phosphocreb ser 133 Search Results


rabbit anti phosphocreb 1 ser133  (Bioss)
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phosphocreb ser133  (Cell Signaling Technology Inc)
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Phosphocreb Ser133, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti phosphocreb ser133 antibodies  (Cell Signaling Technology Inc)
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phosphocreb ser 133  (Cell Signaling Technology Inc)
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Phosphocreb Ser 133, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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phosphocreb1 ser133 antibodies  (Cell Signaling Technology Inc)
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Phosphocreb1 Ser133 Antibodies, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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phosphocreb(ser 133) antibody  (Upstate Biotechnology Inc)
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phosphocreb ser133 analysis  (Cell Signaling Technology Inc)
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Figure 6. Protein kinase A (PKA) activity is increased by LY294002 and LY303511 and required for enhanced gap junctional intercellular communication (GJIC). A, immunofluorescence analysis of CREB phosphorylated at <t>Ser133</t> in MDA-MB-231 revealed an increase in phosphorylation after 2 hours treatment with LY294002 (10 mmol/L) and LY303511 (10 mmol/ L). B, analysis of CREB at Ser133 in nuclear extracts from MDA-MB- 231 treated with LY294002 (10 mmol/L) showed phosphorylation of CREB within 15 minutes. C, treatment with the PKA agonist 8- bromo cAMP (8-BR-cAMP; 0.1, 0.5, and 1.0 mmol/L) increased GJIC in a dose-dependent manner in MDA-MB-231. **, P < 0.01. Inhibition of PKA activity with H89 (10 mmol/L) when cotreated with LY294002 (10 mmol/L) inhibited GJIC compared with LY294002 alone (D, calcein; E, quantified, *, P < 0.05). Pretreatment of cells with the adenylate cyclase inhibitor 20,50-dideoxyadenosine (F) or SQ 22,536 (G) (10, 75, and 100 mmol/ L) did not reduce the ability of LY294002 (10 mmol/L) to increase GJIC. NT, nontreated.
Phosphocreb Ser133 Analysis, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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phosphorcreb  (Cell Signaling Technology Inc)
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Figure 6. Protein kinase A (PKA) activity is increased by LY294002 and LY303511 and required for enhanced gap junctional intercellular communication (GJIC). A, immunofluorescence analysis of CREB phosphorylated at <t>Ser133</t> in MDA-MB-231 revealed an increase in phosphorylation after 2 hours treatment with LY294002 (10 mmol/L) and LY303511 (10 mmol/ L). B, analysis of CREB at Ser133 in nuclear extracts from MDA-MB- 231 treated with LY294002 (10 mmol/L) showed phosphorylation of CREB within 15 minutes. C, treatment with the PKA agonist 8- bromo cAMP (8-BR-cAMP; 0.1, 0.5, and 1.0 mmol/L) increased GJIC in a dose-dependent manner in MDA-MB-231. **, P < 0.01. Inhibition of PKA activity with H89 (10 mmol/L) when cotreated with LY294002 (10 mmol/L) inhibited GJIC compared with LY294002 alone (D, calcein; E, quantified, *, P < 0.05). Pretreatment of cells with the adenylate cyclase inhibitor 20,50-dideoxyadenosine (F) or SQ 22,536 (G) (10, 75, and 100 mmol/ L) did not reduce the ability of LY294002 (10 mmol/L) to increase GJIC. NT, nontreated.
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phosphocreb (ser133  (Cell Signaling Technology Inc)
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Figure 6. Protein kinase A (PKA) activity is increased by LY294002 and LY303511 and required for enhanced gap junctional intercellular communication (GJIC). A, immunofluorescence analysis of CREB phosphorylated at <t>Ser133</t> in MDA-MB-231 revealed an increase in phosphorylation after 2 hours treatment with LY294002 (10 mmol/L) and LY303511 (10 mmol/ L). B, analysis of CREB at Ser133 in nuclear extracts from MDA-MB- 231 treated with LY294002 (10 mmol/L) showed phosphorylation of CREB within 15 minutes. C, treatment with the PKA agonist 8- bromo cAMP (8-BR-cAMP; 0.1, 0.5, and 1.0 mmol/L) increased GJIC in a dose-dependent manner in MDA-MB-231. **, P < 0.01. Inhibition of PKA activity with H89 (10 mmol/L) when cotreated with LY294002 (10 mmol/L) inhibited GJIC compared with LY294002 alone (D, calcein; E, quantified, *, P < 0.05). Pretreatment of cells with the adenylate cyclase inhibitor 20,50-dideoxyadenosine (F) or SQ 22,536 (G) (10, 75, and 100 mmol/ L) did not reduce the ability of LY294002 (10 mmol/L) to increase GJIC. NT, nontreated.
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phosphocreb (ser133) (87g3) rabbit mab 9198t antibody  (Cell Signaling Technology Inc)
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Figure 6. Protein kinase A (PKA) activity is increased by LY294002 and LY303511 and required for enhanced gap junctional intercellular communication (GJIC). A, immunofluorescence analysis of CREB phosphorylated at <t>Ser133</t> in MDA-MB-231 revealed an increase in phosphorylation after 2 hours treatment with LY294002 (10 mmol/L) and LY303511 (10 mmol/ L). B, analysis of CREB at Ser133 in nuclear extracts from MDA-MB- 231 treated with LY294002 (10 mmol/L) showed phosphorylation of CREB within 15 minutes. C, treatment with the PKA agonist 8- bromo cAMP (8-BR-cAMP; 0.1, 0.5, and 1.0 mmol/L) increased GJIC in a dose-dependent manner in MDA-MB-231. **, P < 0.01. Inhibition of PKA activity with H89 (10 mmol/L) when cotreated with LY294002 (10 mmol/L) inhibited GJIC compared with LY294002 alone (D, calcein; E, quantified, *, P < 0.05). Pretreatment of cells with the adenylate cyclase inhibitor 20,50-dideoxyadenosine (F) or SQ 22,536 (G) (10, 75, and 100 mmol/ L) did not reduce the ability of LY294002 (10 mmol/L) to increase GJIC. NT, nontreated.
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anti-phosphocreb-1 (ser 133)  (Santa Cruz Biotechnology)
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Figure 6. Protein kinase A (PKA) activity is increased by LY294002 and LY303511 and required for enhanced gap junctional intercellular communication (GJIC). A, immunofluorescence analysis of CREB phosphorylated at <t>Ser133</t> in MDA-MB-231 revealed an increase in phosphorylation after 2 hours treatment with LY294002 (10 mmol/L) and LY303511 (10 mmol/ L). B, analysis of CREB at Ser133 in nuclear extracts from MDA-MB- 231 treated with LY294002 (10 mmol/L) showed phosphorylation of CREB within 15 minutes. C, treatment with the PKA agonist 8- bromo cAMP (8-BR-cAMP; 0.1, 0.5, and 1.0 mmol/L) increased GJIC in a dose-dependent manner in MDA-MB-231. **, P < 0.01. Inhibition of PKA activity with H89 (10 mmol/L) when cotreated with LY294002 (10 mmol/L) inhibited GJIC compared with LY294002 alone (D, calcein; E, quantified, *, P < 0.05). Pretreatment of cells with the adenylate cyclase inhibitor 20,50-dideoxyadenosine (F) or SQ 22,536 (G) (10, 75, and 100 mmol/ L) did not reduce the ability of LY294002 (10 mmol/L) to increase GJIC. NT, nontreated.
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Image Search Results


Figure 6. Protein kinase A (PKA) activity is increased by LY294002 and LY303511 and required for enhanced gap junctional intercellular communication (GJIC). A, immunofluorescence analysis of CREB phosphorylated at Ser133 in MDA-MB-231 revealed an increase in phosphorylation after 2 hours treatment with LY294002 (10 mmol/L) and LY303511 (10 mmol/ L). B, analysis of CREB at Ser133 in nuclear extracts from MDA-MB- 231 treated with LY294002 (10 mmol/L) showed phosphorylation of CREB within 15 minutes. C, treatment with the PKA agonist 8- bromo cAMP (8-BR-cAMP; 0.1, 0.5, and 1.0 mmol/L) increased GJIC in a dose-dependent manner in MDA-MB-231. **, P < 0.01. Inhibition of PKA activity with H89 (10 mmol/L) when cotreated with LY294002 (10 mmol/L) inhibited GJIC compared with LY294002 alone (D, calcein; E, quantified, *, P < 0.05). Pretreatment of cells with the adenylate cyclase inhibitor 20,50-dideoxyadenosine (F) or SQ 22,536 (G) (10, 75, and 100 mmol/ L) did not reduce the ability of LY294002 (10 mmol/L) to increase GJIC. NT, nontreated.

Journal: Cancer Research

Article Title: Homotypic Gap Junctional Communication Associated with Metastasis Suppression Increases with PKA Activity and Is Unaffected by PI3K Inhibition

doi: 10.1158/0008-5472.can-10-2606

Figure Lengend Snippet: Figure 6. Protein kinase A (PKA) activity is increased by LY294002 and LY303511 and required for enhanced gap junctional intercellular communication (GJIC). A, immunofluorescence analysis of CREB phosphorylated at Ser133 in MDA-MB-231 revealed an increase in phosphorylation after 2 hours treatment with LY294002 (10 mmol/L) and LY303511 (10 mmol/ L). B, analysis of CREB at Ser133 in nuclear extracts from MDA-MB- 231 treated with LY294002 (10 mmol/L) showed phosphorylation of CREB within 15 minutes. C, treatment with the PKA agonist 8- bromo cAMP (8-BR-cAMP; 0.1, 0.5, and 1.0 mmol/L) increased GJIC in a dose-dependent manner in MDA-MB-231. **, P < 0.01. Inhibition of PKA activity with H89 (10 mmol/L) when cotreated with LY294002 (10 mmol/L) inhibited GJIC compared with LY294002 alone (D, calcein; E, quantified, *, P < 0.05). Pretreatment of cells with the adenylate cyclase inhibitor 20,50-dideoxyadenosine (F) or SQ 22,536 (G) (10, 75, and 100 mmol/ L) did not reduce the ability of LY294002 (10 mmol/L) to increase GJIC. NT, nontreated.

Article Snippet: For phosphoCREB Ser133 analysis, Alexa Fluor 488–conjugate antibody (#9187; Cell Signaling) was used.

Techniques: Activity Assay, Immunofluorescence, Phospho-proteomics, Inhibition