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Image Search Results
Journal: Cell reports
Article Title: BIRC2 Expression Impairs Anti-Cancer Immunity and Immunotherapy Efficacy.
doi: 10.1016/j.celrep.2020.108073
Figure Lengend Snippet: Figure 4. BIRC2 Knockdown in Melanoma Cells Decreases Tumor Growth and Alters Inflammatory Cell Recruitment to the Tumor Micro- environment (A) B16F10 subclones expressing NTC or BIRC2 shRNA (sh3 or sh4) were implanted subcutaneously in female C57BL/6 mice, and tumor growth was monitored. (B–F) Tumors were harvested on day 35 and the percentage of CD8+/CD44+/CD69+ activated T cells (B), CD11b+/NK1.1+ NK cells (C), CD11b+/CD11c+/F4/80
Article Snippet: REAGENT or RESOURCE SOURCE IDENTIFIER Antibodies Anti-mouse BIRC2 Novus Biologicals Cat# NB100-56889 Anti-mouse b-Actin Santa Cruz Biotechnology Cat# sc-47778 Anti-mouse CD3 BioLegend Cat# 102102 Anti-mouse CD3 Novus Biologicals Cat# FAB4841G-100 Anti-mouse CD4 Novus Biologicals Cat# FAB554A-100 Anti-mouse CD8A Novus Biologicals Cat# NBP1-49045PE Anti-mouse CD11b Novus Biologicals Cat# NB110-89474AF405 Anti-mouse CD11c Novus Biologicals Cat# NB110-40766AF488 Anti-mouse CD25 Novus Biologicals Cat# NBP2-27425AF488 Anti-mouse CD28 BioLegend Cat# 100223 Anti-mouse CD44 Novus Biologicals Cat# NBP1-47386APC Anti-mouse CD45 Novus Biologicals Cat# NB100-77417AF488 Anti-mouse CD45 Novus Biologicals Cat#
Techniques: Knockdown, Expressing, shRNA
Journal: Cell reports
Article Title: BIRC2 Expression Impairs Anti-Cancer Immunity and Immunotherapy Efficacy.
doi: 10.1016/j.celrep.2020.108073
Figure Lengend Snippet: Figure 5. BIRC2 Knockdown in Breast Can- cer Cells Decreases Tumor Growth and Al- ters Inflammatory Cell Recruitment to the Tumor Microenvironment (A) EMT6 subclones expressing NTC or either of two shRNAs targeting BIRC2 (sh4 and sh5) were cultured at 20% O2 and analyzed for expression of BIRC2 protein by immunoblot assay. (B) EMT6 subclones (NTC, sh4, and sh5) were im- planted into the mammary fat pad of female BALB/c mice, and tumor volumes were determined (mean ± SEM; n = 4); *p < 0.05 (Kruskal-Wallis test with Benjamini-Hochberg post-test). (C–F) Tumors were harvested on day 13, and the percentage of CD8+/CD44+/CD69+ activated T cells (C), CD3/NK1.1+ NK cells (D), CD11b+/F4/ 80/CD11c+ DCs (E), and CD11b+/Ly6C+ MDSCs (F) was determined (mean ± SEM; n = 4); *p < 0.05 for the indicated pairs (Kruskal-Wallis test with Benjamini-Hochberg post-test). All immune cell populations were calculated as a percentage of the total number of live cells (based on forward and side scatter). (G) EMT6 subclones were implanted into the mammary fat pad of female SCID mice, and tumor growth was monitored. See also Figure S3B.
Article Snippet: REAGENT or RESOURCE SOURCE IDENTIFIER Antibodies Anti-mouse BIRC2 Novus Biologicals Cat# NB100-56889 Anti-mouse b-Actin Santa Cruz Biotechnology Cat# sc-47778 Anti-mouse CD3 BioLegend Cat# 102102 Anti-mouse CD3 Novus Biologicals Cat# FAB4841G-100 Anti-mouse CD4 Novus Biologicals Cat# FAB554A-100 Anti-mouse CD8A Novus Biologicals Cat# NBP1-49045PE Anti-mouse CD11b Novus Biologicals Cat# NB110-89474AF405 Anti-mouse CD11c Novus Biologicals Cat# NB110-40766AF488 Anti-mouse CD25 Novus Biologicals Cat# NBP2-27425AF488 Anti-mouse CD28 BioLegend Cat# 100223 Anti-mouse CD44 Novus Biologicals Cat# NBP1-47386APC Anti-mouse CD45 Novus Biologicals Cat# NB100-77417AF488 Anti-mouse CD45 Novus Biologicals Cat#
Techniques: Knockdown, Expressing, Cell Culture, Western Blot
Journal: Cell reports
Article Title: BIRC2 Expression Impairs Anti-Cancer Immunity and Immunotherapy Efficacy.
doi: 10.1016/j.celrep.2020.108073
Figure Lengend Snippet: Figure 6. BIRC2 Knockdown in B16F10 Cells Increases Anti-tumor Immunity by Increasing CXCL9 Expression (A) NTC and BIRC2-KD subclones were implanted into C57BL/6 mice. When BIRC2-KD tumors became palpable, mice were treated with anti-CXCL9 or IgG every 3 days. Tumor volumes were determined (mean ± SEM; n = 4); *p < 0.05 (Kruskal-Wallis test with Benjamini-Hochberg post-test). (B–E) Tumors were harvested on day 35, and the percentage of CD8+ T cells (relative to CD45+ population) (B), CD8+/CD44+/CD69+ T cells (C), CD3/NK1.1+ NK cells (D), and CD11b+/CD11c+/F4/80 DCs (E) was determined (mean ± SEM; n = 4); *p < 0.05 (Kruskal-Wallis test with Benjamini-Hochberg post-test). All immune cell populations (except B) were calculated as a percentage of the total live cells (based on forward and side scatter). (F–H) The Pearson correlation test was performed to compare CXCL9 mRNA expression with CD8+ T cell score (F), NK cell score (G), and DC score (H), using TCGA data from 481 human melanomas. See also Figures S3C and S4.
Article Snippet: REAGENT or RESOURCE SOURCE IDENTIFIER Antibodies Anti-mouse BIRC2 Novus Biologicals Cat# NB100-56889 Anti-mouse b-Actin Santa Cruz Biotechnology Cat# sc-47778 Anti-mouse CD3 BioLegend Cat# 102102 Anti-mouse CD3 Novus Biologicals Cat# FAB4841G-100 Anti-mouse CD4 Novus Biologicals Cat# FAB554A-100 Anti-mouse CD8A Novus Biologicals Cat# NBP1-49045PE Anti-mouse CD11b Novus Biologicals Cat# NB110-89474AF405 Anti-mouse CD11c Novus Biologicals Cat# NB110-40766AF488 Anti-mouse CD25 Novus Biologicals Cat# NBP2-27425AF488 Anti-mouse CD28 BioLegend Cat# 100223 Anti-mouse CD44 Novus Biologicals Cat# NBP1-47386APC Anti-mouse CD45 Novus Biologicals Cat# NB100-77417AF488 Anti-mouse CD45 Novus Biologicals Cat#
Techniques: Knockdown, Expressing
Journal: The Journal of Neuroscience
Article Title: Retinal Ganglion Cell Axon Regeneration Requires Complement and Myeloid Cell Activity within the Optic Nerve
doi: 10.1523/jneurosci.0555-21.2021
Figure Lengend Snippet: Figure 5. Marked increase in CR3 near the site of ONI. Complement C3b phagocytosis receptor CR3 is microglia/monocyte-specific, and CR31 microglia/monocyte number and phagocytic activation increase within the injured optic nerve. A, Representative images of CR3 immunolabeled uninjured (–) and injured (1, 3, 5, 7, 14 DPI) optic nerves at the injury site. Indicated regions (☐) are shown enlarged to the right of each image. Note the accumulation of CR31 cells and the increased cellular signal intensity following ONI. B, C, Quantitation confirms that the approximate number of CR31 cells (B) increases rapidly (by 1 DPI) and is sustained for at least 14 DPI, with a 30-fold peak at 5 DPI; likewise, CR3 immunofluorescence intensity (C) is elevated at all postinjury time points evaluated (1-14 DPI). D, The specificity of the CR3 (CD11b) antibody was verified using 14 DPI nerves from CR31/1 (left) and CR3/ mice (right). E, The approximate number of Iba11 microglia/monocytes in the nerve increases dramatically by 5 DPI and remains elevated until at least 14 DPI. F, Quantitation of CR31Iba1 (red), CR3-Iba11 (green), and colocalized CR31Iba11 (yellow) cells at/near the injury site. While most CR31 optic nerve cells are microglia, some CR31 cells in the injured nerve are likely infiltrating peripheral blood monocytes. G, CR3 (red) colocalization with Iba1 (green; microglia) at nerve injury site (3, 5 DPI), in the distal nerve (3 DPI), and in the chiasm (14 DPI). H–J, Presence of myeloid cell markers CD206 (H), CD45 (I), and P2RY12 (J) in 14 DPI optic nerves. Iba11 and CR31 microglia/monocytes at/near the injury are large, round, and lack processes: morphologic changes associated with phagocytic activation. L, Similarly, these Iba11 (green) microglia/monocytes express strikingly high levels of lysosome marker CD68 (red; observed 3-14 DPI, 14 DPI shown). M, C1q deletion dampens the CR31 cell response to injury plus zymosan 1 CPT-cAMP treatment at 5 and 14 DPI. N, Pro-regenerative treatments may augment the CR31 cell response in the injured nerve at 14 DPI. Scale bars: A, 50 mm, 10 mm; D, G, H, I, J, L, 50 mm. Graphs represent either mean 6 SEM or 25th to 75th percentile (box), median (line), range (whiskers), and individual data points (circles). B, C, E, K, *p , 0.05, **p , 0.01, ***p , 0.001, ****p , 0.0001, one-way ANOVA with Dunnett post-test vs uninjured or untreated. J, **p , 0.01, t test.
Article Snippet: Antibodies used in immunohistochemistry experiments Antibody Target (specificity) Host species Manufacturer Dilution C1q Complement C1q (C1q) Rabbit Abcam #ab182451 1:250 C3 Complement C3 (C3) Goat MP/Cappel #55730 1:1000 C3d Complement C3d (C3d opsonin) Rabbit Dako #A0063 1:1000 CC1 CC1, APC (mature oligodendrocytes) Mouse Abcam #ab16794 1:100 CD11b Complement receptor 3, CR3, Mac1, integrin aMb 2 (monocytes, microglia, PMNs) Rat Bio-Rad #MCA711G 1:1000
Techniques: Activation Assay, Immunolabeling, Quantitation Assay, Immunofluorescence, Marker
Journal: International Journal of Molecular Sciences
Article Title: Enteropathogenic Escherichia coli (EPEC) Recruitment of PAR Polarity Protein Atypical PKCζ to Pedestals and Cell–Cell Contacts Precedes Disruption of Tight Junctions in Intestinal Epithelial Cells
doi: 10.3390/ijms21020527
Figure Lengend Snippet: Temporal redistribution of TJ proteins and barrier dysfunction caused by EPEC. ( A–C ) SKCO-15 cells were plated on Transwells and infected or not (UI) with EPEC. Total JAM-A, JAM-A S285, JAM-A Y280, occludin, and ZO-1 localization and TER were determined. ( A ) EPEC does not alter the distribution of total JAM-A. In contrast, JAM-A S285 is displaced from the cell–cell contacts to the cytoplasm at 30 min post-infection. Tyrosine phosphorylation of JAM-A Y280 is apparent at 60–120 min post-infection. Scale bars, 10 µm. ( B ) EPEC induces the endocytosis of occludin and ZO-1 at 1 and 2 h post-infection, respectively. Scale bars, 10 µm. ( C ) TER drops significantly as early as 45 min post-infection and progressively decreases over time as more TJ proteins are displaced. TER reported as percent change from baseline. * p < 0.01, *** p < 0.001.
Article Snippet: Par3 (07-330, EMD Millipore), Par6 (ab49776 and ab6022, Abcam, Cambridge, MA, USA), aPKCζ (sc-17781, Santa Cruz Biotechnology, Dallas, TX, USA), p-aPKCζ–T560 (ab62372, Abcam, Cambridge, MA, USA), p-aPKCζ–T410 (sc-12894R, Santa Cruz Biotechnology, Dallas, TX, USA), actin (A2066, Sigma-Aldrich, St. Louis, MO, USA), F-actin BODIPY 558/568 Phalloidin (B3475, Invitrogen, Life Technologies Carlsbad, CA, USA), occludin (33-1500, Invitrogen, Life Technologies, Carlsbad, CA, USA), JAM-A S285 (sc-17430, Santa Cruz Biotechnology, Dallas, TX, USA),
Techniques: Infection, Phospho-proteomics
Journal: iScience
Article Title: NF1-dependent disruption of the blood-nerve-barrier is improved by blockade of P2RY14
doi: 10.1016/j.isci.2024.110294
Figure Lengend Snippet:
Article Snippet: Primary antibody incubation occurred overnight at 4 degree Celsius with the following antibodies: Anti-Glut1 antibody (1:300, Abcam, Cat#ab115730), Fibrinogen antibody (1:500, Agilent DAKO, Cat#: A008002-2), CD31 antibody (1:100, BD Biosciences, Cat#: 553370), pPKA antibody (1:200, Cell Signaling, Cat#: 9621S), Cav1 antibody (1:400, Cell Signaling, Cat#:3238S),
Techniques: Recombinant, Gene Expression, Microarray, Software