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mouse anti ck2 β primary antibody  (Santa Cruz Biotechnology)


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    Santa Cruz Biotechnology mouse anti ck2 β primary antibody
    Sequences of two <t> CK2 </t> β -specific siRNAs and one control siRNA These siRNAs were conjugated to chitosan and then administered through intrathecal catheters in rats.
    Mouse Anti Ck2 β Primary Antibody, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 46 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mouse+anti+ck2+%CE%B2+primary+antibody/pmc04109487-123-32-38?v=Santa+Cruz+Biotechnology
    Average 93 stars, based on 46 article reviews
    mouse anti ck2 β primary antibody - by Bioz Stars, 2026-08
    93/100 stars

    Images

    1) Product Images from "Casein Kinase II Regulates N -Methyl- d -Aspartate Receptor Activity in Spinal Cords and Pain Hypersensitivity Induced by Nerve Injury"

    Article Title: Casein Kinase II Regulates N -Methyl- d -Aspartate Receptor Activity in Spinal Cords and Pain Hypersensitivity Induced by Nerve Injury

    Journal: The Journal of Pharmacology and Experimental Therapeutics

    doi: 10.1124/jpet.114.215855

    Sequences of two CK2 β -specific siRNAs and one control siRNA These siRNAs were conjugated to chitosan and then administered through intrathecal catheters in rats.
    Figure Legend Snippet: Sequences of two CK2 β -specific siRNAs and one control siRNA These siRNAs were conjugated to chitosan and then administered through intrathecal catheters in rats.

    Techniques Used: Control, Sequencing

    CK2 contributes to the increased NMDAR activity of spinal dorsal horn neurons caused by nerve injury. (A and B) Representative recordings (A) and mean changes (B) in the amplitude of evoked NMDAR-EPSCs and AMPAR-EPSCs of lamina II neurons in SNL rat spinal cord slices treated with vehicle (dimethylsulfoxide, n = 16 neurons), 100 μM DRB (n = 10 neurons), or 2 μM TBB (n = 10 neurons). (C and D) Representative recordings (C) and mean changes (D) in the amplitude of evoked NMDAR-EPSCs and AMPAR-EPSCs of lamina II neurons in control rat spinal slices treated with vehicle (n = 13 neurons) or 100 μM DRB (n = 11 neurons). *P < 0.05 compared with the vehicle control group. Error bars represent the S.E.M.
    Figure Legend Snippet: CK2 contributes to the increased NMDAR activity of spinal dorsal horn neurons caused by nerve injury. (A and B) Representative recordings (A) and mean changes (B) in the amplitude of evoked NMDAR-EPSCs and AMPAR-EPSCs of lamina II neurons in SNL rat spinal cord slices treated with vehicle (dimethylsulfoxide, n = 16 neurons), 100 μM DRB (n = 10 neurons), or 2 μM TBB (n = 10 neurons). (C and D) Representative recordings (C) and mean changes (D) in the amplitude of evoked NMDAR-EPSCs and AMPAR-EPSCs of lamina II neurons in control rat spinal slices treated with vehicle (n = 13 neurons) or 100 μM DRB (n = 11 neurons). *P < 0.05 compared with the vehicle control group. Error bars represent the S.E.M.

    Techniques Used: Activity Assay, Control

    CK2 plays a critical role in nerve injury–induced increase in the postsynaptic NMDAR activity of spinal dorsal horn neurons. (A and B) Original traces (A) and mean changes (B) in the NMDAR currents elicited by puff NMDA to lamina II neurons in SNL rat spinal slices treated with vehicle (dimethylsulfoxide, n = 19 neurons) or DRB (n = 23 neurons). (C) Summary data show AMPAR- and NMDAR-mediated mEPSCs of lamina II neurons in spinal cord slices treated with vehicle or DRB in sham control and SNL rats. *P < 0.05 compared with the vehicle control group. Error bars represent the S.E.M.
    Figure Legend Snippet: CK2 plays a critical role in nerve injury–induced increase in the postsynaptic NMDAR activity of spinal dorsal horn neurons. (A and B) Original traces (A) and mean changes (B) in the NMDAR currents elicited by puff NMDA to lamina II neurons in SNL rat spinal slices treated with vehicle (dimethylsulfoxide, n = 19 neurons) or DRB (n = 23 neurons). (C) Summary data show AMPAR- and NMDAR-mediated mEPSCs of lamina II neurons in spinal cord slices treated with vehicle or DRB in sham control and SNL rats. *P < 0.05 compared with the vehicle control group. Error bars represent the S.E.M.

    Techniques Used: Activity Assay, Control

    NMDAR activity of spinal dorsal horn neurons is dynamically controlled by CK2 and calcineurin. (A and B) Representative recordings (A) and mean changes (B) in the amplitude of evoked NMDAR-EPSCs and AMPAR-EPSCs of lamina II neurons in control rat spinal slices treated with vehicle (dimethylsulfoxide, n = 13 neurons), 1 μM FK-506 (n = 10 neurons), 0.1 μM okadaic acid (n = 12 neurons), FK-506 plus DRB (n = 10 neurons), or FK-506 plus TBB (n = 10 neurons). (C) Mean changes in the amplitude of evoked NMDAR-EPSCs and AMPAR-EPSCs of lamina II neurons in SNL rat spinal cord slices treated with vehicle (n = 16 neurons) or 1 μM FK-506 (n = 14 neurons). *P < 0.05 compared with the vehicle control group. Error bars represent the S.E.M.
    Figure Legend Snippet: NMDAR activity of spinal dorsal horn neurons is dynamically controlled by CK2 and calcineurin. (A and B) Representative recordings (A) and mean changes (B) in the amplitude of evoked NMDAR-EPSCs and AMPAR-EPSCs of lamina II neurons in control rat spinal slices treated with vehicle (dimethylsulfoxide, n = 13 neurons), 1 μM FK-506 (n = 10 neurons), 0.1 μM okadaic acid (n = 12 neurons), FK-506 plus DRB (n = 10 neurons), or FK-506 plus TBB (n = 10 neurons). (C) Mean changes in the amplitude of evoked NMDAR-EPSCs and AMPAR-EPSCs of lamina II neurons in SNL rat spinal cord slices treated with vehicle (n = 16 neurons) or 1 μM FK-506 (n = 14 neurons). *P < 0.05 compared with the vehicle control group. Error bars represent the S.E.M.

    Techniques Used: Activity Assay, Control

    Nerve injury increases CK2α and CK2β protein levels in the dorsal spinal cord. (A–C) Immunoblotting gel images (A) and quantification of CK2α (approximately 45 kDa) (B), and CK2β (approximately 25 kDa) (C) protein levels in the dorsal spinal cord ipsilateral to SNL and contralateral (sham) controls (n = 6 rats in each group). The dorsal spinal cord tissues were obtained 3, 7, 14, and 28 days after surgery. The CK2α and CK2β protein amounts were normalized to β-actin (loading controls) in each sample. *P < 0.05 compared with the contralateral control. Error bars represent the S.E.M.
    Figure Legend Snippet: Nerve injury increases CK2α and CK2β protein levels in the dorsal spinal cord. (A–C) Immunoblotting gel images (A) and quantification of CK2α (approximately 45 kDa) (B), and CK2β (approximately 25 kDa) (C) protein levels in the dorsal spinal cord ipsilateral to SNL and contralateral (sham) controls (n = 6 rats in each group). The dorsal spinal cord tissues were obtained 3, 7, 14, and 28 days after surgery. The CK2α and CK2β protein amounts were normalized to β-actin (loading controls) in each sample. *P < 0.05 compared with the contralateral control. Error bars represent the S.E.M.

    Techniques Used: Western Blot, Control

    Inhibition of CK2 and siRNA knockdown of CK2β expression at the spinal level reduces pain hypersensitivity induced by nerve injury. (A and B) Time course of the effects of intrathecal injection of 100, 200, and 500 ng TBB and vehicle (10% dimethylsulfoxide) on the withdrawal threshold measured with von Frey filaments (A) and a pressure stimulus (B) in rats 3 weeks after SNL or sham surgery (n = 7 to 8 rats per group). (C) Quantitative PCR analysis of CK2α and CK2β mRNA levels in the dorsal spinal cord ipsilateral (Ipsi) and contralateral (Cont) to nerve ligation of SNL rats treated with the two CK2β-specific siRNAs and a scramble control siRNA (n = 4 samples in each group). (D) Immunoblotting gel images (top) and mean changes (bottom) show the CK2β protein levels in the dorsal spinal cord of SNL rats treated with the two CK2β-specific siRNAs and a scramble control siRNA (n = 6 samples in each group). (E) Mean changes in the amplitude and ratio of NMDAR-EPSCs to AMPAR-EPSCs of lamina II neurons recorded from SNL rats treated with the scramble control siRNA (n = 11 neurons) or CK2β-specific siRNA (n = 12 neurons). (F and G) Changes in the paw withdrawal threshold measured with von Frey filaments (F) and a pressure stimulus (G) (n = 7 to 8 rats in each group) of SNL rats treated intrathecally with the two CK2β-specific siRNAs and a scramble control siRNA (n = 7 rats in each group). Threshold tests were performed before siRNA injection each day (indicated by arrows). *P < 0.05 compared with the respective predrug control or the control siRNA group. Error bars represent the S.E.M.
    Figure Legend Snippet: Inhibition of CK2 and siRNA knockdown of CK2β expression at the spinal level reduces pain hypersensitivity induced by nerve injury. (A and B) Time course of the effects of intrathecal injection of 100, 200, and 500 ng TBB and vehicle (10% dimethylsulfoxide) on the withdrawal threshold measured with von Frey filaments (A) and a pressure stimulus (B) in rats 3 weeks after SNL or sham surgery (n = 7 to 8 rats per group). (C) Quantitative PCR analysis of CK2α and CK2β mRNA levels in the dorsal spinal cord ipsilateral (Ipsi) and contralateral (Cont) to nerve ligation of SNL rats treated with the two CK2β-specific siRNAs and a scramble control siRNA (n = 4 samples in each group). (D) Immunoblotting gel images (top) and mean changes (bottom) show the CK2β protein levels in the dorsal spinal cord of SNL rats treated with the two CK2β-specific siRNAs and a scramble control siRNA (n = 6 samples in each group). (E) Mean changes in the amplitude and ratio of NMDAR-EPSCs to AMPAR-EPSCs of lamina II neurons recorded from SNL rats treated with the scramble control siRNA (n = 11 neurons) or CK2β-specific siRNA (n = 12 neurons). (F and G) Changes in the paw withdrawal threshold measured with von Frey filaments (F) and a pressure stimulus (G) (n = 7 to 8 rats in each group) of SNL rats treated intrathecally with the two CK2β-specific siRNAs and a scramble control siRNA (n = 7 rats in each group). Threshold tests were performed before siRNA injection each day (indicated by arrows). *P < 0.05 compared with the respective predrug control or the control siRNA group. Error bars represent the S.E.M.

    Techniques Used: Inhibition, Knockdown, Expressing, Injection, Real-time Polymerase Chain Reaction, Ligation, Control, Western Blot



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    mouse anti ck2 β primary antibody  (Santa Cruz Biotechnology)
    93
    Santa Cruz Biotechnology mouse anti ck2 β primary antibody
    Sequences of two <t> CK2 </t> β -specific siRNAs and one control siRNA These siRNAs were conjugated to chitosan and then administered through intrathecal catheters in rats.
    Mouse Anti Ck2 β Primary Antibody, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mouse+anti+ck2+%CE%B2+primary+antibody/pmc04109487-123-32-38?v=Santa+Cruz+Biotechnology
    Average 93 stars, based on 1 article reviews
    mouse anti ck2 β primary antibody - by Bioz Stars, 2026-08
    93/100 stars
    		  Buy from Supplier

    Image Search Results


    Sequences of two CK2 β -specific siRNAs and one control siRNA These siRNAs were conjugated to chitosan and then administered through intrathecal catheters in rats.

    Journal: The Journal of Pharmacology and Experimental Therapeutics

    Article Title: Casein Kinase II Regulates N -Methyl- d -Aspartate Receptor Activity in Spinal Cords and Pain Hypersensitivity Induced by Nerve Injury

    doi: 10.1124/jpet.114.215855

    Figure Lengend Snippet: Sequences of two CK2 β -specific siRNAs and one control siRNA These siRNAs were conjugated to chitosan and then administered through intrathecal catheters in rats.

    Article Snippet: The membrane was blocked for 30 minutes in 5% skim milk in phosphate-buffered saline containing 0.05% Tween-20 and then incubated with goat anti-CK2 α (sc-6476; Santa Cruz Biotechnology, Santa Cruz, CA) or mouse anti-CK2 β primary antibody (sc-46666; Santa Cruz Biotechnology) ( Ye et al., 2012 ) overnight at 4°C.

    Techniques: Control, Sequencing

    CK2 contributes to the increased NMDAR activity of spinal dorsal horn neurons caused by nerve injury. (A and B) Representative recordings (A) and mean changes (B) in the amplitude of evoked NMDAR-EPSCs and AMPAR-EPSCs of lamina II neurons in SNL rat spinal cord slices treated with vehicle (dimethylsulfoxide, n = 16 neurons), 100 μM DRB (n = 10 neurons), or 2 μM TBB (n = 10 neurons). (C and D) Representative recordings (C) and mean changes (D) in the amplitude of evoked NMDAR-EPSCs and AMPAR-EPSCs of lamina II neurons in control rat spinal slices treated with vehicle (n = 13 neurons) or 100 μM DRB (n = 11 neurons). *P < 0.05 compared with the vehicle control group. Error bars represent the S.E.M.

    Journal: The Journal of Pharmacology and Experimental Therapeutics

    Article Title: Casein Kinase II Regulates N -Methyl- d -Aspartate Receptor Activity in Spinal Cords and Pain Hypersensitivity Induced by Nerve Injury

    doi: 10.1124/jpet.114.215855

    Figure Lengend Snippet: CK2 contributes to the increased NMDAR activity of spinal dorsal horn neurons caused by nerve injury. (A and B) Representative recordings (A) and mean changes (B) in the amplitude of evoked NMDAR-EPSCs and AMPAR-EPSCs of lamina II neurons in SNL rat spinal cord slices treated with vehicle (dimethylsulfoxide, n = 16 neurons), 100 μM DRB (n = 10 neurons), or 2 μM TBB (n = 10 neurons). (C and D) Representative recordings (C) and mean changes (D) in the amplitude of evoked NMDAR-EPSCs and AMPAR-EPSCs of lamina II neurons in control rat spinal slices treated with vehicle (n = 13 neurons) or 100 μM DRB (n = 11 neurons). *P < 0.05 compared with the vehicle control group. Error bars represent the S.E.M.

    Article Snippet: The membrane was blocked for 30 minutes in 5% skim milk in phosphate-buffered saline containing 0.05% Tween-20 and then incubated with goat anti-CK2 α (sc-6476; Santa Cruz Biotechnology, Santa Cruz, CA) or mouse anti-CK2 β primary antibody (sc-46666; Santa Cruz Biotechnology) ( Ye et al., 2012 ) overnight at 4°C.

    Techniques: Activity Assay, Control

    CK2 plays a critical role in nerve injury–induced increase in the postsynaptic NMDAR activity of spinal dorsal horn neurons. (A and B) Original traces (A) and mean changes (B) in the NMDAR currents elicited by puff NMDA to lamina II neurons in SNL rat spinal slices treated with vehicle (dimethylsulfoxide, n = 19 neurons) or DRB (n = 23 neurons). (C) Summary data show AMPAR- and NMDAR-mediated mEPSCs of lamina II neurons in spinal cord slices treated with vehicle or DRB in sham control and SNL rats. *P < 0.05 compared with the vehicle control group. Error bars represent the S.E.M.

    Journal: The Journal of Pharmacology and Experimental Therapeutics

    Article Title: Casein Kinase II Regulates N -Methyl- d -Aspartate Receptor Activity in Spinal Cords and Pain Hypersensitivity Induced by Nerve Injury

    doi: 10.1124/jpet.114.215855

    Figure Lengend Snippet: CK2 plays a critical role in nerve injury–induced increase in the postsynaptic NMDAR activity of spinal dorsal horn neurons. (A and B) Original traces (A) and mean changes (B) in the NMDAR currents elicited by puff NMDA to lamina II neurons in SNL rat spinal slices treated with vehicle (dimethylsulfoxide, n = 19 neurons) or DRB (n = 23 neurons). (C) Summary data show AMPAR- and NMDAR-mediated mEPSCs of lamina II neurons in spinal cord slices treated with vehicle or DRB in sham control and SNL rats. *P < 0.05 compared with the vehicle control group. Error bars represent the S.E.M.

    Article Snippet: The membrane was blocked for 30 minutes in 5% skim milk in phosphate-buffered saline containing 0.05% Tween-20 and then incubated with goat anti-CK2 α (sc-6476; Santa Cruz Biotechnology, Santa Cruz, CA) or mouse anti-CK2 β primary antibody (sc-46666; Santa Cruz Biotechnology) ( Ye et al., 2012 ) overnight at 4°C.

    Techniques: Activity Assay, Control

    NMDAR activity of spinal dorsal horn neurons is dynamically controlled by CK2 and calcineurin. (A and B) Representative recordings (A) and mean changes (B) in the amplitude of evoked NMDAR-EPSCs and AMPAR-EPSCs of lamina II neurons in control rat spinal slices treated with vehicle (dimethylsulfoxide, n = 13 neurons), 1 μM FK-506 (n = 10 neurons), 0.1 μM okadaic acid (n = 12 neurons), FK-506 plus DRB (n = 10 neurons), or FK-506 plus TBB (n = 10 neurons). (C) Mean changes in the amplitude of evoked NMDAR-EPSCs and AMPAR-EPSCs of lamina II neurons in SNL rat spinal cord slices treated with vehicle (n = 16 neurons) or 1 μM FK-506 (n = 14 neurons). *P < 0.05 compared with the vehicle control group. Error bars represent the S.E.M.

    Journal: The Journal of Pharmacology and Experimental Therapeutics

    Article Title: Casein Kinase II Regulates N -Methyl- d -Aspartate Receptor Activity in Spinal Cords and Pain Hypersensitivity Induced by Nerve Injury

    doi: 10.1124/jpet.114.215855

    Figure Lengend Snippet: NMDAR activity of spinal dorsal horn neurons is dynamically controlled by CK2 and calcineurin. (A and B) Representative recordings (A) and mean changes (B) in the amplitude of evoked NMDAR-EPSCs and AMPAR-EPSCs of lamina II neurons in control rat spinal slices treated with vehicle (dimethylsulfoxide, n = 13 neurons), 1 μM FK-506 (n = 10 neurons), 0.1 μM okadaic acid (n = 12 neurons), FK-506 plus DRB (n = 10 neurons), or FK-506 plus TBB (n = 10 neurons). (C) Mean changes in the amplitude of evoked NMDAR-EPSCs and AMPAR-EPSCs of lamina II neurons in SNL rat spinal cord slices treated with vehicle (n = 16 neurons) or 1 μM FK-506 (n = 14 neurons). *P < 0.05 compared with the vehicle control group. Error bars represent the S.E.M.

    Article Snippet: The membrane was blocked for 30 minutes in 5% skim milk in phosphate-buffered saline containing 0.05% Tween-20 and then incubated with goat anti-CK2 α (sc-6476; Santa Cruz Biotechnology, Santa Cruz, CA) or mouse anti-CK2 β primary antibody (sc-46666; Santa Cruz Biotechnology) ( Ye et al., 2012 ) overnight at 4°C.

    Techniques: Activity Assay, Control

    Nerve injury increases CK2α and CK2β protein levels in the dorsal spinal cord. (A–C) Immunoblotting gel images (A) and quantification of CK2α (approximately 45 kDa) (B), and CK2β (approximately 25 kDa) (C) protein levels in the dorsal spinal cord ipsilateral to SNL and contralateral (sham) controls (n = 6 rats in each group). The dorsal spinal cord tissues were obtained 3, 7, 14, and 28 days after surgery. The CK2α and CK2β protein amounts were normalized to β-actin (loading controls) in each sample. *P < 0.05 compared with the contralateral control. Error bars represent the S.E.M.

    Journal: The Journal of Pharmacology and Experimental Therapeutics

    Article Title: Casein Kinase II Regulates N -Methyl- d -Aspartate Receptor Activity in Spinal Cords and Pain Hypersensitivity Induced by Nerve Injury

    doi: 10.1124/jpet.114.215855

    Figure Lengend Snippet: Nerve injury increases CK2α and CK2β protein levels in the dorsal spinal cord. (A–C) Immunoblotting gel images (A) and quantification of CK2α (approximately 45 kDa) (B), and CK2β (approximately 25 kDa) (C) protein levels in the dorsal spinal cord ipsilateral to SNL and contralateral (sham) controls (n = 6 rats in each group). The dorsal spinal cord tissues were obtained 3, 7, 14, and 28 days after surgery. The CK2α and CK2β protein amounts were normalized to β-actin (loading controls) in each sample. *P < 0.05 compared with the contralateral control. Error bars represent the S.E.M.

    Article Snippet: The membrane was blocked for 30 minutes in 5% skim milk in phosphate-buffered saline containing 0.05% Tween-20 and then incubated with goat anti-CK2 α (sc-6476; Santa Cruz Biotechnology, Santa Cruz, CA) or mouse anti-CK2 β primary antibody (sc-46666; Santa Cruz Biotechnology) ( Ye et al., 2012 ) overnight at 4°C.

    Techniques: Western Blot, Control

    Inhibition of CK2 and siRNA knockdown of CK2β expression at the spinal level reduces pain hypersensitivity induced by nerve injury. (A and B) Time course of the effects of intrathecal injection of 100, 200, and 500 ng TBB and vehicle (10% dimethylsulfoxide) on the withdrawal threshold measured with von Frey filaments (A) and a pressure stimulus (B) in rats 3 weeks after SNL or sham surgery (n = 7 to 8 rats per group). (C) Quantitative PCR analysis of CK2α and CK2β mRNA levels in the dorsal spinal cord ipsilateral (Ipsi) and contralateral (Cont) to nerve ligation of SNL rats treated with the two CK2β-specific siRNAs and a scramble control siRNA (n = 4 samples in each group). (D) Immunoblotting gel images (top) and mean changes (bottom) show the CK2β protein levels in the dorsal spinal cord of SNL rats treated with the two CK2β-specific siRNAs and a scramble control siRNA (n = 6 samples in each group). (E) Mean changes in the amplitude and ratio of NMDAR-EPSCs to AMPAR-EPSCs of lamina II neurons recorded from SNL rats treated with the scramble control siRNA (n = 11 neurons) or CK2β-specific siRNA (n = 12 neurons). (F and G) Changes in the paw withdrawal threshold measured with von Frey filaments (F) and a pressure stimulus (G) (n = 7 to 8 rats in each group) of SNL rats treated intrathecally with the two CK2β-specific siRNAs and a scramble control siRNA (n = 7 rats in each group). Threshold tests were performed before siRNA injection each day (indicated by arrows). *P < 0.05 compared with the respective predrug control or the control siRNA group. Error bars represent the S.E.M.

    Journal: The Journal of Pharmacology and Experimental Therapeutics

    Article Title: Casein Kinase II Regulates N -Methyl- d -Aspartate Receptor Activity in Spinal Cords and Pain Hypersensitivity Induced by Nerve Injury

    doi: 10.1124/jpet.114.215855

    Figure Lengend Snippet: Inhibition of CK2 and siRNA knockdown of CK2β expression at the spinal level reduces pain hypersensitivity induced by nerve injury. (A and B) Time course of the effects of intrathecal injection of 100, 200, and 500 ng TBB and vehicle (10% dimethylsulfoxide) on the withdrawal threshold measured with von Frey filaments (A) and a pressure stimulus (B) in rats 3 weeks after SNL or sham surgery (n = 7 to 8 rats per group). (C) Quantitative PCR analysis of CK2α and CK2β mRNA levels in the dorsal spinal cord ipsilateral (Ipsi) and contralateral (Cont) to nerve ligation of SNL rats treated with the two CK2β-specific siRNAs and a scramble control siRNA (n = 4 samples in each group). (D) Immunoblotting gel images (top) and mean changes (bottom) show the CK2β protein levels in the dorsal spinal cord of SNL rats treated with the two CK2β-specific siRNAs and a scramble control siRNA (n = 6 samples in each group). (E) Mean changes in the amplitude and ratio of NMDAR-EPSCs to AMPAR-EPSCs of lamina II neurons recorded from SNL rats treated with the scramble control siRNA (n = 11 neurons) or CK2β-specific siRNA (n = 12 neurons). (F and G) Changes in the paw withdrawal threshold measured with von Frey filaments (F) and a pressure stimulus (G) (n = 7 to 8 rats in each group) of SNL rats treated intrathecally with the two CK2β-specific siRNAs and a scramble control siRNA (n = 7 rats in each group). Threshold tests were performed before siRNA injection each day (indicated by arrows). *P < 0.05 compared with the respective predrug control or the control siRNA group. Error bars represent the S.E.M.

    Article Snippet: The membrane was blocked for 30 minutes in 5% skim milk in phosphate-buffered saline containing 0.05% Tween-20 and then incubated with goat anti-CK2 α (sc-6476; Santa Cruz Biotechnology, Santa Cruz, CA) or mouse anti-CK2 β primary antibody (sc-46666; Santa Cruz Biotechnology) ( Ye et al., 2012 ) overnight at 4°C.

    Techniques: Inhibition, Knockdown, Expressing, Injection, Real-time Polymerase Chain Reaction, Ligation, Control, Western Blot