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  • 99
    Millipore neun mouse anti neun
    CXCR4 modulates neuropathic pain. a – c CXCR4 immunofluorescent co-staining with <t>NeuN</t> (a neuron marker) ( a , a′ ), <t>GFAP</t> (an astrocyte marker) ( b , b′ ) or IBA1 (a microglial marker) ( c , c′ ) in the lumbar segment of the spinal cord at 7 days after pSNL surgery. * p
    Neun Mouse Anti Neun, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 88 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore neun
    Ago2 is dispensable for brain organization and neuronal maintenance in the adult brain. (A) Conditional inactivation of Ago2 in adult neurons. Expression of Ago2 was analyzed by Western blotting of the striatal protein lysates derived from three Ago2 fl/fl mice (lanes 1–3), and three Camk2a -Cre; Ago2 fl/fl mice (lanes 4–6). The lysates derived from Ago2 −/− and WT mouse embryonic fibroblasts (MEF) were used as controls for the specificity of the anti-Ago2 antibodies. Equal protein concentration in the samples was controlled by β actin loading. (B and C) Ago2 deficiency in the forebrain does not affect brain morphology. (B) The overall brain morphology of 12-wk-old Camk2a -Cre; Ago2 fl/fl and Ago2 fl/fl control mice was analyzed using standard Nissl-stain ( n = 3/genotype). Two representative images from sagittal brain sections of mice of both genotypes are shown. (C) Saggital brain sections of Ago2 fl/fl and Camk2a -Cre; Ago2 fl/fl mice are shown ( n = 3/genotype). Striatal morphology was analyzed by visualizing Drd1 and Drd2 MSNs (top) using antibodies against the MSN-enriched protein <t>DARPP-32</t> (green) and the Drd2-MSN–specific adenosine 2A (A2A) receptor (red); the dopaminergic terminals (bottom) were visualized by expression of the dopamine-producing enzyme TH (green), and neuronal nuclei in the striatum were visualized by using the neuron-specific marker <t>NeuN</t> (red). The nucleus of each cell was visualized using Draq5 DNA staining (blue). Bar, 100 µm.
    Neun, supplied by Millipore, used in various techniques. Bioz Stars score: 94/100, based on 13758 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Millipore antibodies neun
    Gprin3-BacTRAP mice allow for the isolation of translating mRNA from CA3 neurons A) Immunohistochemical labeling for the EGFP fusion proteins shows expression in several brain regions, but in hippocampus the labeling is primarily in the CA3 region. B–C) Double labeling for either <t>NeuN</t> or <t>GFAP</t> confirm that Gprin3-EFGP-L10a positive cells are neuronal. D) qRT-PCR from TRAP-IP and Unbound (UnB) mRNA isolations demonstrates significant enrichment for Gprin3 in the TRAP fraction and the glial specific marker Gfap in the unbound fraction. E) Read density plots from RNA-Seq data of the canonically neuronal gene Tuj1 and the glial gene Aqp4 demonstrate enrichment of neuronal genes in the TRAP fraction and glial genes in the unbound fraction across stress conditions (FST= forced swim test; CRS= Chronic Restraint Stress). F) Heatmap of genes expressed in either dentate gyrus (black) or CA3 (red) shows that the TRAP-IP is highly enriched in CA3 specific genes, whereas dentate specific genes are enriched in the unbound fraction. (*p
    Antibodies Neun, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 57 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    ABclonal rabbit anti neun
    Gprin3-BacTRAP mice allow for the isolation of translating mRNA from CA3 neurons A) Immunohistochemical labeling for the EGFP fusion proteins shows expression in several brain regions, but in hippocampus the labeling is primarily in the CA3 region. B–C) Double labeling for either <t>NeuN</t> or <t>GFAP</t> confirm that Gprin3-EFGP-L10a positive cells are neuronal. D) qRT-PCR from TRAP-IP and Unbound (UnB) mRNA isolations demonstrates significant enrichment for Gprin3 in the TRAP fraction and the glial specific marker Gfap in the unbound fraction. E) Read density plots from RNA-Seq data of the canonically neuronal gene Tuj1 and the glial gene Aqp4 demonstrate enrichment of neuronal genes in the TRAP fraction and glial genes in the unbound fraction across stress conditions (FST= forced swim test; CRS= Chronic Restraint Stress). F) Heatmap of genes expressed in either dentate gyrus (black) or CA3 (red) shows that the TRAP-IP is highly enriched in CA3 specific genes, whereas dentate specific genes are enriched in the unbound fraction. (*p
    Rabbit Anti Neun, supplied by ABclonal, used in various techniques. Bioz Stars score: 93/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    85
    Millipore marker neun
    Gprin3-BacTRAP mice allow for the isolation of translating mRNA from CA3 neurons A) Immunohistochemical labeling for the EGFP fusion proteins shows expression in several brain regions, but in hippocampus the labeling is primarily in the CA3 region. B–C) Double labeling for either <t>NeuN</t> or <t>GFAP</t> confirm that Gprin3-EFGP-L10a positive cells are neuronal. D) qRT-PCR from TRAP-IP and Unbound (UnB) mRNA isolations demonstrates significant enrichment for Gprin3 in the TRAP fraction and the glial specific marker Gfap in the unbound fraction. E) Read density plots from RNA-Seq data of the canonically neuronal gene Tuj1 and the glial gene Aqp4 demonstrate enrichment of neuronal genes in the TRAP fraction and glial genes in the unbound fraction across stress conditions (FST= forced swim test; CRS= Chronic Restraint Stress). F) Heatmap of genes expressed in either dentate gyrus (black) or CA3 (red) shows that the TRAP-IP is highly enriched in CA3 specific genes, whereas dentate specific genes are enriched in the unbound fraction. (*p
    Marker Neun, supplied by Millipore, used in various techniques. Bioz Stars score: 85/100, based on 31 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Thermo Fisher neun
    CD24+ Ptch1 lox/lox ;GFAP cre cells co-label with markers of neural progenitors and granule cell precursors. (A-R) Co-immunolabelling of cytospun flow-sorted CD24+ and CD24- Ptch1 lox/lox ;GFAP cre primary cells with markers of progenitor and differentiated cells. Adjacent bar graphs illustrate the percentage of CD24+ (white bars) and CD24- (black bars) cells that co-labelled with their respective secondary marker. Co-labelled antibodies were <t>PCNA:</t> proliferating cells (A-C), Sox2: stem/progenitor cells (D-F), <t>NeuN:</t> mature neurons (G-I), βIIItubulin: neural progenitors (J-L), Pax6: radial glial progenitors (M-O) and BLBP: radial glial cells (P-R). Inset images show magnified images of the co-staining. Scale bar A, H, J, K and P 200μm, scale bar B, D, E, G, M, N and Q 100μm. NS: non-significant, *p
    Neun, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 92/100, based on 541 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    CXCR4 modulates neuropathic pain. a – c CXCR4 immunofluorescent co-staining with NeuN (a neuron marker) ( a , a′ ), GFAP (an astrocyte marker) ( b , b′ ) or IBA1 (a microglial marker) ( c , c′ ) in the lumbar segment of the spinal cord at 7 days after pSNL surgery. * p

    Journal: Journal of Neuroinflammation

    Article Title: miRNA-23a/CXCR4 regulates neuropathic pain via directly targeting TXNIP/NLRP3 inflammasome axis

    doi: 10.1186/s12974-018-1073-0

    Figure Lengend Snippet: CXCR4 modulates neuropathic pain. a – c CXCR4 immunofluorescent co-staining with NeuN (a neuron marker) ( a , a′ ), GFAP (an astrocyte marker) ( b , b′ ) or IBA1 (a microglial marker) ( c , c′ ) in the lumbar segment of the spinal cord at 7 days after pSNL surgery. * p

    Article Snippet: The sections were then incubated with fluorescent-conjugated secondary antibody ( , , ; , Invitrogen) at 37 °C for 1 h. For fluorescence in situ hybridization (FISH) and IF co-staining, CXCR4 antisense or sense probe (CDS: 356-916 in ) or TXNIP antisense or sense probe (883–1185 in NM_001009935.3) with digoxin modification were hybridized to spinal slices as instructed in the FISH kit (Guangzhou Exon) and incubated with fluorescent-conjugated EGFP secondary anti-digoxin and then incubated with NeuN antibody (1:500, MAB377; Millipore), GFAP antibody (1:500, ab10062, ab7260, Abcam), and IBA1 antibody (1:200, WAKO, 019–19,741), respectively, and finally incubated with AlexaFluor 568 antibody (Abcam).

    Techniques: Staining, Marker

    Ago2 is dispensable for brain organization and neuronal maintenance in the adult brain. (A) Conditional inactivation of Ago2 in adult neurons. Expression of Ago2 was analyzed by Western blotting of the striatal protein lysates derived from three Ago2 fl/fl mice (lanes 1–3), and three Camk2a -Cre; Ago2 fl/fl mice (lanes 4–6). The lysates derived from Ago2 −/− and WT mouse embryonic fibroblasts (MEF) were used as controls for the specificity of the anti-Ago2 antibodies. Equal protein concentration in the samples was controlled by β actin loading. (B and C) Ago2 deficiency in the forebrain does not affect brain morphology. (B) The overall brain morphology of 12-wk-old Camk2a -Cre; Ago2 fl/fl and Ago2 fl/fl control mice was analyzed using standard Nissl-stain ( n = 3/genotype). Two representative images from sagittal brain sections of mice of both genotypes are shown. (C) Saggital brain sections of Ago2 fl/fl and Camk2a -Cre; Ago2 fl/fl mice are shown ( n = 3/genotype). Striatal morphology was analyzed by visualizing Drd1 and Drd2 MSNs (top) using antibodies against the MSN-enriched protein DARPP-32 (green) and the Drd2-MSN–specific adenosine 2A (A2A) receptor (red); the dopaminergic terminals (bottom) were visualized by expression of the dopamine-producing enzyme TH (green), and neuronal nuclei in the striatum were visualized by using the neuron-specific marker NeuN (red). The nucleus of each cell was visualized using Draq5 DNA staining (blue). Bar, 100 µm.

    Journal: The Journal of Experimental Medicine

    Article Title: Argonaute 2 in dopamine 2 receptor-expressing neurons regulates cocaine addiction

    doi: 10.1084/jem.20100451

    Figure Lengend Snippet: Ago2 is dispensable for brain organization and neuronal maintenance in the adult brain. (A) Conditional inactivation of Ago2 in adult neurons. Expression of Ago2 was analyzed by Western blotting of the striatal protein lysates derived from three Ago2 fl/fl mice (lanes 1–3), and three Camk2a -Cre; Ago2 fl/fl mice (lanes 4–6). The lysates derived from Ago2 −/− and WT mouse embryonic fibroblasts (MEF) were used as controls for the specificity of the anti-Ago2 antibodies. Equal protein concentration in the samples was controlled by β actin loading. (B and C) Ago2 deficiency in the forebrain does not affect brain morphology. (B) The overall brain morphology of 12-wk-old Camk2a -Cre; Ago2 fl/fl and Ago2 fl/fl control mice was analyzed using standard Nissl-stain ( n = 3/genotype). Two representative images from sagittal brain sections of mice of both genotypes are shown. (C) Saggital brain sections of Ago2 fl/fl and Camk2a -Cre; Ago2 fl/fl mice are shown ( n = 3/genotype). Striatal morphology was analyzed by visualizing Drd1 and Drd2 MSNs (top) using antibodies against the MSN-enriched protein DARPP-32 (green) and the Drd2-MSN–specific adenosine 2A (A2A) receptor (red); the dopaminergic terminals (bottom) were visualized by expression of the dopamine-producing enzyme TH (green), and neuronal nuclei in the striatum were visualized by using the neuron-specific marker NeuN (red). The nucleus of each cell was visualized using Draq5 DNA staining (blue). Bar, 100 µm.

    Article Snippet: DARPP-32 (1:1,000; Novus Biologicals), NeuN (1:1,000; Millipore), TH (1:500; Millipore), and A2A (1:100; Millipore) were visualized using immunofluorescence analysis (Alexa Fluor 546/488–labeled goat anti–mouse/anti–rabbit IgGs [H+L] dilution 1:500; Invitrogen).

    Techniques: Expressing, Western Blot, Derivative Assay, Mouse Assay, Protein Concentration, Staining, Marker

    SVCT2 is upregulated after stroke and mainly localized in endothelial structures. Sections of brain tissue from mice with MCAO were stained with SVCT2 (red, left column) and co-stained with occludin (B, B'), NeuN (E, E'), GFAP (H, H'). Intense SVCT2- immunoreactivity was found in the infarct area (ipsilateral), compared to only weak expression on the contralateral side (compare A to A', D to D', G to G'). Co-immunohistochemistry with occludin showed colocalisation in linear, occasionally branched structures reminiscent of capillaries (A–C, D–F, G–I, arrows). Co-stainings with NeuN showed weak SVCT2-immunoreactivity in NeuN positive cells in both hemispheres (D–F, D'–F', arrowheads). Co-stainings with GFAP showed no SVCT2-immunoreactivity in GFAP-positive cells (G–I, G'–I'). Size bars: 10 µm.

    Journal: PLoS ONE

    Article Title: Sodium-Dependent Vitamin C Transporter 2 (SVCT2) Expression and Activity in Brain Capillary Endothelial Cells after Transient Ischemia in Mice

    doi: 10.1371/journal.pone.0017139

    Figure Lengend Snippet: SVCT2 is upregulated after stroke and mainly localized in endothelial structures. Sections of brain tissue from mice with MCAO were stained with SVCT2 (red, left column) and co-stained with occludin (B, B'), NeuN (E, E'), GFAP (H, H'). Intense SVCT2- immunoreactivity was found in the infarct area (ipsilateral), compared to only weak expression on the contralateral side (compare A to A', D to D', G to G'). Co-immunohistochemistry with occludin showed colocalisation in linear, occasionally branched structures reminiscent of capillaries (A–C, D–F, G–I, arrows). Co-stainings with NeuN showed weak SVCT2-immunoreactivity in NeuN positive cells in both hemispheres (D–F, D'–F', arrowheads). Co-stainings with GFAP showed no SVCT2-immunoreactivity in GFAP-positive cells (G–I, G'–I'). Size bars: 10 µm.

    Article Snippet: Double fluorescent staining was performed using SVCT2 in combination with the Zonula occludens marker Occludin (1∶100, Zymed Laboratories), the neuronal marker NeuN (Chemicon), the glial marker GFAP (Sigma), the endothelial marker Von-Willebrand-Factor (1∶50, Santa Cruz) and CD34 (1∶100, BD Biosciences).

    Techniques: Mouse Assay, Staining, Expressing, Immunohistochemistry

    Microscopic and histological views of transgene expression. ( A ) A light field microscope view of V1. An optrode (arrow) inserted through a hole between the mesh-ECoG (blue squares) on V1. ( B ) A fluorescent microscope view of the same area as in A. EYFP fluorescence was observed around the injection site (arrowhead). The optrode insertion site (arrow) was within the fluorescence-positive area. ( C ) GFP immunostaining of a coronal section. The hChR2-EYFP fluorescence-positive cells were mainly observed in layers V and VI. Arrowhead indicates the injection site. Roman numbers indicate layers whose laminar borders were estimated from the result of Vglut1 in situ hybridization (ISH) of the adjacent section. ( D ) Double labeling for GFP and NeuN. Almost all ChR2-YFP expressing cells (detected by GFP probe, dark blue) were positive for NeuN, a mature neuron marker (detected by immunostaining, brown). ( E ) Double labeling for vGlut1 and GFP. Numerous ChR2-YFP-expressing cells (detected by GFP immunostaining, brown) were also positive for Vglut1 , an excitatory neuron marker (detected by an ISH probe, dark blue) in the visual cortex. In D and E, double positive cells are indicated by arrowheads.

    Journal: Scientific Reports

    Article Title: Locally induced neuronal synchrony precisely propagates to specific cortical areas without rhythm distortion

    doi: 10.1038/s41598-018-26054-8

    Figure Lengend Snippet: Microscopic and histological views of transgene expression. ( A ) A light field microscope view of V1. An optrode (arrow) inserted through a hole between the mesh-ECoG (blue squares) on V1. ( B ) A fluorescent microscope view of the same area as in A. EYFP fluorescence was observed around the injection site (arrowhead). The optrode insertion site (arrow) was within the fluorescence-positive area. ( C ) GFP immunostaining of a coronal section. The hChR2-EYFP fluorescence-positive cells were mainly observed in layers V and VI. Arrowhead indicates the injection site. Roman numbers indicate layers whose laminar borders were estimated from the result of Vglut1 in situ hybridization (ISH) of the adjacent section. ( D ) Double labeling for GFP and NeuN. Almost all ChR2-YFP expressing cells (detected by GFP probe, dark blue) were positive for NeuN, a mature neuron marker (detected by immunostaining, brown). ( E ) Double labeling for vGlut1 and GFP. Numerous ChR2-YFP-expressing cells (detected by GFP immunostaining, brown) were also positive for Vglut1 , an excitatory neuron marker (detected by an ISH probe, dark blue) in the visual cortex. In D and E, double positive cells are indicated by arrowheads.

    Article Snippet: After obtaining dark blue-coloured ISH signals via the reaction of alkaline phosphatase and nitroblue tetrazolium (NBT)/5-Bromo-4-Chloro-3-Indolyl Phosphate (BCIP), immunohistochemical staining on the same section was performed using antibodies against NeuN (A60; Millipore, Temecula, CA; 1:200) or GFP (GF090R; Nacalai, Kyoto, Japan; 1:2,000).

    Techniques: Expressing, Microscopy, Fluorescence, Injection, Immunostaining, In Situ Hybridization, Labeling, Marker

    ( A ) Rates of cells having neurites for treated cells. The greatest of rate of cells having neurites was found for VHL(157–171) peptide-treated cells, with the rate being very low for the others; ( B ) Immunocytochemical microphotographs for TAT(YARAAARQARA)-treated cells ( left ), VHL(157–168)-treated cell ( center ), and VHL(157–171)-treated cells ( right ). Immunocytochemistry using anti-NFH antibody for neuron (green) and DAPI for nuclei (blue). Scale bar = 20 μm; ( C ) Confocal microscope images of engrafted cells with PKH26PCL-prelabeling in the non-treated group ( left ), VHL(157–168)-treated group ( center ), and the VHL(157–171)-treated group ( right ). Immunohistochemistry using anti-NeuN antibody (green) and PKH26PCL (red).

    Journal: International Journal of Molecular Sciences

    Article Title: BC-Box Motif-Mediated Neuronal Differentiation of Somatic Stem Cells

    doi: 10.3390/ijms19020466

    Figure Lengend Snippet: ( A ) Rates of cells having neurites for treated cells. The greatest of rate of cells having neurites was found for VHL(157–171) peptide-treated cells, with the rate being very low for the others; ( B ) Immunocytochemical microphotographs for TAT(YARAAARQARA)-treated cells ( left ), VHL(157–168)-treated cell ( center ), and VHL(157–171)-treated cells ( right ). Immunocytochemistry using anti-NFH antibody for neuron (green) and DAPI for nuclei (blue). Scale bar = 20 μm; ( C ) Confocal microscope images of engrafted cells with PKH26PCL-prelabeling in the non-treated group ( left ), VHL(157–168)-treated group ( center ), and the VHL(157–171)-treated group ( right ). Immunohistochemistry using anti-NeuN antibody (green) and PKH26PCL (red).

    Article Snippet: Antibodies against anti-MAP2 antibody (Sigma-Aldrich, St. Louis, MO, USA), anti-Neurofilment-H (NFH) antibody (Sigma-Aldrich), anti-NeuN antibody (Merk Millipore, Billerica, MA, USA), anti-GFAP antibody (DAKO, Santa Clara, CA, USA), anti-tyrosine hydroxylase (TH) antibody (Merk Millipore, Billerica, MA, USA), anti-choline acetyl transferase (ChAT) antibody (Abbiotec, San Diego, CA, USA), anti-glutamic acid decaboxylase (GAD) antibody (Enzo Life Sciences, Flamingdale, NY, USA), and anti-rhodopsin antibody (Santa Cruz, San Diego, CA, USA) were used.

    Techniques: Immunocytochemistry, Microscopy, Immunohistochemistry

    Most BrdU positive cells in the DG, independent of genotype or strain, express the neuronal marker, NeuN A) Fluorescent immunohistochemistry for BrdU (red) and NeuN (green). Merged image shows co-localization of BrdU and NeuN; scale bar = 50μm B) Fluorescent immunohistochemistry for BrdU (red) and GFAP (green). Dapi (blue) was used as a background nuclear stain in order to visualize the GCL of the DG. Merged image shows that BrdU and GFAP do not co-localize; scale bar = 50μm C) Percent of BrdU positive cells that co-localize with NeuN or GFAP in (+/+) and MOR-1 (−/−) C57BL/6 mice. D) Percent of BrdU positive cells that co-localize with NeuN or GFAP in (+/+) and MOR-1 (−/−) 129S6 mice. (n=4–5 per group)

    Journal: Neuroscience

    Article Title: Loss of MOR-1 on different genetic backgrounds leads to increased BrdU labeling in the dentate gyrus only after repeated injection

    doi: 10.1016/j.neuroscience.2011.12.046

    Figure Lengend Snippet: Most BrdU positive cells in the DG, independent of genotype or strain, express the neuronal marker, NeuN A) Fluorescent immunohistochemistry for BrdU (red) and NeuN (green). Merged image shows co-localization of BrdU and NeuN; scale bar = 50μm B) Fluorescent immunohistochemistry for BrdU (red) and GFAP (green). Dapi (blue) was used as a background nuclear stain in order to visualize the GCL of the DG. Merged image shows that BrdU and GFAP do not co-localize; scale bar = 50μm C) Percent of BrdU positive cells that co-localize with NeuN or GFAP in (+/+) and MOR-1 (−/−) C57BL/6 mice. D) Percent of BrdU positive cells that co-localize with NeuN or GFAP in (+/+) and MOR-1 (−/−) 129S6 mice. (n=4–5 per group)

    Article Snippet: After pretreatment (described above) and blocking step with 5% goat serum sections were incubated sequentially with BrdU primary antibody (Rat anti BrdU; Serotec; 1:100) and secondary antibody (Alexa Fluor 594 goat anti-rat; Invitrogen; 1:250) and then with either NeuN primary antibody (mouse anti-NeuN; Chemicon; 1:100) or GFAP primary antibody (rabbit anti-GFAP; Dako; 1:1000) and their respective secondary antibodies (Alexa Fluor 488 goat anti-mouse; Invitrogen; 1:250 and Alexa Fluor 488 goat anti-rabbit; Invitrogen; 1:1000).

    Techniques: Marker, Immunohistochemistry, Staining, Mouse Assay

    H3.X/Y protein expression in human brain. (A) Overview IF picture of commercially available human hippocampus section stained with DAPI (DNA, gray). (B) Human hippocampus sections were costained with α-H3.X/Y (red), α-NeuN (neuronal marker, green), and DAPI (DNA, blue). The boxed section from A is shown. Arrows indicate neuronal cells with positive α-H3.X/Y staining in the region above DG. One out of three representative stainings is shown. (C) The boxed section and the α-H3.X/Y–positive cell marked with an asterisk in B are shown in higher resolution. Costainings with astrocyte marker antibody (α-GFAP) are shown in Fig. S5 . Bars: (A and B) 200 µm; (C, top) 2 µm; (C, bottom) 10 µm.

    Journal: The Journal of Cell Biology

    Article Title: Identification and characterization of two novel primate-specific histone H3 variants, H3.X and H3.Y

    doi: 10.1083/jcb.201002043

    Figure Lengend Snippet: H3.X/Y protein expression in human brain. (A) Overview IF picture of commercially available human hippocampus section stained with DAPI (DNA, gray). (B) Human hippocampus sections were costained with α-H3.X/Y (red), α-NeuN (neuronal marker, green), and DAPI (DNA, blue). The boxed section from A is shown. Arrows indicate neuronal cells with positive α-H3.X/Y staining in the region above DG. One out of three representative stainings is shown. (C) The boxed section and the α-H3.X/Y–positive cell marked with an asterisk in B are shown in higher resolution. Costainings with astrocyte marker antibody (α-GFAP) are shown in Fig. S5 . Bars: (A and B) 200 µm; (C, top) 2 µm; (C, bottom) 10 µm.

    Article Snippet: The following primary antibodies were used in this study: α-HA (clone 12CA5; Roche), α-H3S10ph (Millipore), α-H3 (C terminus; Abcam), α-NeuN (Millipore), and α-GFAP (Dako).

    Techniques: Expressing, Staining, Marker

    The iron levels and apoptosis in neurons in the cortex and hippocampus in wild-type and GFAP-shhepcidin mice following LPS injection. Double immunofluorescence labeling of FPN1 ( a ), Ferritin-L ( b ) or cleaved caspase 3 ( c ) and NeuN (staining for neurons) was carried out in cortical and hippocampal sections. Scale bar=100 μ m. Values are presented as the mean±S.D. ** P

    Journal: Cell Death & Disease

    Article Title: Astrocyte hepcidin is a key factor in LPS-induced neuronal apoptosis

    doi: 10.1038/cddis.2017.93

    Figure Lengend Snippet: The iron levels and apoptosis in neurons in the cortex and hippocampus in wild-type and GFAP-shhepcidin mice following LPS injection. Double immunofluorescence labeling of FPN1 ( a ), Ferritin-L ( b ) or cleaved caspase 3 ( c ) and NeuN (staining for neurons) was carried out in cortical and hippocampal sections. Scale bar=100 μ m. Values are presented as the mean±S.D. ** P

    Article Snippet: After blocking for 1 h with normal goat serum prepared in 0.01 M PBS, the slices were incubated overnight at 4 °C with mouse anti-GFAP monoclonal antibody (1:400) (MAB360; Millipore, Temecula, CA, USA), mouse anti-CD11b monoclonal antibody (1:400) (ab1211; Abcam), anti-NeuN monoclonal antibody (1:100) (MAB377; Millipore), rabbit anti-FPN1 antibody (1:400) (MTP11-A; Alpha Diagnostic International), rabbit anti-caspase-3 (1:300) (9662 and 9661; Cell Signaling Technology, Danvers, MA, USA), rabbit anti-mouse ferritin light chain (1:10 000) (FERL14-S; Alpha Diagnostic International) or rabbit anti-mouse ferritin heavy chain (1 : 200) (ab65080; Abcam).

    Techniques: Mouse Assay, Injection, Immunofluorescence, Labeling, Staining

    Spatial distribution and cell type of CYLD ischemic cortical borders after 2 h of focal cerebral ischemia and 72 h of reperfusion, n = 6 (Scale bar = 100 μm). (A) Co-expression of CYLD (green) and NeuN (red, neurons). (B) Microglia co-expressing CYLD (green) and Iba1 (red, microglia). (C) Astrocytes co-expressing CYLD (green) and GFAP (red, astrocytes). 1–3 were magnified from a merged image and show CYLD. Yellow arrows indicate co-expression between CYLD and neurons (Scale bar = 50 μm).

    Journal: Frontiers in Molecular Neuroscience

    Article Title: Electroacupuncture Suppresses the NF-κB Signaling Pathway by Upregulating Cylindromatosis to Alleviate Inflammatory Injury in Cerebral Ischemia/Reperfusion Rats

    doi: 10.3389/fnmol.2017.00363

    Figure Lengend Snippet: Spatial distribution and cell type of CYLD ischemic cortical borders after 2 h of focal cerebral ischemia and 72 h of reperfusion, n = 6 (Scale bar = 100 μm). (A) Co-expression of CYLD (green) and NeuN (red, neurons). (B) Microglia co-expressing CYLD (green) and Iba1 (red, microglia). (C) Astrocytes co-expressing CYLD (green) and GFAP (red, astrocytes). 1–3 were magnified from a merged image and show CYLD. Yellow arrows indicate co-expression between CYLD and neurons (Scale bar = 50 μm).

    Article Snippet: Sections were subsequently incubated with prepared primary antibodies at 4°C overnight as follows: Anti-NeuN mouse (labeled neurons, MAB377, Millipore, 1:100), anti-GFAP mouse (labeled astrocytes, BM0055, Boster, 1:100), anti-Iba1 goat (to label microglia, NB100-1028SS, Novus, 1:50), anti-CYLD rabbit (11110-1-AP, Proteintech, 1:100), anti-CYLD mouse (SC-74435, Santa Cruz, 1:100), anti-NF-κB p65 rabbit (#8242, Cell Signaling Technology, 1:50) and anti-CX3CL1 rabbit (ab25088, Abcam, 1:100).

    Techniques: Expressing

    Dendritic spine density is decreased in peri-lesional tissues. (a) Two days post-occlusion, absence of NeuN staining demarcates the microinfarct core, the border of which is traced with a yellow dashed line. Viable neurons exist beyond the microinfarct core, evidenced by robust NeuN staining, but C-fos studies in Figure 4 demonstrated functional deficits up to 700 um beyond the core (blue dashed line). (b) In the same slice, YFP brightly labels layer 2/3 cortical neurons and their processes. Colored squares highlight example YFP and NeuN-positive pyramidal neurons that were selected for high resolution imaging of dendrites. (c) High resolution confocal microscopy of dendrites. Images shown are 30 µm average intensity projections. Small colored rectangles indicate a typical dendritic segment used for spine counting. (d) Individual spines were manually counted along isolated dendritic segments (arrowheads), and divided by the length of dendritic segment analyzed to provide a measure of spine density. An average spine density for each neuron (n = 28 neurons in total) was calculated from several dendritic segments. (e) Mean spine density per neuron versus the neuron’s distance from the microinfarct core. Spine density decreases closer to the microinfarct core (Pearson, R 2 = 0.38, p = 0.0005). (f) Cells within the peri-lesional region show a significant ∼25% decrease in spine density compared to cells beyond the peri-lesional region (n = 14 neurons/group compiled over two mice, p = 0.005 by Wilcoxon Rank-sum test). Data are mean ± SEM.

    Journal: Journal of Cerebral Blood Flow & Metabolism

    Article Title: Functional deficits induced by cortical microinfarcts

    doi: 10.1177/0271678X16685573

    Figure Lengend Snippet: Dendritic spine density is decreased in peri-lesional tissues. (a) Two days post-occlusion, absence of NeuN staining demarcates the microinfarct core, the border of which is traced with a yellow dashed line. Viable neurons exist beyond the microinfarct core, evidenced by robust NeuN staining, but C-fos studies in Figure 4 demonstrated functional deficits up to 700 um beyond the core (blue dashed line). (b) In the same slice, YFP brightly labels layer 2/3 cortical neurons and their processes. Colored squares highlight example YFP and NeuN-positive pyramidal neurons that were selected for high resolution imaging of dendrites. (c) High resolution confocal microscopy of dendrites. Images shown are 30 µm average intensity projections. Small colored rectangles indicate a typical dendritic segment used for spine counting. (d) Individual spines were manually counted along isolated dendritic segments (arrowheads), and divided by the length of dendritic segment analyzed to provide a measure of spine density. An average spine density for each neuron (n = 28 neurons in total) was calculated from several dendritic segments. (e) Mean spine density per neuron versus the neuron’s distance from the microinfarct core. Spine density decreases closer to the microinfarct core (Pearson, R 2 = 0.38, p = 0.0005). (f) Cells within the peri-lesional region show a significant ∼25% decrease in spine density compared to cells beyond the peri-lesional region (n = 14 neurons/group compiled over two mice, p = 0.005 by Wilcoxon Rank-sum test). Data are mean ± SEM.

    Article Snippet: Immunohistochemistry for c-Fos studies was performed with anti-c-Fos primary antibody from rabbit host (sc-52; 1:500 dilution; Santa Cruz Biotech), anti-NeuN primary antibody from mouse host (MAB339; 1:500; Millipore), and anti-VGlut2 primary antibody from guinea pig host (AF1042; 1:5,000 dilution; R & D Systems;).

    Techniques: Staining, Functional Assay, Imaging, Confocal Microscopy, Isolation, Mouse Assay

    Apoptosis of dentate gyrus neurons induced by adenovirally delivered ICER overexpression. A , β-Galactosidase enzymatic activity in dentate gyrus neurons (note brownish MAP2 immunostaining) infected with an adenoviral vector encoding β-galactosidase (Ad-βgal; arrows). B , RT-PCR analysis of expression of exogenous recombinant adenovirus-delivered ICERIIγgene. RNA was isolated 24 hr after infection (with either Ad-βgal or the adenovirus-carrying ICERIIγgene Ad-ICER). The primers were designed to recognize only the transgenes that were used: Ad-ICER, cDNA from cultures treated with Ad-ICER was used for the reaction; Ad-βgal, cDNA from cultures treated with Ad-βgal; pRSV-ICER, pRSV-ICER plasmid DNA was used as a template for positive control of the reaction. C , Quantitative analysis of neurons with altered chromatin morphology after exposure to Ad-ICER. The cultures were exposed overnight to either Ad-βgal or Ad-ICER (MOI, 50, for both). Cells were fixed 24 hr after infection and stained with Hoechst 33285 and an anti body against NeuN. For each experimental variant, the cells were counted from 24 incidental microscopic fields from four independent cultures grown on 10 mm glass coverslips. Results are shown as an average percentage of neurons with changed chromatin morphology per coverslip ± SEM; *** p

    Journal: The Journal of Neuroscience

    Article Title: Inducible cAMP Early Repressor, an Endogenous Antagonist of cAMP Responsive Element-Binding Protein, Evokes Neuronal Apoptosis In Vitro

    doi: 10.1523/JNEUROSCI.23-11-04519.2003

    Figure Lengend Snippet: Apoptosis of dentate gyrus neurons induced by adenovirally delivered ICER overexpression. A , β-Galactosidase enzymatic activity in dentate gyrus neurons (note brownish MAP2 immunostaining) infected with an adenoviral vector encoding β-galactosidase (Ad-βgal; arrows). B , RT-PCR analysis of expression of exogenous recombinant adenovirus-delivered ICERIIγgene. RNA was isolated 24 hr after infection (with either Ad-βgal or the adenovirus-carrying ICERIIγgene Ad-ICER). The primers were designed to recognize only the transgenes that were used: Ad-ICER, cDNA from cultures treated with Ad-ICER was used for the reaction; Ad-βgal, cDNA from cultures treated with Ad-βgal; pRSV-ICER, pRSV-ICER plasmid DNA was used as a template for positive control of the reaction. C , Quantitative analysis of neurons with altered chromatin morphology after exposure to Ad-ICER. The cultures were exposed overnight to either Ad-βgal or Ad-ICER (MOI, 50, for both). Cells were fixed 24 hr after infection and stained with Hoechst 33285 and an anti body against NeuN. For each experimental variant, the cells were counted from 24 incidental microscopic fields from four independent cultures grown on 10 mm glass coverslips. Results are shown as an average percentage of neurons with changed chromatin morphology per coverslip ± SEM; *** p

    Article Snippet: Primary antibodies were as follows: monoclonal anti-MAP2 protein (Sigma) diluted 1:400, monoclonal anti-NeuN (Chemicon, Temecula, CA) diluted 1:500, and polyclonal ICER 1:20,000 ( ).

    Techniques: Over Expression, Activity Assay, Immunostaining, Infection, Plasmid Preparation, Reverse Transcription Polymerase Chain Reaction, Expressing, Recombinant, Isolation, Positive Control, Staining, Variant Assay

    History of alcohol dependence increases DNMT1 expression in neuronal cells in mPFC. A , Western blot analysis shows no difference in DNMT1, DNMT3a, and DNMT3b protein expression. Black bars indicate mean values (± SEM) of control rats. Gray bars indicate mean values (± SEM) of PD rats. Protein expression is represented as DNMT/β-tubulin relative to control. B , C , Immunohistochemical detection of DNMT1 (green) and neuronal cells (red) in the mPFC of control (top) and PD rats (bottom). Right top and bottom, Merge DNMT1/NeuN. C , Average density of DNMT1 in neuronal cells. # p

    Journal: The Journal of Neuroscience

    Article Title: DNA Methylation in the Medial Prefrontal Cortex Regulates Alcohol-Induced Behavior and Plasticity

    doi: 10.1523/JNEUROSCI.4571-14.2015

    Figure Lengend Snippet: History of alcohol dependence increases DNMT1 expression in neuronal cells in mPFC. A , Western blot analysis shows no difference in DNMT1, DNMT3a, and DNMT3b protein expression. Black bars indicate mean values (± SEM) of control rats. Gray bars indicate mean values (± SEM) of PD rats. Protein expression is represented as DNMT/β-tubulin relative to control. B , C , Immunohistochemical detection of DNMT1 (green) and neuronal cells (red) in the mPFC of control (top) and PD rats (bottom). Right top and bottom, Merge DNMT1/NeuN. C , Average density of DNMT1 in neuronal cells. # p

    Article Snippet: Sections were incubated in rabbit anti-DNMT1 (1 μg/ml; Abcam) or mouse anti-5Mec (1:300, Acris) and chicken anti-NeuN (1:500; EMD Millipore) for 48 h at 4°C and with the secondary antibody for 2 h at room temperature (donkey anti-rabbit 488 for DNMT1, donkey anti-mouse 555 for 5MeC, and donkey anti-chicken 633 for NeuN, 1:1000; Invitrogen).

    Techniques: Expressing, Western Blot, Immunohistochemistry

    A , Immunohistochemical detection of 5MeC (red) and neuronal cells (green) in the mPFC of control (top) and PD (bottom). Right top and bottom, Merge 5MeC/NeuN. B , Average density of 5MeC in neuronal cells. # p

    Journal: The Journal of Neuroscience

    Article Title: DNA Methylation in the Medial Prefrontal Cortex Regulates Alcohol-Induced Behavior and Plasticity

    doi: 10.1523/JNEUROSCI.4571-14.2015

    Figure Lengend Snippet: A , Immunohistochemical detection of 5MeC (red) and neuronal cells (green) in the mPFC of control (top) and PD (bottom). Right top and bottom, Merge 5MeC/NeuN. B , Average density of 5MeC in neuronal cells. # p

    Article Snippet: Sections were incubated in rabbit anti-DNMT1 (1 μg/ml; Abcam) or mouse anti-5Mec (1:300, Acris) and chicken anti-NeuN (1:500; EMD Millipore) for 48 h at 4°C and with the secondary antibody for 2 h at room temperature (donkey anti-rabbit 488 for DNMT1, donkey anti-mouse 555 for 5MeC, and donkey anti-chicken 633 for NeuN, 1:1000; Invitrogen).

    Techniques: Immunohistochemistry

    TRAPed Cells Are Primarily Direct Pathway Medium Spiny Neurons (A-F) Representative 40x confocal images from the striatum of FosTRAP mice treated with 6-OHDA and levodopa, immunostained for different cellular markers. Left columns show TRAP-tdTomato, middle columns show antibody staining for NeuN (A), Choline Acetyltransferase (ChAT, B), Neuropeptide Y (NPY, C), Parvalbumin (PV, D), DARPP-32 (E), D2-GFP (F), and right columns show merged images. White arrowheads denote colocalization, while white arrows show non-colocalized cells. (G) Percent of TRAPed striatal cells positive for each cellular marker. .

    Journal: Neuron

    Article Title: A Subpopulation of Striatal Neurons Mediates Levodopa-Induced Dyskinesia

    doi: 10.1016/j.neuron.2018.01.017

    Figure Lengend Snippet: TRAPed Cells Are Primarily Direct Pathway Medium Spiny Neurons (A-F) Representative 40x confocal images from the striatum of FosTRAP mice treated with 6-OHDA and levodopa, immunostained for different cellular markers. Left columns show TRAP-tdTomato, middle columns show antibody staining for NeuN (A), Choline Acetyltransferase (ChAT, B), Neuropeptide Y (NPY, C), Parvalbumin (PV, D), DARPP-32 (E), D2-GFP (F), and right columns show merged images. White arrowheads denote colocalization, while white arrows show non-colocalized cells. (G) Percent of TRAPed striatal cells positive for each cellular marker. .

    Article Snippet: Primary antibodies used: Rabbit anti-TH (Pel-Freez, 1:1,000), Chicken anti-TH (Sigma, 1:1,000), Rabbit anti-c-Fos (Cell Signalizing Technology, 1:1,000), Rabbit anti-c-Fos (Santa Cruz, 1:1,000), Goat anti-ChAT (Millipore, 1:500), Rabbit anti-DARPP-32 (Cell Signaling Technology, 1:1,000), Mouse anti-RFP (Rockland Immunochemicals, 1:500), Rabbit anti-NeuN (Millipore, 1:1,000), Rabbit anti-NPY (Cell Signaling Technology, 1:1,000), Rabbit anti-PV (Swant, 1:2,000), Rabbit anti-Erg-1 (Cell Signaling Technology, 1:500), or Goat anti-ΔFosB (Santa Cruz Biotechnology, 1:500).

    Techniques: Mouse Assay, Staining, Marker

    ALDH7A1 expression is not heterogeneous across brain regions or sexes. (A-D) Co-immunostaining of ALDH7A1 with (A) neuronal marker NeuN, (B) microglia marker Iba1, (C) mature oligodendrocyte (OL) marker CC1, and (D) the oligodendrocyte precursor cell (OPC) marker NG2 + in adult mouse cortex. Scale bars: 50 µm. Boxed insets displayed at higher magnification in right three panels. Inset scale bars: 10 µm. ALDH7A1 did not co-localize with these cell-type markers (A-D, arrowheads). (E-H) ALDH7A1 immunofluorescence (red) in the (E) cerebellum, (F) dentate gyrus, (G) corpus callosum, and (H) olfactory bulb of adult GLT1-eGFP reporter mice. Arrowheads indicate colocalization of ALDH7A1 with GFP in Bergmann glia in (E), adult neural stem cells in (F), fibrous astrocytes in (G), and olfactory bulb astrocytes in (H). Arrows indicate colocalization of ALDH7A1 in velate astrocytes in (E) and hippocampal astrocytes in (F). Scale bars: 100 µm. (I-J) Western blot of ALDH7A1 in adult cortical tissue of male (♂) and female (♀) mice. Expression is normalized to GAPDH for quantification in (J). No differences were observed (male, n = 3 mice; female, n = 3 mice; P = 0.8992, t 4 = 0.1349, two-sided Welch’s t -test).

    Journal: bioRxiv

    Article Title: Astrocyte redox dysregulation causes prefrontal hypoactivity: sulforaphane treats non-ictal pathophysiology in ALDH7A1-mediated epilepsy

    doi: 10.1101/796474

    Figure Lengend Snippet: ALDH7A1 expression is not heterogeneous across brain regions or sexes. (A-D) Co-immunostaining of ALDH7A1 with (A) neuronal marker NeuN, (B) microglia marker Iba1, (C) mature oligodendrocyte (OL) marker CC1, and (D) the oligodendrocyte precursor cell (OPC) marker NG2 + in adult mouse cortex. Scale bars: 50 µm. Boxed insets displayed at higher magnification in right three panels. Inset scale bars: 10 µm. ALDH7A1 did not co-localize with these cell-type markers (A-D, arrowheads). (E-H) ALDH7A1 immunofluorescence (red) in the (E) cerebellum, (F) dentate gyrus, (G) corpus callosum, and (H) olfactory bulb of adult GLT1-eGFP reporter mice. Arrowheads indicate colocalization of ALDH7A1 with GFP in Bergmann glia in (E), adult neural stem cells in (F), fibrous astrocytes in (G), and olfactory bulb astrocytes in (H). Arrows indicate colocalization of ALDH7A1 in velate astrocytes in (E) and hippocampal astrocytes in (F). Scale bars: 100 µm. (I-J) Western blot of ALDH7A1 in adult cortical tissue of male (♂) and female (♀) mice. Expression is normalized to GAPDH for quantification in (J). No differences were observed (male, n = 3 mice; female, n = 3 mice; P = 0.8992, t 4 = 0.1349, two-sided Welch’s t -test).

    Article Snippet: Antibodies used: rabbit anti-ALDH7A1 EP1935Y (Abcam 53278; 1:250), chicken anti-GFP (Abcam 13970; 1:2,000), mouse anti-ALDH1L1 (Millipore MABN495; 1:1,000), mouse anti-CC1 (Calbiochem OP80; 1:50), guinea pig anti-NG2 (William Stallcup, Burnham Institute; 1:1,000), goat anti-Iba1 (Novus NB100-1028; 1:250), mouse anti-NeuN (Millipore MAB377; 1:500), mouse anti-GFAP (Millipore MAB360; 1:400), mouse anti-8-oxo-dG (Trevigen 4354-MC-050; 1:250), guinea pig anti-VGAT (synaptic systems 131 004; 1:250), mouse anti-gephyrin (synaptic systems 147 021; 1:500), AlexaFluor 568 anti-IgG1 for gephyrin antibodies, and AlexaFluor 405-, 488-, 568-, 647-conjugated secondary antibodies.

    Techniques: Expressing, Immunostaining, Marker, Immunofluorescence, Mouse Assay, Western Blot

    Gprin3-BacTRAP mice allow for the isolation of translating mRNA from CA3 neurons A) Immunohistochemical labeling for the EGFP fusion proteins shows expression in several brain regions, but in hippocampus the labeling is primarily in the CA3 region. B–C) Double labeling for either NeuN or GFAP confirm that Gprin3-EFGP-L10a positive cells are neuronal. D) qRT-PCR from TRAP-IP and Unbound (UnB) mRNA isolations demonstrates significant enrichment for Gprin3 in the TRAP fraction and the glial specific marker Gfap in the unbound fraction. E) Read density plots from RNA-Seq data of the canonically neuronal gene Tuj1 and the glial gene Aqp4 demonstrate enrichment of neuronal genes in the TRAP fraction and glial genes in the unbound fraction across stress conditions (FST= forced swim test; CRS= Chronic Restraint Stress). F) Heatmap of genes expressed in either dentate gyrus (black) or CA3 (red) shows that the TRAP-IP is highly enriched in CA3 specific genes, whereas dentate specific genes are enriched in the unbound fraction. (*p

    Journal: Molecular psychiatry

    Article Title: Translational profiling of stress-induced neuroplasticity in the CA3 pyramidal neurons of BDNF Val66Met mice

    doi: 10.1038/mp.2016.219

    Figure Lengend Snippet: Gprin3-BacTRAP mice allow for the isolation of translating mRNA from CA3 neurons A) Immunohistochemical labeling for the EGFP fusion proteins shows expression in several brain regions, but in hippocampus the labeling is primarily in the CA3 region. B–C) Double labeling for either NeuN or GFAP confirm that Gprin3-EFGP-L10a positive cells are neuronal. D) qRT-PCR from TRAP-IP and Unbound (UnB) mRNA isolations demonstrates significant enrichment for Gprin3 in the TRAP fraction and the glial specific marker Gfap in the unbound fraction. E) Read density plots from RNA-Seq data of the canonically neuronal gene Tuj1 and the glial gene Aqp4 demonstrate enrichment of neuronal genes in the TRAP fraction and glial genes in the unbound fraction across stress conditions (FST= forced swim test; CRS= Chronic Restraint Stress). F) Heatmap of genes expressed in either dentate gyrus (black) or CA3 (red) shows that the TRAP-IP is highly enriched in CA3 specific genes, whereas dentate specific genes are enriched in the unbound fraction. (*p

    Article Snippet: Antibodies NeuN (1:1,000; MAB377, Chemicon) and GFAP (1:1,000; AB7260 Abcam) were diluted in the blocking solution overnight at 4 °C.

    Techniques: Mouse Assay, Isolation, Immunohistochemistry, Labeling, Expressing, Quantitative RT-PCR, Marker, RNA Sequencing Assay

    CD24+ Ptch1 lox/lox ;GFAP cre cells co-label with markers of neural progenitors and granule cell precursors. (A-R) Co-immunolabelling of cytospun flow-sorted CD24+ and CD24- Ptch1 lox/lox ;GFAP cre primary cells with markers of progenitor and differentiated cells. Adjacent bar graphs illustrate the percentage of CD24+ (white bars) and CD24- (black bars) cells that co-labelled with their respective secondary marker. Co-labelled antibodies were PCNA: proliferating cells (A-C), Sox2: stem/progenitor cells (D-F), NeuN: mature neurons (G-I), βIIItubulin: neural progenitors (J-L), Pax6: radial glial progenitors (M-O) and BLBP: radial glial cells (P-R). Inset images show magnified images of the co-staining. Scale bar A, H, J, K and P 200μm, scale bar B, D, E, G, M, N and Q 100μm. NS: non-significant, *p

    Journal: PLoS ONE

    Article Title: Identification of CD24 as a marker of Patched1 deleted medulloblastoma-initiating neural progenitor cells

    doi: 10.1371/journal.pone.0210665

    Figure Lengend Snippet: CD24+ Ptch1 lox/lox ;GFAP cre cells co-label with markers of neural progenitors and granule cell precursors. (A-R) Co-immunolabelling of cytospun flow-sorted CD24+ and CD24- Ptch1 lox/lox ;GFAP cre primary cells with markers of progenitor and differentiated cells. Adjacent bar graphs illustrate the percentage of CD24+ (white bars) and CD24- (black bars) cells that co-labelled with their respective secondary marker. Co-labelled antibodies were PCNA: proliferating cells (A-C), Sox2: stem/progenitor cells (D-F), NeuN: mature neurons (G-I), βIIItubulin: neural progenitors (J-L), Pax6: radial glial progenitors (M-O) and BLBP: radial glial cells (P-R). Inset images show magnified images of the co-staining. Scale bar A, H, J, K and P 200μm, scale bar B, D, E, G, M, N and Q 100μm. NS: non-significant, *p

    Article Snippet: For murine tissue immunohistochemistry, antibodies used were Olig2 (Millipore, Massachusetts, USA, AB9610), CNPase (Millipore, MAB326), PCNA (Zymed/Thermo-Fisher, 13–3900), Calbindin (Sigma, C9848), NeuN (Chemicon/Thermo-Fisher, MAB377), Pax6 (Covance, USA, PRB-278P), Sox2 (Merck, New Jersey, USA, AB5603), βIIItubulin (Promega, Wisconsin, USA, G712A), BLBP (Millipore, ABN14).

    Techniques: Flow Cytometry, Marker, Staining