rabbit polyclonal anti human jak2  (Cell Signaling Technology Inc)

Journal: International Journal of Molecular Sciences

Article Title: dCas9-Based PDGFR–β Activation ADSCs Accelerate Wound Healing in Diabetic Mice through Angiogenesis and ECM Remodeling

doi: 10.3390/ijms24065949

Figure Lengend Snippet: PDGFR–β is dynamically downregulated with ADSC passage. ( A ) Cell surface co–expression of the antigens, CD44, CD73, CD90, and CD105 in MSCs. ( B ) Differentiation potential of MSCs in osteogenic, chrondrogenic, and adipogenic lineages using Alizarin red, Alcian blue, and oil red O staining, respectively. ( C ) Flow cytometry analysis indicating the expression pattern of PDGFR–β in single cell suspensions of ADSCs (CD105–PE, CD90–PE, CD73–CY5.5, CD44-PE, CD29-APC, CD45-FITC, HLA-DR-CY5.5, CD34-FITC, CD14-PE, CD19-FITC). ( D ) PDGFR–β expression and ( E ) levels relative to β–ACTIN in P4–P6 ADSCs ( n = 3). Data are shown as mean ± SD. Independent–sample t test (two–tailed) was used for statistical comparisons between 2 groups; One–way ANOVA followed by Tukey post hoc test was used for statistical comparisons between multiple groups. * * p < 0.01; ** * p < 0.001.

Article Snippet: The antibodies used were as follows: FITC anti–human CD34 (Abcam, ab195013, Waltham, MA, USA), FITC anti–human CD45, (BD Biosciences, 557803, Piscataway, NJ, USA), PE–Cy7 anti–human CD14 (BD Biosciences, 561385, Piscataway, NJ, USA), PERCP–CY5.5 anti–human HLA–DR (BD Biosciences, 552764, Piscataway, NJ, USA), PERCP–CY5.5 anti–human CD73 (BD Biosciences, 561260, Piscataway, NJ, USA), PE anti–human CD90 (BD Biosciences, 555596, Piscataway, NJ, USA), APC anti–human CD19 (eBioscience, 11–0199042, San Diego, CA, USA), PE anti–CD105 (eBioscience, 25–1057–42, San Diego, CA, USA), PE anti–human CD44 (BD Biosciences, 555479, Piscataway, NJ, USA), APC anti–human CD29 (BD Biosciences, 559883, Piscataway, NJ, USA), and BV421 anti–human PDGFR–β (BD Biosciences, 564124, Piscataway, NJ, USA).

Techniques: Expressing, Staining, Flow Cytometry, Two Tailed Test

Journal: eLife

Article Title: Genetic depletion studies inform receptor usage by virulent hantaviruses in human endothelial cells

doi: 10.7554/eLife.69708

Figure Lengend Snippet:

Article Snippet: Antibody , AF480-α-Human-vWF (Rabbit monoclonal) , Abcam , Cat. # ab195028 , Flow 1:250.

Techniques: Plasmid Preparation, Expressing, Transduction, Recombinant, Sequencing, Staining, Software, Imaging

Journal: Cell Reports

Article Title: Metabolic programs define dysfunctional immune responses in severe COVID-19 patients

doi: 10.1016/j.celrep.2021.108863

Figure Lengend Snippet: Novel H3K27me3 + VDAC1 + T cells are unique in COVID-19 compared with other viral infections (A) UMAP projection of pooled donors with active infection, color coded by disease. (B) UMAP projection of COVID-A and recovered COVID-19 (COVID-R) patients compared with HCs. (C) UMAP projection of influenza and COVID-A patients compared with HCs. (D) Frequency of H3K27Me3 + VDAC1 + CD4 and CD8 T cells as percent of total live cells. (E) Representative gating of H3K27Me3 + VDAC1 + CD4 T cells from multiple disease states. (F) Hierarchical clustering of H3K27Me3 + VDAC1 + CD4 T cells based on expression (MFI values) of indicated proteins. Comparison of hospitalized COVID-A infection (dark blue), COVID-R (light blue), and hospitalized influenza (red). (G) Normalized MFI of GLUT1, TOMM20, and KLRG1 on H3K27Me3 + VDAC1 + CD4 T cells in all patients where H3K27Me3 + VDAC + T cells compromise greater than 10% of the total CD4 population and representative histogram overlays of MFI. Each dot represents one patient sample; significance was tested using unpaired Kruskal-Wallis test compared with HC (D) or every combination (G). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Article Snippet: Anti-human GLUT1 AF647 , Abcam , Cat# ab195020.

Techniques: Infection, Expressing

Journal: Cell Reports

Article Title: Metabolic programs define dysfunctional immune responses in severe COVID-19 patients

doi: 10.1016/j.celrep.2021.108863

Figure Lengend Snippet: Loss of T cell survival can be rescued by targeting VDAC1 or caspases (A) PBMCs from COVID-A patients or HCs were cultured for 48 h in media, rapamycin (100 nM), VBIT-4 (300 nM), or ZVAD (60 nM). T cell survival was calculated as the percent CD4 or CD8 T cells remaining from initial plating. Significance was tested using two-way ANOVA with each drug compared with the media control, n = 9. (B) T cells were stimulated with anti-CD3/CD28 (purple) for 48 h, and surviving T cells from COVID-19 patients are able to respond by upregulating HLA-DR, CD69, CD25, and GLUT1 to the same extent as HCs compared with unstimulated controls (gray). (C) Graphical depiction of proposed mechanism of mitochondrial cell death signaling in COVID-19 T cells. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Article Snippet: Anti-human GLUT1 AF647 , Abcam , Cat# ab195020.

Techniques: Cell Culture

Journal: Cell Reports

Article Title: Metabolic programs define dysfunctional immune responses in severe COVID-19 patients

doi: 10.1016/j.celrep.2021.108863

Figure Lengend Snippet:

Article Snippet: Anti-human GLUT1 AF647 , Abcam , Cat# ab195020.

Techniques: Recombinant, Conjugation Assay, Antibody Labeling, Staining, Blocking Assay, Software