rabbit polyclonal anti-creb serum (Upstate Biotechnology Inc)
90
Structured Review
Upstate Biotechnology Inc
rabbit polyclonal anti-creb serum
Rabbit Polyclonal Anti Creb Serum, supplied by Upstate Biotechnology 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/rabbit+polyclonal+anti-creb+serum/anti+caspase+3+antibody/pm15935216-55-55-73
Average 90 stars, based on 1 article reviews
Rabbit Polyclonal Anti Creb Serum, supplied by Upstate Biotechnology 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/rabbit+polyclonal+anti-creb+serum/anti+caspase+3+antibody/pm15935216-55-55-73
Average 90 stars, based on 1 article reviews
rabbit polyclonal anti-creb serum - by Bioz Stars,
2026-09
90/100 stars
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Membrane:Article Title: HIV-1 Tat protein down-regulates CREB transcription factor expression in PC12 neuronal cells through a phosphatidylinositol 3-kinase/AKT/cyclic nucleoside phosphodiesterase pathway. Article Snippet: The addition of low concentrations (0.1–1 nM) of extracellular HIV-1 Tat protein to PC12 neuronal cells stimulated a rapid (peak at 5 min) elevation of the cAMP intracellular levels, which in turn induced the phosphorylation of CREB transcription factor (peak at 15 min) on serine-133 (Ser-133).. On the contrary, at later time points (60–120 min) Tat induced a significant decline of intracellular cAMP with respect to the basal levels observed in control cells treated with bovine serum albumin.. In blocking experiments performed with pharmacological inhibitors, Tat decreased the intracellular levels of cAMP and CREB Ser-133 phosphorylation through a signal transduction pathway involving the sequential activation of phosphatidylinositol 3-kinase, AKT, and cyclic nucleoside phosphodiesterases. Article Title: Nitric Oxide Protects Neuroblastoma Cells from Apoptosis Induced by Serum Deprivation through cAMP-response Element-binding Protein (CREB) Activation Article Snippet: The gel was then blotted onto a nitrocellulose membrane, and equal loading of protein in each lane was assessed by brief staining of the blot with 0.1% Ponceau S. Blotted membranes were blocked for 1 h in a 4% suspension of dried skimmed milk in PBS and incubated overnight at 4 °C with the following: 1) a rabbit polyclonal anti-CREB serum; 2) a rabbit serum directed against the phosphorylated Ser133 form of Article Title: Neurochemical correlates of nicotine neurotoxicity on rat habenulo-interpeduncular cholinergic neurons. Article Snippet: Chronic administration of high doses of nicotine results in axonal degeneration in the central core of the fasciculus retroflexus, a fiber tract connecting the habenulae (Hb) to the interpeduncular nucleus (IPN).. An important part of this connection is cholinergic and neurons of origin are located in the medial Hb.. We have undertaken the present investigation in order to ascertain whether the cholinergic Hb–IPN neurons are the actual target of nicotine toxicity and to begin studying molecular correlates of this action. Staining:Article Title: HIV-1 Tat protein down-regulates CREB transcription factor expression in PC12 neuronal cells through a phosphatidylinositol 3-kinase/AKT/cyclic nucleoside phosphodiesterase pathway. Article Snippet: The addition of low concentrations (0.1–1 nM) of extracellular HIV-1 Tat protein to PC12 neuronal cells stimulated a rapid (peak at 5 min) elevation of the cAMP intracellular levels, which in turn induced the phosphorylation of CREB transcription factor (peak at 15 min) on serine-133 (Ser-133).. On the contrary, at later time points (60–120 min) Tat induced a significant decline of intracellular cAMP with respect to the basal levels observed in control cells treated with bovine serum albumin.. In blocking experiments performed with pharmacological inhibitors, Tat decreased the intracellular levels of cAMP and CREB Ser-133 phosphorylation through a signal transduction pathway involving the sequential activation of phosphatidylinositol 3-kinase, AKT, and cyclic nucleoside phosphodiesterases. Article Title: Nitric Oxide Protects Neuroblastoma Cells from Apoptosis Induced by Serum Deprivation through cAMP-response Element-binding Protein (CREB) Activation Article Snippet: The gel was then blotted onto a nitrocellulose membrane, and equal loading of protein in each lane was assessed by brief staining of the blot with 0.1% Ponceau S. Blotted membranes were blocked for 1 h in a 4% suspension of dried skimmed milk in PBS and incubated overnight at 4 °C with the following: 1) a rabbit polyclonal anti-CREB serum; 2) a rabbit serum directed against the phosphorylated Ser133 form of Article Title: Neurochemical correlates of nicotine neurotoxicity on rat habenulo-interpeduncular cholinergic neurons. Article Snippet: Chronic administration of high doses of nicotine results in axonal degeneration in the central core of the fasciculus retroflexus, a fiber tract connecting the habenulae (Hb) to the interpeduncular nucleus (IPN).. An important part of this connection is cholinergic and neurons of origin are located in the medial Hb.. We have undertaken the present investigation in order to ascertain whether the cholinergic Hb–IPN neurons are the actual target of nicotine toxicity and to begin studying molecular correlates of this action. Suspension:Article Title: HIV-1 Tat protein down-regulates CREB transcription factor expression in PC12 neuronal cells through a phosphatidylinositol 3-kinase/AKT/cyclic nucleoside phosphodiesterase pathway. Article Snippet: The addition of low concentrations (0.1–1 nM) of extracellular HIV-1 Tat protein to PC12 neuronal cells stimulated a rapid (peak at 5 min) elevation of the cAMP intracellular levels, which in turn induced the phosphorylation of CREB transcription factor (peak at 15 min) on serine-133 (Ser-133).. On the contrary, at later time points (60–120 min) Tat induced a significant decline of intracellular cAMP with respect to the basal levels observed in control cells treated with bovine serum albumin.. In blocking experiments performed with pharmacological inhibitors, Tat decreased the intracellular levels of cAMP and CREB Ser-133 phosphorylation through a signal transduction pathway involving the sequential activation of phosphatidylinositol 3-kinase, AKT, and cyclic nucleoside phosphodiesterases. Article Title: Nitric Oxide Protects Neuroblastoma Cells from Apoptosis Induced by Serum Deprivation through cAMP-response Element-binding Protein (CREB) Activation Article Snippet: The gel was then blotted onto a nitrocellulose membrane, and equal loading of protein in each lane was assessed by brief staining of the blot with 0.1% Ponceau S. Blotted membranes were blocked for 1 h in a 4% suspension of dried skimmed milk in PBS and incubated overnight at 4 °C with the following: 1) a rabbit polyclonal anti-CREB serum; 2) a rabbit serum directed against the phosphorylated Ser133 form of Article Title: Neurochemical correlates of nicotine neurotoxicity on rat habenulo-interpeduncular cholinergic neurons. Article Snippet: Chronic administration of high doses of nicotine results in axonal degeneration in the central core of the fasciculus retroflexus, a fiber tract connecting the habenulae (Hb) to the interpeduncular nucleus (IPN).. An important part of this connection is cholinergic and neurons of origin are located in the medial Hb.. We have undertaken the present investigation in order to ascertain whether the cholinergic Hb–IPN neurons are the actual target of nicotine toxicity and to begin studying molecular correlates of this action. Incubation:Article Title: HIV-1 Tat protein down-regulates CREB transcription factor expression in PC12 neuronal cells through a phosphatidylinositol 3-kinase/AKT/cyclic nucleoside phosphodiesterase pathway. Article Snippet: The addition of low concentrations (0.1–1 nM) of extracellular HIV-1 Tat protein to PC12 neuronal cells stimulated a rapid (peak at 5 min) elevation of the cAMP intracellular levels, which in turn induced the phosphorylation of CREB transcription factor (peak at 15 min) on serine-133 (Ser-133).. On the contrary, at later time points (60–120 min) Tat induced a significant decline of intracellular cAMP with respect to the basal levels observed in control cells treated with bovine serum albumin.. In blocking experiments performed with pharmacological inhibitors, Tat decreased the intracellular levels of cAMP and CREB Ser-133 phosphorylation through a signal transduction pathway involving the sequential activation of phosphatidylinositol 3-kinase, AKT, and cyclic nucleoside phosphodiesterases. Article Title: Nitric Oxide Protects Neuroblastoma Cells from Apoptosis Induced by Serum Deprivation through cAMP-response Element-binding Protein (CREB) Activation Article Snippet: The gel was then blotted onto a nitrocellulose membrane, and equal loading of protein in each lane was assessed by brief staining of the blot with 0.1% Ponceau S. Blotted membranes were blocked for 1 h in a 4% suspension of dried skimmed milk in PBS and incubated overnight at 4 °C with the following: 1) a rabbit polyclonal anti-CREB serum; 2) a rabbit serum directed against the phosphorylated Ser133 form of Article Title: Neurochemical correlates of nicotine neurotoxicity on rat habenulo-interpeduncular cholinergic neurons. Article Snippet: Chronic administration of high doses of nicotine results in axonal degeneration in the central core of the fasciculus retroflexus, a fiber tract connecting the habenulae (Hb) to the interpeduncular nucleus (IPN).. An important part of this connection is cholinergic and neurons of origin are located in the medial Hb.. We have undertaken the present investigation in order to ascertain whether the cholinergic Hb–IPN neurons are the actual target of nicotine toxicity and to begin studying molecular correlates of this action. |