rabbit anti cyclin d1  (Proteintech)

Journal: Scientific Reports

Article Title: The local anesthetic, lidocaine, suppresses the growth of colon cancer SW480 cells by decreasing the voltage-gated sodium channel subunit Na v 1.5

doi: 10.1038/s41598-025-29505-1

Figure Lengend Snippet: Cyclin D1 and mutant p53 levels decreased in lidocaine-treated SW480 cells. ( A ) Decrease of cyclin D1 and mutant p53 levels in lidocaine-treated SW480 cells. The cell lysates of SW480 cells which were treated with or without 5 mM lidocaine for 24 h were subjected to western blot analysis. The arrow indicates Na v 1.5. The relative expression levels of Na v 1.5, cyclin D1 and mutant p53 were normalized to GAPDH levels in each sample. The results of each sample assayed in triplicate are presented as the mean ± SD. * p < 0.05. ( B ) The SCN5A mRNA levels in siRNA-transfected SW480 cells. Total RNAs extracted from control or SCN5A siRNA-transfected SW480 cells were subjected to qPCR analysis. The expression levels of SCN5A mRNA were normalized to GAPDH levels in each sample. The results of each sample assayed in triplicate are presented as the mean ± SD. ** p < 0.01. ( C ) The Na v 1.5 expression levels in control or SCN5A siRNA-transfected SW480 cells. Twenty-four hours after transfection, SW480 cells were treated with or without 5 mM lidocaine for 24 h and the cell lysates were subjected to western blot analysis. The expression levels of Na v 1.5 were normalized to GAPDH levels in each sample. The results of each sample assayed in triplicate are presented as the mean ± SD. * p < 0.05, ** p < 0.01. ( D ) Cyclin D1 and mutant p53 levels in SCN5A siRNA-transfected SW480 cells with or without lidocaine treatment. The lysates of control or SCN5A siRNA-2 transfected SW480 cells were subjected to western blot analysis. The arrow indicates Na v 1.5. The expression levels of Na v 1.5 were normalized to α-tubulin levels in each sample. The results of each sample assayed in triplicate are presented as the mean ± SD. * p < 0.05, ** p < 0.01.

Article Snippet: The antibodies used in this study were rabbit anti-Na v 1.5 antibody (Proteintech, IL, USA, 23016-1-AP), mouse anti-Ki67 antibody (SantaCruz Bio, TX, USA, sc-23900), rabbit anti-ATP1A1 antibody (Proteintech, IL, USA, 55187-1-AP), rabbit anti-GDF-15 antibody (Proteintech, IL, USA, 27455-1-AP), rabbit anti-cyclin D1 antibody (Proteintech, IL, USA, 26929-1-AP), mouse anti-p53 antibody (Cell Signaling Technology, MA, USA, #2524), anti-rabbit cleaved caspase-3 antibody (Cell Signaling Technology, MA, USA, #9664), mouse anti-GAPDH antibody (Fujifilm-Wako, Osaka, Japan, 014-25524), mouse α-tubulin antibody (DM1A) (SantaCruz Bio, TX, USA, sc-32293), goat Cy3-conjugated anti-mouse IgG antibody, and donkey Cy2-conjugated anti-rabbit IgG antibody (Jackson ImmunoResearch Laboratories, PA, USA).

Techniques: Mutagenesis, Western Blot, Expressing, Transfection, Control

Journal: Scientific Reports

Article Title: The local anesthetic, lidocaine, suppresses the growth of colon cancer SW480 cells by decreasing the voltage-gated sodium channel subunit Na v 1.5

doi: 10.1038/s41598-025-29505-1

Figure Lengend Snippet: Schematic representation of the mechanism of lidocaine-induced growth suppression in colon cancer SW480 cells. Colon cancer SW480 cells expressed Na v 1.5 in the cell membrane. Lidocaine treatment induced growth suppression of SW480 cells, along with a decrease of Na v 1.5. Lidocaine treatment also induced a decrease of the cell cycle promoter, cyclin D1, and mutant p53, having transforming activity, which was independent of the Na v 1.5-related signaling pathway.

Article Snippet: The antibodies used in this study were rabbit anti-Na v 1.5 antibody (Proteintech, IL, USA, 23016-1-AP), mouse anti-Ki67 antibody (SantaCruz Bio, TX, USA, sc-23900), rabbit anti-ATP1A1 antibody (Proteintech, IL, USA, 55187-1-AP), rabbit anti-GDF-15 antibody (Proteintech, IL, USA, 27455-1-AP), rabbit anti-cyclin D1 antibody (Proteintech, IL, USA, 26929-1-AP), mouse anti-p53 antibody (Cell Signaling Technology, MA, USA, #2524), anti-rabbit cleaved caspase-3 antibody (Cell Signaling Technology, MA, USA, #9664), mouse anti-GAPDH antibody (Fujifilm-Wako, Osaka, Japan, 014-25524), mouse α-tubulin antibody (DM1A) (SantaCruz Bio, TX, USA, sc-32293), goat Cy3-conjugated anti-mouse IgG antibody, and donkey Cy2-conjugated anti-rabbit IgG antibody (Jackson ImmunoResearch Laboratories, PA, USA).

Techniques: Membrane, Mutagenesis, Activity Assay

Journal: Journal of translational medicine

Article Title: METTL3 regulates Ambra1 expression in an m6A-YTHDF2-dependent manner to promote mantle cell lymphoma progression.

doi: 10.1186/s12967-025-06647-4

Figure Lengend Snippet: Fig. 8 METTL3/YTHDF2/Ambra1 promotes MCL progression. (A) Representative images of tumors from each group on day 28. (B-C) Changes in tumor size and weight in the indicated groups. (D) METTL3 and Ambra1 mRNA and protein expression in the tumor tissues of the indicated groups. (E) Immu noblots showing the expression of Bcl2, BAX, cleaved caspase-3, and PARP in the tumor tissues. (F-G) Representative IHC images showing expression of cyclin D1, CDK4, and CDK6 in the tumor tissues. n = 5, *P < 0.05 vs. sh-NC + sh-NC group, #P < 0.05 vs. sh-METTL3 + sh-NC group, &P < 0.05 vs. sh-NC + sh- Ambra1 group

Article Snippet: After blocking with 5% BSA, the sections were incubated overnight with rabbit polyclonal antibodies against cyclin D1 (AWA10518, Abiowell), CDK4 (11026-1-AP, ProteinTech), and CDK6 (14052-1-AP, ProteinTech) (dilution 1:200) at 4 °C.

Techniques: Expressing