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(A) Venn diagram showing overlap of B cell-specific CREB1 and CREBBP ChIP-seq targets. All targets identified in each dataset were used to determine overlap, and the top 1,500 common targets were selected for downstream analyses. (B) RNA expression data from the TCGA MDACC B-cell malignancies cohort. Heatmaps showing correlations between OSTM1, CREB1, or PDE3B mRNA levels and the top 1,500 CREB1/CREBBP co-occupied target genes identified in ( A ). (C) Venn diagrams showing overlap among genes significantly correlated with OSTM1, CREB1, or PDE3B within the top 1,500 CREB1/CREBBP targets. As OSTM1 negatively regulates PDE3B, genes positively correlated with OSTM1 and CREB1 expression and negatively correlated with PDE3B expression showed substantial overlap (78.2%). Conversely, genes negatively correlated with OSTM1 and CREB1 expression and positively correlated with PDE3B expression also overlapped significantly (66.8%). (D) CRISPR gene-effect scores from the CCLE database for OSTM1 and PDE3B across BCL lines, showing generally negative effects upon PDE3B silencing and positive effects upon OSTM1 silencing. (E) Pde3b was silenced by sgRNA in sg Ostm1 clone #3 Ba/F3 cells. PDE3B protein levels were determined by IB, and sg Ostm1/Pde3b double knockout (DKO) Ba/F3 cells were selected for subsequent experiments. (F) sgControl, sg Ostm1 , and DKO Ba/F3 cells were cutured in the presense or absence of IL3. Pde3b silencing reversed IL3-independence in sg Ostm1 cells. (G) GFP-expressing sg Ostm1 or DKO Ba/F3 cells were transplanted into nude mice via i.p. injection. Mice were harvested at the endpoint of the sg Ostm1 cohort. Spleens and livers were photographed and weighed. P values were calculated using Student’s t-test. GFP-positive tumor cells were detected only in sg Ostm1 recipients, but not in DKO recipients. (H) qRT-PCR in sgControl and sg Ostm1 Ba/F3 cells showing that Ostm1 silencing reduced expression of PKA/CREB/CREBBP target genes. (I) sgCtrl, sg Ostm1 , and DKO Ba/F3 cells were probed for phospho-PKA substrates and phospho-CREB <t>(Ser133).</t> (J) OSTM1 was silenced using two independent sgRNAs in SU-DHL-5 cells. Left: qPCR validation of OSTM1 knockout using on-target primers. Right: IB showing stablization of PDE3B and downregulation of cAMP/PKA signaling upon OSTM1 deletion. (K) OSTM1 was silenced in ARH-77 cells. IB of two clones shows increased PDE3B protein levles and decreased cAMP/PKA signaling upon OSTM1 silencing. (L) PDE3B-His was stably expressed in SU-DHL-10 cell line, which suppressed cAMP/PKA signaling. (M) OSTM1-Flag or OSTM1Δ31-Flag was stably expressed in OPM2 and RPMI-8226 cells. IB shows that OSTM1Δ31, but not the full-length OSTM1, promoted PDE3B degradation and enhanced cAMP/PKA signaling. (N) IB of whole-spleen lysates from indicated age-matched mice collected at the endpoints of O +/- ;C -/- or DKO cohorts. Phosphorylation levels of CREB and PKA substrates were generally reduced in the O -/- , O +/- C -/- , and DKO mice. (O) Bulk RNA-seq of purified splenic B cells from the indicated genotypes (as in ). Genes up-or down-regulated in DKO versus C -/- mice were intersected with the CREB1/CREBBP ChIP-seq targets identified in (A) . (P) Spleens from two-month-old C -/- and DKO mice were harvested, and 10,000 cells per mouse were analyzed by scRNA-seq. UMAP plots of B-cell subpopulations are shown by genotype. Bar graphs show the relative proportions of B-cell subsets. (Q) Genes down-regulated in DKO vs C -/- B cells, as identified by both bulk RNA-seq of splenic B cells and scRNA-seq of follicular B cells, were intersected with CREB1/CREBBP targets. Eight genes were commonly identified across all 4 datasets.

P Creb Ser133 87g3, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 2141 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "OSTM1 is a ubiquitin E3 ligase that suppresses B-cell malignancy by activating the cAMP/PKA/CREB pathway"

Article Title: OSTM1 is a ubiquitin E3 ligase that suppresses B-cell malignancy by activating the cAMP/PKA/CREB pathway

Journal: bioRxiv

doi: 10.64898/2026.01.23.701155

Figure Legend Snippet: (A) Venn diagram showing overlap of B cell-specific CREB1 and CREBBP ChIP-seq targets. All targets identified in each dataset were used to determine overlap, and the top 1,500 common targets were selected for downstream analyses. (B) RNA expression data from the TCGA MDACC B-cell malignancies cohort. Heatmaps showing correlations between OSTM1, CREB1, or PDE3B mRNA levels and the top 1,500 CREB1/CREBBP co-occupied target genes identified in ( A ). (C) Venn diagrams showing overlap among genes significantly correlated with OSTM1, CREB1, or PDE3B within the top 1,500 CREB1/CREBBP targets. As OSTM1 negatively regulates PDE3B, genes positively correlated with OSTM1 and CREB1 expression and negatively correlated with PDE3B expression showed substantial overlap (78.2%). Conversely, genes negatively correlated with OSTM1 and CREB1 expression and positively correlated with PDE3B expression also overlapped significantly (66.8%). (D) CRISPR gene-effect scores from the CCLE database for OSTM1 and PDE3B across BCL lines, showing generally negative effects upon PDE3B silencing and positive effects upon OSTM1 silencing. (E) Pde3b was silenced by sgRNA in sg Ostm1 clone #3 Ba/F3 cells. PDE3B protein levels were determined by IB, and sg Ostm1/Pde3b double knockout (DKO) Ba/F3 cells were selected for subsequent experiments. (F) sgControl, sg Ostm1 , and DKO Ba/F3 cells were cutured in the presense or absence of IL3. Pde3b silencing reversed IL3-independence in sg Ostm1 cells. (G) GFP-expressing sg Ostm1 or DKO Ba/F3 cells were transplanted into nude mice via i.p. injection. Mice were harvested at the endpoint of the sg Ostm1 cohort. Spleens and livers were photographed and weighed. P values were calculated using Student’s t-test. GFP-positive tumor cells were detected only in sg Ostm1 recipients, but not in DKO recipients. (H) qRT-PCR in sgControl and sg Ostm1 Ba/F3 cells showing that Ostm1 silencing reduced expression of PKA/CREB/CREBBP target genes. (I) sgCtrl, sg Ostm1 , and DKO Ba/F3 cells were probed for phospho-PKA substrates and phospho-CREB (Ser133). (J) OSTM1 was silenced using two independent sgRNAs in SU-DHL-5 cells. Left: qPCR validation of OSTM1 knockout using on-target primers. Right: IB showing stablization of PDE3B and downregulation of cAMP/PKA signaling upon OSTM1 deletion. (K) OSTM1 was silenced in ARH-77 cells. IB of two clones shows increased PDE3B protein levles and decreased cAMP/PKA signaling upon OSTM1 silencing. (L) PDE3B-His was stably expressed in SU-DHL-10 cell line, which suppressed cAMP/PKA signaling. (M) OSTM1-Flag or OSTM1Δ31-Flag was stably expressed in OPM2 and RPMI-8226 cells. IB shows that OSTM1Δ31, but not the full-length OSTM1, promoted PDE3B degradation and enhanced cAMP/PKA signaling. (N) IB of whole-spleen lysates from indicated age-matched mice collected at the endpoints of O +/- ;C -/- or DKO cohorts. Phosphorylation levels of CREB and PKA substrates were generally reduced in the O -/- , O +/- C -/- , and DKO mice. (O) Bulk RNA-seq of purified splenic B cells from the indicated genotypes (as in ). Genes up-or down-regulated in DKO versus C -/- mice were intersected with the CREB1/CREBBP ChIP-seq targets identified in (A) . (P) Spleens from two-month-old C -/- and DKO mice were harvested, and 10,000 cells per mouse were analyzed by scRNA-seq. UMAP plots of B-cell subpopulations are shown by genotype. Bar graphs show the relative proportions of B-cell subsets. (Q) Genes down-regulated in DKO vs C -/- B cells, as identified by both bulk RNA-seq of splenic B cells and scRNA-seq of follicular B cells, were intersected with CREB1/CREBBP targets. Eight genes were commonly identified across all 4 datasets.

Techniques Used: ChIP-sequencing, RNA Expression, Expressing, CRISPR, Double Knockout, Injection, Quantitative RT-PCR, Biomarker Discovery, Knock-Out, Clone Assay, Stable Transfection, Phospho-proteomics, RNA Sequencing, Purification

Membrane:

Article Title: Transcriptomic and epigenomic consequences of heterozygous loss-of-function mutations in AKAP11, a shared risk gene for bipolar disorder and schizophrenia.
Article Snippet: The gene A-kinase anchoring protein 11 (AKAP11) recently emerged as a shared risk factor between bipolar disorder and schizophrenia, driven by large-effect loss-of-function (LoF) variants.. Recent research has uncovered the neurophysiological characteristics and synapse proteomics profile of Akap11-mutant mouse models.. Considering the role of AKAP11 in binding cAMPdependent protein kinase A (PKA) and mediating phosphorylation of numerous substrates, such as transcription factors and epigenetic regulators, and given that chromatin alterations have been implicated in the brains of patients with bipolar disorder and schizophrenia, it is crucial to uncover the transcriptomic and chromatin dysregulations following the heterozygous knockout of AKAP11, particularly in human neurons.

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Article Title: Comparative analysis of ERK and CREB activity in normal and cryptorchid testes of bulls.
Article Snippet: After antigen retrieval, sections were treated with 0.3% (v/v) hydrogen peroxide in distilled water for 20 min to quench endogenous peroxidase activity, followed by blocking with 1% (v/v) normal goat serum (NGS) (S-1000; Vector Laboratories) and 0.5% (v/v) bovine serum albumin (BSA) (A9647; Sigma-Aldrich, USA) in phosphate-buffered saline (PBS). .. Phospho-p44/42 mitogen-activated protein kinase (MAPK) (Erk1/2) (Thr202/Tyr204) (20G11) Rabbit mAb (1:100 dilution, 4370S; Cell Signaling Technology), Phospho-CREB (Ser133) (87G3) Rabbit mAb (1:200 dilution, 9198S; Cell Signaling Technology), or mouse antivimentin (1:200 dilution, Clone V9; Neomarkers, USA) was added to antibody diluent (003218; Life Technologies, USA) and incubated overnight at 4°C. .. After three washes in PBS with Tween 20, the sections were incubated in anti-Mouse Secondary Antibody, Alexa Fluor 488 (1:500 dilution, A28175; Thermo Fisher Scientific, USA) or anti-Rabbit Secondary Antibody Alexa Fluor Plus 594 (1:500 dilution, A32754; Thermo Fisher Scientific) in blocking solution for 2 h at room temperature.

Article Title: Bisphenol S causes excessive estrogen synthesis by activating FSHR and the downstream cAMP/PKA signaling pathway.
Article Snippet: The cell lysatewas electrophoresed on 10% SDS-PAGE gel and then transferred onto polyvinylidene fluoride membrane (MerckMillipore,Darmstadt,Germany). .. Themembranewas blocked with 5% nonfat dry milk solution, incubated with primary antibodies (Phospho-CREB (Ser133) (87G3) Rabbit mAb, CST, Danvers, MA, USA, 1:500, CREB (48H2) Rabbit mAb, CST, Danvers, MA, USA, 1:500, ADCY against mole ratio of BPS/FSHR. .. Communications Biology | (2024) 7:844 8 Rabbit pAb, Abclonal, Wuhan, China, 1:1000, CYP11A1 Rabbit mAb, Abclonal,Wuhan,China, 1:1000 orGAPDHRabbit pAb,Abbkine,Wuhan, China, 1:10,000) at 4 °C overnight, and incubated with secondary antibody (HRP Goat Anti-Rabbit lgG, Abbkine, Wuhan, China, 1:10,000) at room temperature for 1 h. Immunoblot membrane was developed with Ultrasensitive ECL Chemiluminescence Kit (Beyotime, Shanghai, China).

Article Title: Comparative analysis of ERK and CREB activity in normal and cryptorchid testes of bulls
Article Snippet: After antigen retrieval, sections were treated with 0.3% (v/v) hydrogen peroxide in distilled water for 20 min to quench endogenous peroxidase activity, followed by blocking with 1% (v/v) normal goat serum (NGS) (S-1000; Vector Laboratories) and 0.5% (v/v) bovine serum albumin (BSA) (A9647; Sigma-Aldrich, USA) in phosphate-buffered saline (PBS). .. Phospho-p44/42 mitogen-activated protein kinase (MAPK) (Erk1/2) (Thr202/Tyr204) (20G11) Rabbit mAb (1:100 dilution, 4370S; Cell Signaling Technology), Phospho-CREB (Ser133) (87G3) Rabbit mAb (1:200 dilution, 9198S; Cell Signaling Technology), or mouse anti-vimentin (1:200 dilution, Clone V9; Neomarkers, USA) was added to antibody diluent (003218; Life Technologies, USA) and incubated overnight at 4°C. .. After three washes in PBS with Tween 20, the sections were incubated in anti-Mouse Secondary Antibody, Alexa Fluor 488 (1:500 dilution, A28175; Thermo Fisher Scientific, USA) or anti-Rabbit Secondary Antibody Alexa Fluor Plus 594 (1:500 dilution, A32754; Thermo Fisher Scientific) in blocking solution for 2 h at room temperature.

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Journal: bioRxiv

Article Title: OSTM1 is a ubiquitin E3 ligase that suppresses B-cell malignancy by activating the cAMP/PKA/CREB pathway

doi: 10.64898/2026.01.23.701155

Figure Lengend Snippet: (A) Venn diagram showing overlap of B cell-specific CREB1 and CREBBP ChIP-seq targets. All targets identified in each dataset were used to determine overlap, and the top 1,500 common targets were selected for downstream analyses. (B) RNA expression data from the TCGA MDACC B-cell malignancies cohort. Heatmaps showing correlations between OSTM1, CREB1, or PDE3B mRNA levels and the top 1,500 CREB1/CREBBP co-occupied target genes identified in ( A ). (C) Venn diagrams showing overlap among genes significantly correlated with OSTM1, CREB1, or PDE3B within the top 1,500 CREB1/CREBBP targets. As OSTM1 negatively regulates PDE3B, genes positively correlated with OSTM1 and CREB1 expression and negatively correlated with PDE3B expression showed substantial overlap (78.2%). Conversely, genes negatively correlated with OSTM1 and CREB1 expression and positively correlated with PDE3B expression also overlapped significantly (66.8%). (D) CRISPR gene-effect scores from the CCLE database for OSTM1 and PDE3B across BCL lines, showing generally negative effects upon PDE3B silencing and positive effects upon OSTM1 silencing. (E) Pde3b was silenced by sgRNA in sg Ostm1 clone #3 Ba/F3 cells. PDE3B protein levels were determined by IB, and sg Ostm1/Pde3b double knockout (DKO) Ba/F3 cells were selected for subsequent experiments. (F) sgControl, sg Ostm1 , and DKO Ba/F3 cells were cutured in the presense or absence of IL3. Pde3b silencing reversed IL3-independence in sg Ostm1 cells. (G) GFP-expressing sg Ostm1 or DKO Ba/F3 cells were transplanted into nude mice via i.p. injection. Mice were harvested at the endpoint of the sg Ostm1 cohort. Spleens and livers were photographed and weighed. P values were calculated using Student’s t-test. GFP-positive tumor cells were detected only in sg Ostm1 recipients, but not in DKO recipients. (H) qRT-PCR in sgControl and sg Ostm1 Ba/F3 cells showing that Ostm1 silencing reduced expression of PKA/CREB/CREBBP target genes. (I) sgCtrl, sg Ostm1 , and DKO Ba/F3 cells were probed for phospho-PKA substrates and phospho-CREB (Ser133). (J) OSTM1 was silenced using two independent sgRNAs in SU-DHL-5 cells. Left: qPCR validation of OSTM1 knockout using on-target primers. Right: IB showing stablization of PDE3B and downregulation of cAMP/PKA signaling upon OSTM1 deletion. (K) OSTM1 was silenced in ARH-77 cells. IB of two clones shows increased PDE3B protein levles and decreased cAMP/PKA signaling upon OSTM1 silencing. (L) PDE3B-His was stably expressed in SU-DHL-10 cell line, which suppressed cAMP/PKA signaling. (M) OSTM1-Flag or OSTM1Δ31-Flag was stably expressed in OPM2 and RPMI-8226 cells. IB shows that OSTM1Δ31, but not the full-length OSTM1, promoted PDE3B degradation and enhanced cAMP/PKA signaling. (N) IB of whole-spleen lysates from indicated age-matched mice collected at the endpoints of O +/- ;C -/- or DKO cohorts. Phosphorylation levels of CREB and PKA substrates were generally reduced in the O -/- , O +/- C -/- , and DKO mice. (O) Bulk RNA-seq of purified splenic B cells from the indicated genotypes (as in ). Genes up-or down-regulated in DKO versus C -/- mice were intersected with the CREB1/CREBBP ChIP-seq targets identified in (A) . (P) Spleens from two-month-old C -/- and DKO mice were harvested, and 10,000 cells per mouse were analyzed by scRNA-seq. UMAP plots of B-cell subpopulations are shown by genotype. Bar graphs show the relative proportions of B-cell subsets. (Q) Genes down-regulated in DKO vs C -/- B cells, as identified by both bulk RNA-seq of splenic B cells and scRNA-seq of follicular B cells, were intersected with CREB1/CREBBP targets. Eight genes were commonly identified across all 4 datasets.

Article Snippet: Flag-M2 (Millipore Sigma, F1804), Flag (Millipore Sigma, F7425), 6X-His (Thermo Fisher Scientific, MA1-21315), p-AKT Ser-473 (Cell Signaling Technology, 4060), t-AKT (Cell Signaling Technology, 9272), GAPDH (ProteinTech, 10494-1-AP), p-S6 Ser235/236 (Cell Signaling Technology, 4858), t-S6 (Cell Signaling Technology, 2217), p-STAT5 Y694 (Cell Signaling Technology, 9359), t-STAT5 (Cell Signaling Technology, 25656), p-p44/42 MAPK (Erk1/2) Thr202/Tyr204 (Cell Signaling Technology, 4376), t-p44/42 MAPK (Erk1/2) (Cell Signaling Technology, 9102), PDE3B (SMCP3B) (used for IB) (Novus Biologicals, NBP1-43333), PDE3B (used for IP) (Abcam, ab99290), Ubiquitin (P37) (Cell Signaling Technology, 58395), LC3B (Cell Signaling Technology, 2775), K48-linkage specific polyubiquitin (D9D5) (Cell Signaling Technology, 8081), GFP (Santa Cruz, sc-8334), BiP/GRP78 (BD Biosciences, 610978), calnexin (Transduction Labs, C45520-050), CLC7 (Thermo Fisher, A305-381A-T), p-CREB Ser133 (87G3) (Cell Signaling Technology, 9198), t-CREB (48H2) (Cell Signaling Technology, 9197), p-(Ser/Thr) PKA substrates (Cell Signaling Technology, 9621), OSTM1 (Millipore Sigma, ABN1365), goat anti-mouse IgG (H+L) cross-adsorbed secondary antibody, Alexa Fluor 680 (Thermo Fisher, A-21057), goat anti-rabbit IgG (H+L) cross-adsorbed secondary antibody, Alexa FluorTM 594 (Thermo Fisher, A11012), goat anti-rabbit IgG (H+L) cross-adsorbed secondary antibody, Alexa Fluor 488 (Thermo Fisher, A11008), goat anti-rabbit secondary antibody (LI-COR, 926-32211), goat anti-rat secondary antibody for 680 channel (Thermo Fisher, A-21096)

Techniques: ChIP-sequencing, RNA Expression, Expressing, CRISPR, Double Knockout, Injection, Quantitative RT-PCR, Biomarker Discovery, Knock-Out, Clone Assay, Stable Transfection, Phospho-proteomics, RNA Sequencing, Purification

Effect of Selinexor on MGMT expression and phosphorylation of serine 133 of CREBB protein (p-CREBB S133 ). T98G, GBM43, GBM14 and GBM6, cells were treated with the indicated concentrations of Selinexor, and protein lysates were used for western blotting evaluation of (A) MGMT expression and (B) phosphorylation of serine 133 of CREBB protein (p-CREBB S133 ). (C) Western blotting showing the effect of PKA inhibitor H89 on Selinexor-induced MGMT and p-CREBB S133 . (D) qRT-PCR displaying MGMT and XPO1 mRNA in GBM6 cells treated with the indicated concentration of selinexor. (E) The ChIP assay showed the increased trimethylation of lysine 4 of histone H3 (H3K4me3) within the MGMT promoter region of GBM6 when treated with Selinexor. Data in (D, E) are presented as mean ± SEM from n = 3 independent biological replicates, each performed in technical triplicates. Statistical significance was determined using a one-way ANOVA with Tukey’s multiple comparison test. Error bars represent SEM. Representative western blots in (A–C) are shown from n = 3 independent experiments.

Journal: Frontiers in Oncology

Article Title: XPO1-inhibitor Selinexor induces MGMT expression by activating PKA-CREB signaling in IDH wildtype glioblastoma

doi: 10.3389/fonc.2025.1633580

Figure Lengend Snippet: Effect of Selinexor on MGMT expression and phosphorylation of serine 133 of CREBB protein (p-CREBB S133 ). T98G, GBM43, GBM14 and GBM6, cells were treated with the indicated concentrations of Selinexor, and protein lysates were used for western blotting evaluation of (A) MGMT expression and (B) phosphorylation of serine 133 of CREBB protein (p-CREBB S133 ). (C) Western blotting showing the effect of PKA inhibitor H89 on Selinexor-induced MGMT and p-CREBB S133 . (D) qRT-PCR displaying MGMT and XPO1 mRNA in GBM6 cells treated with the indicated concentration of selinexor. (E) The ChIP assay showed the increased trimethylation of lysine 4 of histone H3 (H3K4me3) within the MGMT promoter region of GBM6 when treated with Selinexor. Data in (D, E) are presented as mean ± SEM from n = 3 independent biological replicates, each performed in technical triplicates. Statistical significance was determined using a one-way ANOVA with Tukey’s multiple comparison test. Error bars represent SEM. Representative western blots in (A–C) are shown from n = 3 independent experiments.

Article Snippet: The primary antibodies included XPO1 (Exporitin-1/CRM1 (D6V7N) rabbit mAb, Cell signaling cat# 46249S), phospho-CREB S133 (87G3) rabbit mAb (Cell Signaling Cat# 9198S), CREB (48H2) rabbit mAb (Cell Signaling Cat# 9197S), anti-vinculin (E1E9V) XP(R) rabbit mAb (Cell Signaling cat# 13901S), beta-actin rabbit Ab (Cell Signaling Cat# 4967S), and secondary antibody was anti-Rabbit IgG, HRP-linked antibody (Cell signaling Cat. # 7074S).

Techniques: Expressing, Phospho-proteomics, Western Blot, Quantitative RT-PCR, Concentration Assay, Comparison