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Image Search Results
Journal: The Journal of Neuroscience
Article Title: Protogenin Defines a Transition Stage during Embryonic Neurogenesis and Prevents Precocious Neuronal Differentiation
doi: 10.1523/JNEUROSCI.0473-10.2010
Figure Lengend Snippet: Expression of PRTG protein in the mouse embryo. A, Expression of rat prtg in the nervous system at different stages of development as analyzed by the Northern blot. Ad, Adult; Br, brain; Nt, neural tube. B, Specificity of PRTG antibodies. Cell lysates of HEK293T cells transfected with the control vector, prPRTGf (rat full-length PRTG), prPRTGΔc (rat PRTG without cytoplasmic domain), or prPRTGc (rat cytoplasmic tail), and rat E10.5 neural tube lysate (Embryo) were subjected to Western blot using α-PRTG1 and α-PRTG2 mAbs. Addition of peptide E (E; ectodomain) or peptide C (C; cytoplasmic tail) competes out the bands recognized by the monoclonal antibodies. C, Schematic structure of PRTG. Peptide E or C for generating antibodies is marked in blue. D–H, Transverse sections through the mid-body level of mouse at E7 (D), E7.75 (E), E8.25 (F), E9.5 (G), and E10.5 (H) were stained using α-PRTG2 mAb (red). The dorsal is up in all panels. D, At E7, PRTG labeling is weakly detected in the mesoderm (me), whereas Oct4 is restricted to the ectoderm (ec; green). E, At E7.75, PRTG is detected in neuroepithelium, mesoderm, endoderm, and posterior epiblasts (arrows). The yolk sac (ys) surrounding the embryo is nonspecifically stained by the secondary antibodies. F, G, PRTG protein is present in almost all cells between E8.25 and E9.5 (red) but not in the notochord (n), differentiating cardiac cells, and some mesenchymal cells. The endocardium is labeled with anti-endoglin antibody (green). ac, Atrial chamber; dm, dermomyotome; vc, ventricular chamber; sc, spinal cord. H, PRTG is not detectable at E10.5. I, Expression of PRTG (red) and SSEA1 (green) in a transverse section of E7 and E8.25 mouse embryos. J–N, Expression of PRTG (red) and nestin (J), Ascl1 (K), TuJ1 (L), MAP2 (M), and NeuN (N) (green) in adjacent transverse sections through the thoracic level of E9.5 (top) and E10.5 (bottom) mouse embryos.
Article Snippet:
Techniques: Expressing, Northern Blot, Transfection, Control, Plasmid Preparation, Western Blot, Bioprocessing, Staining, Labeling
Journal: Clinical Cancer Research
Article Title: Mesenchymal Stem Cell Targeting of Microscopic Tumors and Tumor Stroma Development Monitored by Noninvasive In vivo Positron Emission Tomography Imaging
doi: 10.1158/1078-0432.ccr-05-0876
Figure Lengend Snippet: Fig. 5. In situ characterization of EGFP+ cells in HT-29 (s.c.) + TG-hMSC (i.v.) tumors. A, agarose gel electrophoresis of PCR-amplified EGFP sequence (717 bp) done using1 Ag of cellular DNA prepared from loosely associated cell fraction (loose), stromal matrix associated fraction (stroma), and the residue (residue) of HT-29 (s.c.)/TG-hMSC (i.v.) tumor and HT-29 (s.c.) tumor,TG-hMSC, and HT-29 cells. B, cytofluorometric histograms comparing the stromal matrix cell fractions of HT-29 (s.c.) + TG-hMSC (i.v.) tumors (red) and HT-29 (s.c.) tumors (black), examined with anti-GFP specific antibody. EGFP+ cells in the gated area represented 11.5% of total cells. C, histograms showing the presence of human endothelial cell markers but absence of hMSC markers in EGFP+ cells obtained from the HT-29 (s.c.) + TG-hMSC (i.v.) tumor after 30 days of growth in vivo. Stromal matrix ^ associated cell fractions were double stained with FITC-labeled anti-GFP mouse monoclonal antibody, and with a PE-labeled anti-vWF, or anti-CD31, or anti-CD90, or anti-CD105 to assess the expression of these cell surface markers on EGFP+ cells (red). PE-labeled mouse isotype immunoglobulins were included in parallel to serve as the negative control (black).
Article Snippet: © 2005 American Association for Cancerclincancerres.aacrjournals.org Downloaded from anti-mouse IgG antibody or PE-labeled anti-hvWF; and PE-labeled mouse monoclonal antibodies against human CD14 (PharMingen, San Diego, CA), CD31, CD90,
Techniques: In Situ, Agarose Gel Electrophoresis, Amplification, Sequencing, Residue, In Vivo, Staining, Labeling, Expressing, Negative Control
Journal: International Journal of Implant Dentistry
Article Title: Boosting angiogenesis experimentally in ovo by biofunctionalizing collagen membranes with platelet-rich fibrin and hyaluronic acid: implications for regenerative oral surgery?
doi: 10.1186/s40729-026-00669-3
Figure Lengend Snippet: Analysis of ( A ) α-SMA staining, ( B ) CD105 staining, and ( C ) HE staining for each membrane (MM native: native Mucoderm®, A-PRF native, MM + A-PRF: Mucoderm® with A-PRF, BM + i-PRF: Bio-Gide® with i-PRF, Bio-Gide® native, BM + HA: Bio-Gide® with HA, SM + HA: Smartbrane membrane with HA) after 24 h, 48 h, and 72 h. Lines indicate significant differences (based on t-tests), with significance levels denoted as follows: * p < 0.05, ** p < 0.01, *** p < 0.001
Article Snippet: The slides were then incubated with
Techniques: Staining, Membrane
Journal: PLoS ONE
Article Title: Murine Mesenchymal Stem Cells Exhibit a Restricted Repertoire of Functional Chemokine Receptors: Comparison with Human
doi: 10.1371/journal.pone.0002934
Figure Lengend Snippet: A. Flow cytometry analysis of all primary murine MSC cultures (upper panel) and human MSC (lower panel) cultures showed they were CD34 and CD45 negative, and CD105 positive. CD molecule antibody staining is represented by the filled histogram; isotype control staining is represented by the green line. B. Murine MSCs (CD45 − , CD34 − , CD105 + ) incubated in osteogenic medium for 21 days stained positive for alkaline phosphatase activity (top right), whereas murine MSCs incubated in culture medium alone did not stain positive (top left). Murine MSCs incubated in adipogenic medium for 21 days showed fat droplets in the cells stained with Oil Red O (bottom right), whereas murine MSCs incubated in culture medium alone showed no positive staining (bottom left). The black bar represents 200 µm in the top panels and 100 µm in the bottom two panels.
Article Snippet: Antibodies used in this study were as follows: anti-human CCR1 (used at 1 in 100 dilution), CCR2 (1 in 200), CCR3 (1 in 100), CCR5 (1 in 200), CCR6 (1 in 200), CCR7 (1 in 200), CCR8 (1 in 20), CCR9 (1 in 20), CXCR1 (1 in 100), CXCR2 (1 in 100), CXCR3 (1 in 200), CXCR4 (1 in 50), CXCR5 (1 in 50), and CXCR6 (1 in 50), anti-mouse CCR6 (1 in 50), CCR9 (1 in 50), CXCR2 (1 in 50), CXCR3 (1 in 50), and CXCR6 (1 in 50) and
Techniques: Flow Cytometry, Staining, Control, Incubation, Activity Assay