Journal: Proceedings of the National Academy of Sciences of the United States of America

Article Title: Endothelial deletion of EPH receptor A4 alters single-cell profile and Tie2/Akap12 signaling to preserve blood–brain barrier integrity

doi: 10.1073/pnas.2204700120

Figure Lengend Snippet: Raw average gene expression values from all capillary-derived endothelial cells

Article Snippet: Rabbit anti-EphA4 (Proteintech), goat anti-Cd31 (BD Biosciences), rabbit anti-CD45 (Cell Signaling Technology), rat anti-CD68 (Invitrogen), rabbit anti-Akap12 (Alomone, Jerusalem), and goat anti-Tie2 (R&D Systems).

Techniques: Expressing, Activation Assay, Shear, Membrane, Control

Journal: Journal of immunology (Baltimore, Md. : 1950)

Article Title: Systemic lupus erythematosus immune complexes increase the expression of SLAM family members CD319 (CRACC) and CD229 (LY-9) on plasmacytoid dendritic cells and CD319 on CD56(dim) NK cells.

doi: 10.4049/jimmunol.1301022

Figure Lengend Snippet: FIGURE 5. pDCs lack the activating adaptor molecules but express inhibitory adaptor molecules of SLAM receptors. (A) IFN-a production by RNA-IC–stimulated pDCs after cross-linking of CD319, CD229, or BDCA-2 by plate-bound mAbs. IFN-a levels were determined in 20-h cell culture supernatants by an immunoassay and normalized to the IFN-a production in cultures without plate-bound mAb. The dashed line indicates 100%. Data (mean + SD) are from three donors from two independent experiments. Expression of EAT2 and SAP (B) and SHIP-1, SHP-1, SHP- 2, and CSK (C) in cell lysates from isolated pDCs or NK cells from two healthy donors was determined by Western blot. Expression of b-actin was used as control.

Article Snippet: Rabbit polyclonal Abs to Ewing’s sarcoma-activated transcript 2 (EAT2), SHIP-1, SHP-2, CSK (Proteintech Group, Chicago, IL), and a rabbit mAb to SHP-1 (EPR5519; Epitomics, Burlingame, CA), followed by HRP-conjugated goat anti-rabbit IgG (H+L) (Invitrogen), were used to detect the indicated signaling molecules.

Techniques: Cell Culture, Expressing, Isolation, Western Blot, Control

Journal: Journal of Biological Chemistry

Article Title: A potential target for liver cancer management, lysophosphatidic acid receptor 6 (LPAR6), is transcriptionally up-regulated by the NCOA3 coactivator

doi: 10.1074/jbc.ra119.009899

Figure Lengend Snippet: Fig. 5 NCOA3 regulates H3K27ac enrichment at LPAR6 locus (A) Schematic diagram of LPAR6 gene and specific primers designed for qPCR. Black box represents CDS region of LPAR6; Gray boxes represent amplification sites by ChIP-qPCR. (B-C) H3K27ac enrichment in (B) HepG2 or (C) Huh7 cells with or without NCOA3 knockdown. Equal amounts of cells were collected after NCOA3 shRNA or scrambled shRNA transfection for 48h and then subject to ChIP. Primers designed for Site 1 amplified LPAR6 coding sequence, while Site 2 and 3 amplified LPAR6 promoter. Error bars represent S.D. from three independent biological replicates. *p< 0.05 and **p< 0.01, significance of difference was analyzed by unpaired t-test. (D) HGF treatment decreased NCOA3 expression in HepG2

Article Snippet: Antibody against NCOA3 (20032-1-AP) was purchased from Proteintech.

Techniques: Amplification, ChIP-qPCR, Knockdown, shRNA, Transfection, Sequencing, Expressing