creb inhibitor  (MedChemExpress)

Journal: Cellular & Molecular Biology Letters

Article Title: The promoting roles of GLP1R and GIPR in stemness maintenance and multiple lineage-specific differentiation of PDLSCs

doi: 10.1186/s11658-026-00867-2

Figure Lengend Snippet: Enhanced cell growth of PDLSCs facilitated by GIPRA/MAPK/ERK axis. a Western blot assay showing the expression of Ki-67, PCNA, and CCND3 affected by GIPRA as well as inhibition of cAMP/PKA/CREB, MAPK/ERK, Wnt/β-catenin, or JAK/STAT3 signaling pathways. The interpretation of bubble colors in the line chart is illustrated in Fig. a. b CCK-8 assay indicating the cell growth enhanced by GIPRA, but suppressed by ERK Inh ( n = 5 in each group). The interpretation of line colors in the line chart is illustrated in Fig. b. c Venn diagram showing the intersection of differentially binding genes by p-CREB, p-ERK1/2, TCF4, and p-STAT3 (log FC > 1, P < 0.05) compared between GIPRA and NC group. d The bubble plot displays the top ten functions of cell division and cell cycle (GO biological process) associated with the 5994 (red color highlighted) specifically binding genes by p-ERK1/2 in c . e – g IGV showing the binding peaks of p-ERK1/2 on MKI67 ( e ), PCNA ( f ), and CCND3 genes ( g ). The differential binding peaks of p-ERK1/2 on these gene promoters are highlighted by blue boxes. h – k Line plot illustrates the distribution of ChIP-seq signal intensity of p-ERK1/2 ( h ), p-CREB ( i ), TCF4 ( j ), and p-STAT3 ( k ) across the transcription start sites (±3 kb) of differentially binding genes in PDLSCs treated with GIPRA as well as GIPRA plus ERK Inh. NC, normal PDLSCs as negative control; Inh., inhibitor

Article Snippet: The in vitro treatment conditions for the small-molecule compound were as follows: GLP1RA semaglutide acetate (10 nM, 24 h), GIPRA (Pro3) GIP (0.5 nM, 24 h), GLP-1R/GIPR agonist-1 (10 nM, 24 h) also termed as 2GRA in this study, BGM0504 (2 nM, 24 h, BrightGene Pharmaceutical Co., Ltd., China) [ ], CREB inhibitor 666-15 (1 μM, 2 h, HY-101120, MCE), Akt inhibitor MK-2206 (5 μM, 24 h, HY-108232, MCE), ERK1/2 inhibitor SCH772984 (0.5 μM, 24 h, HY-50846, MCE), β-catenin inhibitor IN-3 (5 μM, 24 h, HY-147007, MCE), STAT3-IN-14 (5 μM, 2 h, HY-N10472, MCE).

Techniques: Western Blot, Expressing, Inhibition, Protein-Protein interactions, CCK-8 Assay, Binding Assay, ChIP-sequencing, Negative Control

Journal: Journal of Traditional and Complementary Medicine

Article Title: Role of IGF1/IGFR signaling pathway in neuroprotective effect of Shengmai Dihuang Decoction on CIH-induced cognitive impairment

doi: 10.1016/j.jtcme.2024.11.014

Figure Lengend Snippet: Effects of exogenous IGF1 on cell viability and mitochondrial dysfunction in CIH-exposed HT22 cells. (A) Effects of various IGF1 concentrations on cell viability. (B) TEM was used to detect mitochondria in HT22 cells that had been exposed to CIH (20000 × ). (C and E) Effects of exogenous IGF1 on the mitochondrial membrane potential of HT22 cells (scale bar = 50 μm). (D and F) Effects of exogenous IGF1 on ROS production in the mitochondria of CIH-exposed HT22 cells (scale bar = 25 μm). (G) Effects of exogenous IGF1 on mitochondrial ATP levels in CIH-exposed HT22 cells. (H) Effects of exogenous IGF1 on the level of mitochondrial respiratory chain complex Ι in HT22 cells exposed to CIH. (I) BDNF expression in CIH-exposed HT22 cells. (J) PSD-95 expression in CIH-exposed HT22 cells. (K) P-CREB/CREB expression in HT22 cells exposed to CIH. (L) P-ERK/ERK expression in CIH-exposed HT22 cells. The results are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus the CON group, # P < 0.05, ## P < 0.01, ### P < 0.001 versus the CIH group.

Article Snippet: IGF1 (bs-0014R), IGFR (bs-4985R), P-CREB (bs-5256R), CREB (bsm-33196R), P-ERK (bs-3016R), and ERK (bsm-52259R) were purchased from Bioss Antibodies (Woburn, MA, USA).

Techniques: Membrane, Expressing, Standard Deviation

Journal: Journal of Traditional and Complementary Medicine

Article Title: Role of IGF1/IGFR signaling pathway in neuroprotective effect of Shengmai Dihuang Decoction on CIH-induced cognitive impairment

doi: 10.1016/j.jtcme.2024.11.014

Figure Lengend Snippet: Effects of SDD on cell viability and mitochondrial dysfunction under CIH circumstances in HT22 cells. (A) TEM was used to detect mitochondria in CIH-exposed HT22 cells (20000 × ). (B and D) Impact of SDD on the potential of mitochondria in CIH-exposed HT22 cells (scale bar = 50 μm). (C and E) Effects of SDD on mitochondrial ROS in CIH-exposed HT22 cells (scale bar = 25 μm). (F) Effects of SDD on mitochondrial ATP levels in CIH-exposed HT22 cells. (G) Effects of SDD on the level of mitochondrial respiratory chain complex Ι in CIH-exposed HT22 cells. (H) Cell viability after CIH exposure. (I–J) PSD-95 and BDNF expression in CIH-exposed HT22 cells. (K–L) P-CREB/CREB and P-ERK/ERK expression in CIH-exposed HT22 cells. The results are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus the CON group, # P < 0.05, ## P < 0.01, ### P < 0.001 versus the CIH group.

Article Snippet: IGF1 (bs-0014R), IGFR (bs-4985R), P-CREB (bs-5256R), CREB (bsm-33196R), P-ERK (bs-3016R), and ERK (bsm-52259R) were purchased from Bioss Antibodies (Woburn, MA, USA).

Techniques: Expressing, Standard Deviation

Journal: Journal of Traditional and Complementary Medicine

Article Title: Role of IGF1/IGFR signaling pathway in neuroprotective effect of Shengmai Dihuang Decoction on CIH-induced cognitive impairment

doi: 10.1016/j.jtcme.2024.11.014

Figure Lengend Snippet: Role of IGF1 siRNA and AG1024 in improving the effects of SDD on neuronal injury in CIH-exposed HT22 cells. (A–B) PSD-95 and BDNF expression in CIH-exposed HT22 cells. (C–D) P-CREB/CREB and P-ERK/ERK expression in CIH-exposed HT22 cells. (E) TEM was used to detect mitochondria in CIH-exposed HT22 cells (20000 × ). (F and H) Mitochondrial membrane potential in CIH-exposed HT22 cells (scale bar = 50 μm). (G and I) Mitochondrial ROS in CIH-exposed HT22 cells (scale bar = 25 μm). (J) Mitochondrial ATP levels in CIH-exposed HT22 cells. (K) The level of mitochondrial respiratory chain complex Ι in CIH-exposed HT22 cells. (L) The viability of CIH-exposed HT22 cells. The results are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus the CON group, # P < 0.05, ## P < 0.01 versus the CIH group, △ P < 0.05, △△ P < 0.01, △△△ P < 0.001 versus the SDD group.

Article Snippet: IGF1 (bs-0014R), IGFR (bs-4985R), P-CREB (bs-5256R), CREB (bsm-33196R), P-ERK (bs-3016R), and ERK (bsm-52259R) were purchased from Bioss Antibodies (Woburn, MA, USA).

Techniques: Expressing, Membrane, Standard Deviation