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camp dependent protein kinase inhibitor h89  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc camp dependent protein kinase inhibitor h89
    Camp Dependent Protein Kinase Inhibitor H89, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/camp+dependent+protein+kinase+inhibitor+h89/pka+inhibitor+h89/pm32445645-56-6-7
    Average 90 stars, based on 1 article reviews
    camp dependent protein kinase inhibitor h89 - by Bioz Stars, 2026-10
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    Article Title: ENT1 inhibition attenuates apoptosis by activation of cAMP/pCREB/Bcl2 pathway after MCAO in rats.
    Article Snippet: Background and purpose: The present study was designed to investigate the potential role and the mechanism of equilibrative nucleoside transporter 1 (ENT1) on neuronal apoptosis and neurological deficits after middle cerebral artery occlusion (MCAO) in rats.. Methods: One hundred and thirty-four male Sprague-Dawley rats were subjected to two hours of MCAO followed by reperfusion.. The time course of the expression level of ENT1 and phosphorylation of CREB were detected by western blot and immunofluorescence staining.



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    (A) Effect of <t>PKA</t> inhibitor on HSD3B2 expression in presence and absence of <t>8Br-cAMP</t> stimulation was assessed in NCI-R cells grown either under normal (GM) or starved (SM) conditions for 48 h. Expression was assessed by Western blot analysis using specific antibodies. β-actin served as loading control. Representative Western blots are shown. Quantitative results summarize three independent experiments (mean±SD). (B) HSD3B2 activity under PKA inhibition in presence and absence of 8Br-cAMP stimulation in NCI-R cells grown either in normal (GM) or starved (SM) conditions for 48 h. HSD3B2 activity for converting [3H]DHEA to [3H]androstenedione (%) was assessed. Steroids were extracted and resolved by TLC as depicted. Quantification of three independent experiments (mean±SD) is shown. * p<0.05.
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    (A) Effect of <t>PKA</t> inhibitor on HSD3B2 expression in presence and absence of <t>8Br-cAMP</t> stimulation was assessed in NCI-R cells grown either under normal (GM) or starved (SM) conditions for 48 h. Expression was assessed by Western blot analysis using specific antibodies. β-actin served as loading control. Representative Western blots are shown. Quantitative results summarize three independent experiments (mean±SD). (B) HSD3B2 activity under PKA inhibition in presence and absence of 8Br-cAMP stimulation in NCI-R cells grown either in normal (GM) or starved (SM) conditions for 48 h. HSD3B2 activity for converting [3H]DHEA to [3H]androstenedione (%) was assessed. Steroids were extracted and resolved by TLC as depicted. Quantification of three independent experiments (mean±SD) is shown. * p<0.05.
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    (A) Effect of <t>PKA</t> inhibitor on HSD3B2 expression in presence and absence of <t>8Br-cAMP</t> stimulation was assessed in NCI-R cells grown either under normal (GM) or starved (SM) conditions for 48 h. Expression was assessed by Western blot analysis using specific antibodies. β-actin served as loading control. Representative Western blots are shown. Quantitative results summarize three independent experiments (mean±SD). (B) HSD3B2 activity under PKA inhibition in presence and absence of 8Br-cAMP stimulation in NCI-R cells grown either in normal (GM) or starved (SM) conditions for 48 h. HSD3B2 activity for converting [3H]DHEA to [3H]androstenedione (%) was assessed. Steroids were extracted and resolved by TLC as depicted. Quantification of three independent experiments (mean±SD) is shown. * p<0.05.
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    (A) Effect of PKA inhibitor on HSD3B2 expression in presence and absence of 8Br-cAMP stimulation was assessed in NCI-R cells grown either under normal (GM) or starved (SM) conditions for 48 h. Expression was assessed by Western blot analysis using specific antibodies. β-actin served as loading control. Representative Western blots are shown. Quantitative results summarize three independent experiments (mean±SD). (B) HSD3B2 activity under PKA inhibition in presence and absence of 8Br-cAMP stimulation in NCI-R cells grown either in normal (GM) or starved (SM) conditions for 48 h. HSD3B2 activity for converting [3H]DHEA to [3H]androstenedione (%) was assessed. Steroids were extracted and resolved by TLC as depicted. Quantification of three independent experiments (mean±SD) is shown. * p<0.05.

    Journal: PLoS ONE

    Article Title: Differential Regulation of Human 3β-Hydroxysteroid Dehydrogenase Type 2 for Steroid Hormone Biosynthesis by Starvation and Cyclic Amp Stimulation: Studies in the Human Adrenal NCI-H295R Cell Model

    doi: 10.1371/journal.pone.0068691

    Figure Lengend Snippet: (A) Effect of PKA inhibitor on HSD3B2 expression in presence and absence of 8Br-cAMP stimulation was assessed in NCI-R cells grown either under normal (GM) or starved (SM) conditions for 48 h. Expression was assessed by Western blot analysis using specific antibodies. β-actin served as loading control. Representative Western blots are shown. Quantitative results summarize three independent experiments (mean±SD). (B) HSD3B2 activity under PKA inhibition in presence and absence of 8Br-cAMP stimulation in NCI-R cells grown either in normal (GM) or starved (SM) conditions for 48 h. HSD3B2 activity for converting [3H]DHEA to [3H]androstenedione (%) was assessed. Steroids were extracted and resolved by TLC as depicted. Quantification of three independent experiments (mean±SD) is shown. * p<0.05.

    Article Snippet: Eight-bromoadenosine 3′,5′-cyclic monophosphate (8Br-cAMP), PD98059 mitogen-activated kinase kinase (MEK) inhibitor, U0126 MEK inhibitor and H89 cAMP dependent protein kinase (PKA) inhibitor were purchased from Sigma-Aldrich (Buchs, Switzerland) and dissolved in DMSO.

    Techniques: Expressing, Western Blot, Activity Assay, Inhibition