25504 1 ap  (Proteintech)

Journal: Communications Biology

Article Title: Parkinson’s disease-specific α-Synuclein variants potentially drive Lewy body formation by engaging in promiscuous and non-functional interactions

doi: 10.1038/s42003-025-09395-9

Figure Lengend Snippet: Th-T based aggregation kinetics of 25 μM αSyn 1–103 in the presence of 25 μM representative proteins from each group: LB components (PIN1, LH1.5_GD), known interactors (BSA, lysozyme, SIRT6, and Fyn-SH3 domain), and uncharacterized binders (RNase, TEV protease, GST, and PSIP1-PWWP domain). Controls include αSyn 1–103 alone (red) and individual proteins alone (yellow). Data represent the mean of three individual triplicates ( n = 3) and the error bar shows ±SD. Representative T₅₀ values, derived from one-phase exponential association kinetics, for αSyn 1–103 control and its 1:1 mixtures with cellular proteins are presented as a comparative bar graph. The dashed line indicates the T₅₀ value for the αSyn 1–103 control.

Article Snippet: Pin1 FL (#40773), Tau FL (#16316), and PSIP1-PWWP (1-135) domain (#40744) constructs were obtained from Addgene. (His) 6 -tagged proteins (Pin1 and PSIP1-PWWP domain) were expressed in E. coli BL21(DE3) using 0.5 mM IPTG induction at 37°C for 6 h and purified initially using Ni 2+ -affinity chromatography (HiTrap IMAC FF, Cytiva).

Techniques: Derivative Assay, Control

Journal: Cancer cell international

Article Title: Identifying PSIP1 as a critical R-loop regulator in osteosarcoma via machine-learning and multi-omics analysis.

doi: 10.1186/s12935-025-03775-1

Figure Lengend Snippet: Fig. 5 Identifying therapeutic targets for OS patients. (A) The heatmap of ten RGPSM-related genes in the high- and low-RGPSM patients. (B) The feature plots of six high expressed genes. (C) The K-M plots of PSIP1 in predicting the prognosis of OS patients in various cohorts. (D) The PSIP1 mRNA expression levels between normal samples (normal, N)/cells (osteoblast, OB; mesenchymal stem cell, MSC) and tumor (T)/OS cells. (E) The PSIP1 protein levels in hFOB1.19 and OS cells. *, p < 0.05; **, p < 0.01

Article Snippet: The anti-bodies used in IHC were as followed: anti-PSIP1 antibody (1:100, Cat. #25504- 1-AP, Proteintech) and anti-Ki-67 antibody (1:100, Cat. GB111499-100, Servicebio).

Techniques: Biomarker Discovery, Expressing

Journal: Cancer cell international

Article Title: Identifying PSIP1 as a critical R-loop regulator in osteosarcoma via machine-learning and multi-omics analysis.

doi: 10.1186/s12935-025-03775-1

Figure Lengend Snippet: Fig. 6 Silencing PSIP1 inhibited proliferation, invasion and migration of OS. (A-B) CCK8 (A) and colonies plate information assays (B) were used to mea sure the effects of silencing or up-regulating PSIP1 in OS cells. (C) Transwell migration assays were used to detect the migratory ability of OS cells with silencing or up-regulating PSIP1. (D) The subcutaneous tumor morphology after knockdown of PSIP1. (E-F) The size (E) and weight (F) of tumors. (G) The HE results and IHC results of PSIP1 and Ki-67 of subcutaneous tumors

Article Snippet: The anti-bodies used in IHC were as followed: anti-PSIP1 antibody (1:100, Cat. #25504- 1-AP, Proteintech) and anti-Ki-67 antibody (1:100, Cat. GB111499-100, Servicebio).

Techniques: Migration, Knockdown

Journal: Cancer cell international

Article Title: Identifying PSIP1 as a critical R-loop regulator in osteosarcoma via machine-learning and multi-omics analysis.

doi: 10.1186/s12935-025-03775-1

Figure Lengend Snippet: Fig. 7 Silencing PSIP1 induced R-loop accumulation and DNA damage. (A) The fluorescence intensity of S9.6 after different treatments. (B) The relative γ-H2AX foci intensity (γ-H2AX/DAPI) after different treatments. *, p < 0.05; **, p < 0.01

Article Snippet: The anti-bodies used in IHC were as followed: anti-PSIP1 antibody (1:100, Cat. #25504- 1-AP, Proteintech) and anti-Ki-67 antibody (1:100, Cat. GB111499-100, Servicebio).

Techniques: Fluorescence