- MA5-11192 - Invitrogen Antibodies CREB1 antibody

Submitted references Preventive Effect of Limosilactobacillus fermentum SCHY34 on Lead Acetate-Induced Neurological Damage in SD Rats.

Long X, Wu H, Zhou Y, Wan Y, Kan X, Gong J, Zhao X
Frontiers in nutrition 2022;9:852012

Disturbed flow-induced Gs-mediated signaling protects against endothelial inflammation and atherosclerosis.

Nakayama A, Albarrán-Juárez J, Liang G, Roquid KA, Iring A, Tonack S, Chen M, Müller OJ, Weinstein LS, Offermanns S
JCI insight 2020 Dec 3;5(23)

Human UCB-MSCs treatment upon intraventricular hemorrhage contributes to attenuate hippocampal neuron loss and circuit damage through BDNF-CREB signaling.

Ko HR, Ahn SY, Chang YS, Hwang I, Yun T, Sung DK, Sung SI, Park WS, Ahn JY
Stem cell research & therapy 2018 Nov 21;9(1):326

PKA-RII subunit phosphorylation precedes activation by cAMP and regulates activity termination.

Isensee J, Kaufholz M, Knape MJ, Hasenauer J, Hammerich H, Gonczarowska-Jorge H, Zahedi RP, Schwede F, Herberg FW, Hucho T
The Journal of cell biology 2018 Jun 4;217(6):2167-2184

Sinomenine attenuates cancer-induced bone pain via suppressing microglial JAK2/STAT3 and neuronal CAMKII/CREB cascades in rat models.

Chen SP, Sun J, Zhou YQ, Cao F, Braun C, Luo F, Ye DW, Tian YK
Molecular pain 2018 Jan-Dec;14:1744806918793232

GSK-3β deletion in dentate gyrus excitatory neuron impairs synaptic plasticity and memory.

Liu E, Xie AJ, Zhou Q, Li M, Zhang S, Li S, Wang W, Wang X, Wang Q, Wang JZ
Scientific reports 2017 Jul 18;7(1):5781

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Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 6 GSK-3beta deletion inhibits CaMKII/IV-CREB signaling. ( a,b ) GSK-3beta deletion decreased total and/or the phosphorylated levels of CaMKII, CaMKIV and CREB in DG extracts measured by Western blotting and the quantitative analyses. ( c ) The reduced intensity of pCREB in DG excitatory neurons was also shown by co-immunofluorescent staining. Scale bars, 100 mum. Data were presented as mean +- s.e.m. n = 4 each group, analyzed by unpaired t-test (*) or multiple t-tests (#). * P < 0.05, ** P < 0.01, *** < 0.001 versus Vector, ""#"" indicates that the difference is significant analyzed by multiple t-tests. the absence of asterix indicates that the difference is not significant.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 1 Knockdown of Galpha s increases endothelial inflammation induced by disturbed flow in BAECs. ( A - D ) Confluent BAECs were transfected with control siRNA or siRNA directed against Galpha s and were then exposed to oscillatory (osc.) flow for the indicated time period. p65 and/or CREB phosphorylation was analyzed by immunoblotting ( A and B , n = 3 independent experiments), cellular p65 localization was determined by staining of cells with an anti-p65 antibody ( C , n = 3 independent experiments, at least 3 view fields were analyzed per experiment), and inflammatory gene expression was analyzed by qPCR ( D , n = 4 independent experiments). The diagrams show the densitometric evaluation of p65 phosphorylation ( A and B ) or of nuclear p65 staining ( C ). Scale bar: 20 mum. ( E ) Confluent BAECs were incubated without or with the PKA-inhibitor PKI (1 muM). Inflammatory gene expression after osc. flow induction was analyzed ( n = 4 independent experiments). Data represent mean values +- SD; * P

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 2 Endothelial inflammation induced by disturbed flow is suppressed by cAMP-PKA signaling in HUVECs. ( A and B ) Confluent HUVECs were transfected with control siRNA or siRNA directed against Galpha s and were then exposed to oscillatory (osc.) flow for the indicated time periods. NF-kappaB (p65) phosphorylation, as well as CREB phosphorylation ( A ) or levels of IkappaBalpha ( B ), were determined by immunoblotting. The diagrams show the densitometric evaluation of immunoblots ( n = 3 independent experiments). ( C ) Control or Galpha s knockdown HUVECs were incubated without or with 50 muM db-cAMP for 30 minutes before induction of osc. flow (3 hours). Inflammatory gene expression was analyzed by qPCR ( n = 4 independent experiments). ( D ) Confluent HUVECs were incubated without or with the PKA-inhibitor PKI (1 muM), followed by induction of osc. flow, and inflammatory gene expression ( n = 4 independent experiments) was determined. Data represent mean values +- SD; * P

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 4 Adrenomedullin is released in response to oscillatory flow and activate antiinflammatory signaling though its receptor CALCRL. ( A and B ) Confluent BAECs were transfected with control siRNA (control) or siRNA directed against Galpha s , GPR146, or CALCRL. p65 and CREB phosphorylation before or after oscillatory (osc.) flow induction (15 minutes) were determined. Bar diagrams show the statistical evaluation of immunoblots ( n = 3 independent experiments). ( C ) Confluent BAECs were exposed to osc. flow for the indicated time periods. Thereafter, adrenomedullin concentration in the cell culture medium was determined ( n = 3 independent experiments). ( D and E ) Control, Galpha s -knockdown, or adrenomedullin-knockdown (ADM-knockdown) BAECs were exposed to osc. flow, and p65 phosphorylation was determined by immunoblotting. Bar diagrams show the statistical evaluation of immunoblots ( n = 4 independent experiments). Data represent mean +- SD; * P

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 1. cAMP induces pRII immunoreactivity in intact sensory neurons, but not cell lysates. (A) Representative HCS microscopy images of control (Ctrl; 0.1% DMSO) and 10 uM Fsk-stimulated (15 min) rat sensory neurons. Cultures were stained with UCHL1 to identify the neurons and pRII to quantify PKA-II signaling. Green/red encircled neurons indicate automatically selected/rejected objects. Bar, 100 um. (B) Time course of pRII intensity in sensory neurons after stimulation with Ctrl (0.1% DMSO), 10 uM Fsk, 10 uM Sp-8-Br-cAMPS-AM, or 200 nM 5-HT. (C) Time course of pCREB (Ser133) intensity. (D) Immunoblot of sensory neuron lysates probed with pRII and RIIbeta antibodies (left) and densitometry results (right). The pRII antibody recognized phosphorylated RIIalpha and RIIbeta. Stimulation with 10/100 uM Fsk/IBMX or 10 uM Sp-8-Br-cAMPS-AM for 15 min did not increase the pRII density. (E) Immunoblot and densitometry results of the same cell lysates probed with the pCREB antibody. (F and G) Time course of pRII intensity after stimulation with different doses of 1-10 uM Fsk or 5-200 nM 5-HT. (H and I) Pretreatment of sensory neurons with 4-25 uM H89 (30 min) did not inhibit the pRII response to 3 uM Fsk (H) or 200 nM 5-HT (I). (J and K) Pretreatment with 25 uM H89 (30 min) significantly inhibited the induction of CREB phosphorylation by 10 uM Fsk (H) or 200 nM 5-HT (K). (L and M) Pretreatment with H89 also inhibited the induction of ERK1/2 phosphorylation. HCS res

MA5-11192

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