactions.. Tussilagone (Tus), the main bioactive component derived from Tussilago farfara, has anti-inflammatory effects, but its potential inhibitory effects on pseudo-allergic responses remain unclear.. This research aimed to evaluate the inhibitory role of Tus on pseudo-allergic reactions and its underlying mechanism.

    Article Title: GGPPS Negatively Regulates the Formation of Neutrophil Extracellular Traps in Lipopolysaccharide-Induced Acute Lung Injury.
    Article Snippet: Acute respiratory distress syndrome (ARDS) and acute lung injury (ALI) are life-threatening diseases.. Neutrophil extracellular traps (NETs) play a key role in lung damage.. Geranylgeranyl diphosphate synthase (GGPPS) is associated with the development of inflammatory diseases.

    Saline:

    Article Title: Amyloid β oligomers dysregulate oligodendrocyte differentiation and myelination via PKC in the zebrafish spinal cord
    Article Snippet: Samples were boiled at 95 °C for 8 min, size-separated in 4-20% polyacrylamide-SDS Criterion TGX Precast gels (Bio-Rad) and transferred to Trans-Blot Turbo Midi Nitrocellulose Transfer Packs (Bio-Rad). .. Membranes were blocked in 5% BSA in Tris-buffered saline/0.05% Tween-20 and proteins were detected by specific primary antibodies against PKC (#ab179521, 1:1000; Abcam) and p-PKC (#9371, 1:1000; Cell Signaling). ..

    Article Title: Amyloid‐β Dysregulates Oligodendroglial Lineage Cell Dynamics and Myelination via PKC in the Zebrafish Spinal Cord
    Article Snippet: Samples were boiled at 95 °C for 8 min, size-separated in 4-20% polyacrylamide-SDS Criterion TGX Precast gels (Bio-Rad) and transferred to Trans-Blot Turbo Midi Nitrocellulose Transfer Packs (Bio-Rad). .. Membranes were blocked in 5% BSA in Tris‐buffered saline/0.05% Tween‐20 and proteins were detected by specific primary antibodies against PKC (#ab179521, 1:1000; Abcam) and p-PKC (#9371, 1:1000; Cell Signaling). ..



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    Image Search Results


    The KIBRA and p -PKMζ are activated in contralateral ACC neurons after CPTP. (A-F) Representative blots and columnar statistical charts show KIBRA, p -PKMζ, and PKMζ levels in contralateral ACC at different time points in Thoracotomy pain (A-C) or Thoracotomy no pain (D-F), * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001 vs Sham group; the data were analyzed by 1-way ANOVA followed by Tukey multiple comparisons test, n = 4∼7 rats in each group. (G-H) The photographs of the double immunofluorescence staining show that KIBRA and p -PKMζ are only colocalized with neuron markers (NeuN) but not with astrocyte marker (GFAP) and microglia marker (Iba1) in the Sham and CPTP groups. The white arrowheads indicate the co-immunostaining. Scale bar, 100 μm. ACC, anterior cingulate gyrus; ANOVA, analysis of variance; CPTP, chronic post-thoracotomy pain; GFAP, glial fibrillary acidic protein; Iba1, ionized calcium-binding adapter molecule 1; KIBRA, kidney and brain-expressed protein; NeuN, neuron-specific nuclear protein; PKMζ, protein kinase Mζ; p -PKMζ, phosphorylated protein kinase Mζ.

    Journal: Pain

    Article Title: Kidney and brain-expressed protein upregulation in the anterior cingulate cortex mediates chronic post-thoracotomy pain by the phospho-protein kinase Mζ/glutamate receptor 1 signaling pathway and neuroinflammation in male rats

    doi: 10.1097/j.pain.0000000000003849

    Figure Lengend Snippet: The KIBRA and p -PKMζ are activated in contralateral ACC neurons after CPTP. (A-F) Representative blots and columnar statistical charts show KIBRA, p -PKMζ, and PKMζ levels in contralateral ACC at different time points in Thoracotomy pain (A-C) or Thoracotomy no pain (D-F), * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001 vs Sham group; the data were analyzed by 1-way ANOVA followed by Tukey multiple comparisons test, n = 4∼7 rats in each group. (G-H) The photographs of the double immunofluorescence staining show that KIBRA and p -PKMζ are only colocalized with neuron markers (NeuN) but not with astrocyte marker (GFAP) and microglia marker (Iba1) in the Sham and CPTP groups. The white arrowheads indicate the co-immunostaining. Scale bar, 100 μm. ACC, anterior cingulate gyrus; ANOVA, analysis of variance; CPTP, chronic post-thoracotomy pain; GFAP, glial fibrillary acidic protein; Iba1, ionized calcium-binding adapter molecule 1; KIBRA, kidney and brain-expressed protein; NeuN, neuron-specific nuclear protein; PKMζ, protein kinase Mζ; p -PKMζ, phosphorylated protein kinase Mζ.

    Article Snippet: After using the Pierce Bicinchoninic Acid Assay kit to measure the protein concentration, 30 μg protein was separated with SDS-PAGE gels (Bio-Rad, Hercules, CA) and immunoblotted with antibodies against KIBRA (bs-11570R; Bioss, Woburn, MA), GluR1 (67642-1-lg; Proteintech, Rosemont, IL), p -PKMζ (AF3404; Affinity, Cincinnati, OH), PKMζ (sc-17781; Santa Cruz, Dallas, TX), β-actin (EM21002; HUABIO, Hangzhou, China), tumor necrosis factor-α (TNF-α, BS-1857; Bioworld, Dublin, OH), and interleukin-1β (IL-1β, ab9722; Abcam, Cambridge, United Kingdom).

    Techniques: Double Immunofluorescence Staining, Marker, Immunostaining, Binding Assay

    Knockdown of KIBRA in contralateral ACC prevents the upregulation of KIBRA, p -PKMζ/GluR1 signaling pathways, and neuroinflammation in CPTP rats. (A-F) Representative blots and columnar statistical charts show KIBRA, p -PKMζ, PKMζ, TNF-α, and IL-1β levels in ACC analyzed 21 days after the sham operation, thoracotomy, or KIBRA − + thoracotomy. The data were analyzed by 1-way ANOVA followed by Tukey multiple comparisons test, n = 4∼8 rats in each group. ACC, anterior cingulate gyrus; CPTP, chronic post-thoracotomy pain; GluR1, glutamate receptor 1; IL-1β, interleukin-1β; KIBRA, kidney and brain-expressed protein; PKMζ, protein kinase Mζ; p -PKMζ, phosphorylated protein kinase Mζ; TNF-α, tumor necrosis factor-α.

    Journal: Pain

    Article Title: Kidney and brain-expressed protein upregulation in the anterior cingulate cortex mediates chronic post-thoracotomy pain by the phospho-protein kinase Mζ/glutamate receptor 1 signaling pathway and neuroinflammation in male rats

    doi: 10.1097/j.pain.0000000000003849

    Figure Lengend Snippet: Knockdown of KIBRA in contralateral ACC prevents the upregulation of KIBRA, p -PKMζ/GluR1 signaling pathways, and neuroinflammation in CPTP rats. (A-F) Representative blots and columnar statistical charts show KIBRA, p -PKMζ, PKMζ, TNF-α, and IL-1β levels in ACC analyzed 21 days after the sham operation, thoracotomy, or KIBRA − + thoracotomy. The data were analyzed by 1-way ANOVA followed by Tukey multiple comparisons test, n = 4∼8 rats in each group. ACC, anterior cingulate gyrus; CPTP, chronic post-thoracotomy pain; GluR1, glutamate receptor 1; IL-1β, interleukin-1β; KIBRA, kidney and brain-expressed protein; PKMζ, protein kinase Mζ; p -PKMζ, phosphorylated protein kinase Mζ; TNF-α, tumor necrosis factor-α.

    Article Snippet: After using the Pierce Bicinchoninic Acid Assay kit to measure the protein concentration, 30 μg protein was separated with SDS-PAGE gels (Bio-Rad, Hercules, CA) and immunoblotted with antibodies against KIBRA (bs-11570R; Bioss, Woburn, MA), GluR1 (67642-1-lg; Proteintech, Rosemont, IL), p -PKMζ (AF3404; Affinity, Cincinnati, OH), PKMζ (sc-17781; Santa Cruz, Dallas, TX), β-actin (EM21002; HUABIO, Hangzhou, China), tumor necrosis factor-α (TNF-α, BS-1857; Bioworld, Dublin, OH), and interleukin-1β (IL-1β, ab9722; Abcam, Cambridge, United Kingdom).

    Techniques: Knockdown, Protein-Protein interactions

    Overexpression of KIBRA in ACC causes allodynia and activates p -PKMζ/GluR1 signaling pathways and neuroinflammation. (A) Experiment designs are shown. (B) Mechanical hyperalgesia ratio on 7, 14, and 21 days after thoracotomy or KIBRA overexpression. **** P < 0.0001 vs Thoracotomy pain group; the data were analyzed by Fisher exact test. (C and D) The threshold% and mechanical pain threshold at different time points for pain rats after injection of rAAV-CMV-wwc1-3xFLAG-WPREs or thoracotomy, * P < 0.05, *** P < 0.001, and **** P < 0.0001 vs Sham group, &&&& P < 0.00001 vs KIBRA + pain group, the data were analyzed by 2-way ANOVA followed by Tukey multiple comparisons test, n = 8 in Sham, n = 13 in Thoracotomy pain, n = 12 in KIBRA + pain, n = 8 in KIBRA + no pain group. (E-J) Representative blots and columnar statistical charts show KIBRA, p -PKMζ, PKMζ, GluR1, TNF-α, and IL-1β levels in ACC analyzed 21 days in Sham, KIBRA + pain, and KIBRA + no pain rats. The data were analyzed by 1-way ANOVA followed by Tukey multiple comparisons test, n = 4 in each group. ACC, anterior cingulate gyrus; ANOVA, analysis of variance; GluR1, glutamate receptor 1; IL-1β, interleukin-1β; KIBRA, kidney and brain-expressed protein; PKMζ, protein kinase Mζ; p -PKMζ, phosphorylated protein kinase Mζ; TNF-α, tumor necrosis factor-α.

    Journal: Pain

    Article Title: Kidney and brain-expressed protein upregulation in the anterior cingulate cortex mediates chronic post-thoracotomy pain by the phospho-protein kinase Mζ/glutamate receptor 1 signaling pathway and neuroinflammation in male rats

    doi: 10.1097/j.pain.0000000000003849

    Figure Lengend Snippet: Overexpression of KIBRA in ACC causes allodynia and activates p -PKMζ/GluR1 signaling pathways and neuroinflammation. (A) Experiment designs are shown. (B) Mechanical hyperalgesia ratio on 7, 14, and 21 days after thoracotomy or KIBRA overexpression. **** P < 0.0001 vs Thoracotomy pain group; the data were analyzed by Fisher exact test. (C and D) The threshold% and mechanical pain threshold at different time points for pain rats after injection of rAAV-CMV-wwc1-3xFLAG-WPREs or thoracotomy, * P < 0.05, *** P < 0.001, and **** P < 0.0001 vs Sham group, &&&& P < 0.00001 vs KIBRA + pain group, the data were analyzed by 2-way ANOVA followed by Tukey multiple comparisons test, n = 8 in Sham, n = 13 in Thoracotomy pain, n = 12 in KIBRA + pain, n = 8 in KIBRA + no pain group. (E-J) Representative blots and columnar statistical charts show KIBRA, p -PKMζ, PKMζ, GluR1, TNF-α, and IL-1β levels in ACC analyzed 21 days in Sham, KIBRA + pain, and KIBRA + no pain rats. The data were analyzed by 1-way ANOVA followed by Tukey multiple comparisons test, n = 4 in each group. ACC, anterior cingulate gyrus; ANOVA, analysis of variance; GluR1, glutamate receptor 1; IL-1β, interleukin-1β; KIBRA, kidney and brain-expressed protein; PKMζ, protein kinase Mζ; p -PKMζ, phosphorylated protein kinase Mζ; TNF-α, tumor necrosis factor-α.

    Article Snippet: After using the Pierce Bicinchoninic Acid Assay kit to measure the protein concentration, 30 μg protein was separated with SDS-PAGE gels (Bio-Rad, Hercules, CA) and immunoblotted with antibodies against KIBRA (bs-11570R; Bioss, Woburn, MA), GluR1 (67642-1-lg; Proteintech, Rosemont, IL), p -PKMζ (AF3404; Affinity, Cincinnati, OH), PKMζ (sc-17781; Santa Cruz, Dallas, TX), β-actin (EM21002; HUABIO, Hangzhou, China), tumor necrosis factor-α (TNF-α, BS-1857; Bioworld, Dublin, OH), and interleukin-1β (IL-1β, ab9722; Abcam, Cambridge, United Kingdom).

    Techniques: Over Expression, Protein-Protein interactions, Injection

    ACC overexpression KIBRA combined with thoracotomy induced CPTP in all rats. (A) Experiment designs are shown. (B) Incidence of pain on 7, 14, and 21 days after thoracotomy in KIBRA overexpression rats. ** P < 0.01 vs Thoracotomy pain group; the data were analyzed by Fisher exact test. (C and D) The threshold% and mechanical pain threshold at different time points in KIBRA + no pain + Thoracotomy pain, Thoracotomy pain, or Sham group, **** P < 0.0001 vs Sham group, & P < 0.05 vs Thoracotomy pain group. The data were analyzed by 2-way ANOVA followed by Tukey multiple comparisons test, n = 8 in Sham, n = 13 in Thoracotomy pain, n = 14 in KIBRA + no pain + Thoracotomy pain group. (E-J) Representative blots and columnar statistical charts show KIBRA, p -PKMζ, PKMζ, GluR1, TNF-α, and IL-1β levels in ACC analyzed on POD21 in Sham, Thoracotomy pain, or KIBRA + no pain + Thoracotomy pain rats, n = 4 rats in each group. The data were analyzed by 1-way ANOVA followed by Tukey post hoc test. ACC, anterior cingulate gyrus; ANOVA, analysis of variance; CPTP, chronic post-thoracotomy pain; GluR1, glutamate receptor 1; IL-1β, interleukin-1β; KIBRA, kidney and brain-expressed protein; PKMζ, protein kinase Mζ; p -PKMζ, phosphorylated protein kinase Mζ; TNF-α, tumor necrosis factor-α.

    Journal: Pain

    Article Title: Kidney and brain-expressed protein upregulation in the anterior cingulate cortex mediates chronic post-thoracotomy pain by the phospho-protein kinase Mζ/glutamate receptor 1 signaling pathway and neuroinflammation in male rats

    doi: 10.1097/j.pain.0000000000003849

    Figure Lengend Snippet: ACC overexpression KIBRA combined with thoracotomy induced CPTP in all rats. (A) Experiment designs are shown. (B) Incidence of pain on 7, 14, and 21 days after thoracotomy in KIBRA overexpression rats. ** P < 0.01 vs Thoracotomy pain group; the data were analyzed by Fisher exact test. (C and D) The threshold% and mechanical pain threshold at different time points in KIBRA + no pain + Thoracotomy pain, Thoracotomy pain, or Sham group, **** P < 0.0001 vs Sham group, & P < 0.05 vs Thoracotomy pain group. The data were analyzed by 2-way ANOVA followed by Tukey multiple comparisons test, n = 8 in Sham, n = 13 in Thoracotomy pain, n = 14 in KIBRA + no pain + Thoracotomy pain group. (E-J) Representative blots and columnar statistical charts show KIBRA, p -PKMζ, PKMζ, GluR1, TNF-α, and IL-1β levels in ACC analyzed on POD21 in Sham, Thoracotomy pain, or KIBRA + no pain + Thoracotomy pain rats, n = 4 rats in each group. The data were analyzed by 1-way ANOVA followed by Tukey post hoc test. ACC, anterior cingulate gyrus; ANOVA, analysis of variance; CPTP, chronic post-thoracotomy pain; GluR1, glutamate receptor 1; IL-1β, interleukin-1β; KIBRA, kidney and brain-expressed protein; PKMζ, protein kinase Mζ; p -PKMζ, phosphorylated protein kinase Mζ; TNF-α, tumor necrosis factor-α.

    Article Snippet: After using the Pierce Bicinchoninic Acid Assay kit to measure the protein concentration, 30 μg protein was separated with SDS-PAGE gels (Bio-Rad, Hercules, CA) and immunoblotted with antibodies against KIBRA (bs-11570R; Bioss, Woburn, MA), GluR1 (67642-1-lg; Proteintech, Rosemont, IL), p -PKMζ (AF3404; Affinity, Cincinnati, OH), PKMζ (sc-17781; Santa Cruz, Dallas, TX), β-actin (EM21002; HUABIO, Hangzhou, China), tumor necrosis factor-α (TNF-α, BS-1857; Bioworld, Dublin, OH), and interleukin-1β (IL-1β, ab9722; Abcam, Cambridge, United Kingdom).

    Techniques: Over Expression