anti dek antibody  (Proteintech)

Journal: Cell Death & Disease

Article Title: NAT10-mediated ac4C RNA acetylation stabilizes CXCL5/DEK mRNA to drive proliferation and metastasis in lung adenocarcinoma

doi: 10.1038/s41419-026-08568-6

Figure Lengend Snippet: a , b Distribution of ac4C modification sites on mRNA of CXCL5 and DEK. c , d The ac4C modification of CXCL5 and DEK was verified through acRIP-PCR. e , f The dual fluorescence experiment confirmed the importance of NAT10 recognizing the ac4C modification site of the target gene. g , h Detecting the differential mRNA and protein levels of CXCL5 and DEK before and after NAT10 knockout, as well as cancer tissues and adjacent tissues in LUAD. i Co-localized the intracellular expression of NAT10 with CXCL5 or DEK by Fish and IF. j The half-life changes of CXCL5 and DEK mRNA after inhibiting NAT10. The data in ( e , f ) were normalized to Si-NC levels. The data in ( g ) was normalized to WT levels. The data in ( h ) was normalized to tumor tissue levels. The clinical samples used in Fig. 4h is consistent with those in Fig. .

Article Snippet: The antibodies used in this process consisted of NAT10 (1:1000, Abcam, ab194297), CXCL5 (1:300, Abcam, ab126763), DEK (1:500, CST, 29812 T), GAPDH (1:1000, Abcam, ab181602), HRP-conjugated secondary goat anti-rabbit IgG (1:5000, Proteintech, SA00001-2), and Goat anti-Mouse IgG (1:5000, ABclonal, AS003).

Techniques: Modification, Fluorescence, Knock-Out, Expressing

Journal: Cell Death & Disease

Article Title: NAT10-mediated ac4C RNA acetylation stabilizes CXCL5/DEK mRNA to drive proliferation and metastasis in lung adenocarcinoma

doi: 10.1038/s41419-026-08568-6

Figure Lengend Snippet: a Phenotypic comparison of A549 wild-type and NAT10-knockout cells. b Co-localized the intracellular expression of NAT10 with F-actin by IF. c Prove the effect of overexpression of CXCL5 and DEK separately or simultaneously at the mRNA and protein levels. d Cell proliferation was measured using the CCK8 assay after NAT10 knockout and CXCL5/DEK overexpression. e Inhibition of invasion and metastasis of LUAD cells by NAT10 and its rescue effect on CXCL5/DEK. f Inhibition of cell adhesion of LUAD cells by NAT10 and its rescue effect on CXCL5/DEK. The data in ( c ) was normalized to WT + Vector levels.

Article Snippet: The antibodies used in this process consisted of NAT10 (1:1000, Abcam, ab194297), CXCL5 (1:300, Abcam, ab126763), DEK (1:500, CST, 29812 T), GAPDH (1:1000, Abcam, ab181602), HRP-conjugated secondary goat anti-rabbit IgG (1:5000, Proteintech, SA00001-2), and Goat anti-Mouse IgG (1:5000, ABclonal, AS003).

Techniques: Comparison, Knock-Out, Expressing, Over Expression, CCK-8 Assay, Inhibition, Plasmid Preparation

Journal: Cell Death & Disease

Article Title: NAT10-mediated ac4C RNA acetylation stabilizes CXCL5/DEK mRNA to drive proliferation and metastasis in lung adenocarcinoma

doi: 10.1038/s41419-026-08568-6

Figure Lengend Snippet: Initially, NAT10 acetylates CXCL5 and DEK to maintain their mRNA stability and expression. Then, the increased expression of CXCL5 and DEK promoted tumor adhesion to facilitate LUAD proliferation and metastasis. Created in https://BioRender.com .

Article Snippet: The antibodies used in this process consisted of NAT10 (1:1000, Abcam, ab194297), CXCL5 (1:300, Abcam, ab126763), DEK (1:500, CST, 29812 T), GAPDH (1:1000, Abcam, ab181602), HRP-conjugated secondary goat anti-rabbit IgG (1:5000, Proteintech, SA00001-2), and Goat anti-Mouse IgG (1:5000, ABclonal, AS003).

Techniques: Expressing

Journal: Journal of Advanced Research

Article Title: Genomic landscape of paired primary and peritoneal metastatic lesions in gastric cancer highlights evolutionary dynamics and mutational drivers

doi: 10.1016/j.jare.2025.05.043

Figure Lengend Snippet: Roles of DEK in gastric cancer stemness and peritoneal metastasis. (A) Correlation analysis between DEK expression and cancer stem cell (CSC) signature in the TCGA gastric cancer cohort. (B) Detailed correlations between DEK and the 16 individual members of the CSC signature. (C) Correlations between DEK and two key CSC markers, SOX9 (right) and YAP1 (left), in the TCGA cohort. (D) Assessment of DEK levels in AGS cells transfected with DEK-encoding lentivirus (DEK-OE) or vector, along with their expression levels of YAP1 and SOX9 . (E) mRNA levels of DEK , YAP1 , and SOX9 measured in DEK-OE and control cells by RT-PCR, standardized to the corresponding expression levels in control cells. (F) Tumor sphere formation abilities in DEK-OE and control cells. Photographs of tumor sphere formation at 3-day intervals are shown on the left and quantitative analysis are on the right. (G) Schematic representation of the peritoneal metastasis model using DEK-OE or control tumor cells in mice. (H) Measurements of abdominal circumference (left) and body weight (right) changes in mice with DEK-OE versus control cells. (I-K) Visual (left) and quantitative assessment (right) of peritoneal metastasis models, showing general appearance (I), volume of ascites (J), and peritoneal implants (K) on day 20 for DEK-OE vs. control subcutaneous gastric cancer groups. (L) Kaplan-Meier survival curves for mouse models with DEK-OE versus control cells. (M−N) Protein (M) and mRNA (N) levels of DEK, YAP1, and SOX9 in peritoneal tumors from the mouse models. (O) Schematic representation of competition assays in the peritoneal model with DEK-OE and control cells. (P) Proportions of DEK-OE and control cells in the peritoneum of mice in the competition model, measured by flow cytometry.

Article Snippet: Paraffin-embedded sections were treated with goat serum to block non-specific binding and subsequently stained with anti-DEK antibody (Proteintech, Wuhan, China) and anti-YAP1 antibody (Proteintech, Wuhan, China) using an IHC staining kit (Zsbio, Beijing, China).

Techniques: Expressing, Transfection, Plasmid Preparation, Control, Reverse Transcription Polymerase Chain Reaction, Flow Cytometry