tp53bp2  (Proteintech)

Journal: Cell biology and toxicology

Article Title: ASPP2 deficiency attenuates lipid accumulation through the PPARγ pathway in alcoholic liver injury.

doi: 10.1007/s10565-024-09925-x

Figure Lengend Snippet: Fig. 2 ASPP2 deficiency inhibits the PPARγ and mTOR signaling path- ways. (A and B) Repre- sentative IHC analysis of PPARγ in liver sections, scar bar = 50 µm (A) and quantification analyses (B) of PPARγ positive area (%) in mouse liver tissue from wild-type mice and ASPP2- KD mice. The extended part of the black lines shows the enlarged image from the black box area. (C and D) western blot (C) and quantification analyses (D) of ASPP2, PPARγ, phospho-mTOR, phospho- S6, phospho-p70S6K, and β-actin in mouse liver tissue from wild-type mice and ASPP2-KD mice. (E and F) western blot (E) and quantification analyses (F) of ASPP2, PPARγ, phospho-mTOR, phospho- S6, phospho-p70S6K, and β-actin in primary hepatocytes (Control and ASPP2 siRNA) treated with ethanol for different times. (G and H) western blot (G) and quantification analyses (H) of ASPP2, PPARγ, phospho-mTOR, phospho-S6, phospho- p70S6K, and β-actin in primary hepatocytes (Ad- GFP and Ad-ASPP2) with the indicated treatment. The values represent the means ± SEMs (n = 6 in each group). nsP > 0.05, *P < 0.05, **P < 0.01, ***P < 0.001. Independent- samples T tests between two groups were used for statistical analysis, and one-way ANOVA followed by Bonferroni post hoc tests for multiple comparisons were used for statistical analyses

Article Snippet: Finally, the expression of ASPP2 or PPARγ was observed by microscopy (Leica Microsystems, Mannheim, Germany) after development using a diaminobenzidine kit (Boster, Wuhan, China).

Techniques: Western Blot, Control

Journal: Molecular Therapy. Nucleic Acids

Article Title: LNA-i-miR-221 activity in colorectal cancer: A reverse translational investigation

doi: 10.1016/j.omtn.2024.102221

Figure Lengend Snippet: LNA-i-miR-221 dependent activation of the p53 pathway (A) Expression of TP53 protein after treatment with 15 nM of LNA-NC or LNA-i-miR-221. GAPDH was used to normalize data. Histogram bars in the lower panel are representative of densitometric analysis of bands resulting from the western blots, after normalization on GAPDH and LNA-NC. (B) Fold change values indicating the activity of caspase 3/7 assessed (left); histogram bars showing the percentage of viable cells for each experimental condition at the indicated time points (right). All represented values have been normalized on LNA-NC. To calculate statical significance, Student’s t test was applied. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (C) UCSC Xena browser visual spreadsheet in the COAD dataset. “Null” identifies patients for whom the gene expression has not been collected. Each column identifies an RNA as described on the top. Expression is colored blue to red for low and high expression, respectively. (D) Scatterplot for Spearman correlation. On the x axis miR-221 expression, or the y axis TP53INP1 (left) and TP53BP2 (right) expression.

Article Snippet: The protein expression was checked by using the following primary antibodies: TP53INP1 (ab202026) and TP53BP2 (ab181377) from Abcam (Cambridge, UK), TP53 (2527S) from Cell Signaling Technology (Massachusetts, USA), and GAPDH (SC25778) from Santa Cruz Biotechnology (Dallas, TX, USA).

Techniques: Activation Assay, Expressing, Western Blot, Activity Assay

Journal: Molecular Therapy. Nucleic Acids

Article Title: LNA-i-miR-221 activity in colorectal cancer: A reverse translational investigation

doi: 10.1016/j.omtn.2024.102221

Figure Lengend Snippet: Sequence of primers used in the study

Article Snippet: The protein expression was checked by using the following primary antibodies: TP53INP1 (ab202026) and TP53BP2 (ab181377) from Abcam (Cambridge, UK), TP53 (2527S) from Cell Signaling Technology (Massachusetts, USA), and GAPDH (SC25778) from Santa Cruz Biotechnology (Dallas, TX, USA).

Techniques: Sequencing