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nitrilase superfamily 32 cn hydrolase superfamily protein xanthomonas campestris pv  (ATCC)


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    ATCC nitrilase superfamily 32 cn hydrolase superfamily protein xanthomonas campestris pv
    Nitrilase Superfamily 32 Cn Hydrolase Superfamily Protein Xanthomonas Campestris Pv, supplied by ATCC, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC nitrilase superfamily 32 cn hydrolase superfamily protein xanthomonas campestris pv
    Nitrilase Superfamily 32 Cn Hydrolase Superfamily Protein Xanthomonas Campestris Pv, supplied by ATCC, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Jackson Laboratory offspring pv cre ai 32 mice expressing chr2
    A: We used <t>PV-Cre</t> x <t>Ai-32</t> mice (n = 18, 9 female) with surgically affixed headbars on their skulls, and craniotomies over the striatum. These mice expressed <t>ChR2</t> (EYFP) in PV+ neurons across the brain including the striatum, as visualized in a representative brain slice under fluorescence microscopy (inset). During each recording session, we lowered an optrode into a craniotomy targeting either the dorsal striatum (dStr) or the ventral striatum (vStr) for simultaneous electrophysiological recording and optical stimulation with blue light. B: Recording locations were determined based on a combination of craniotomy coordinates, recording depths, and histology, and classified as either from dorsal striatum (dStr, green square,depth: 2.5 ‒ 3.5 mm), or ventral striatum (vStr, red square, 3.5 ‒ 4.5 mm deep).
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    Abcam anti plvap pv 1 antibody meca 32
    A: We used <t>PV-Cre</t> x <t>Ai-32</t> mice (n = 18, 9 female) with surgically affixed headbars on their skulls, and craniotomies over the striatum. These mice expressed <t>ChR2</t> (EYFP) in PV+ neurons across the brain including the striatum, as visualized in a representative brain slice under fluorescence microscopy (inset). During each recording session, we lowered an optrode into a craniotomy targeting either the dorsal striatum (dStr) or the ventral striatum (vStr) for simultaneous electrophysiological recording and optical stimulation with blue light. B: Recording locations were determined based on a combination of craniotomy coordinates, recording depths, and histology, and classified as either from dorsal striatum (dStr, green square,depth: 2.5 ‒ 3.5 mm), or ventral striatum (vStr, red square, 3.5 ‒ 4.5 mm deep).
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    Becton Dickinson anti pv 1 meca 32 rat polyclonal antibody
    <t>PV-1</t> mRNA expression in intracranial glioma xenografts. A. RT-PCR for PV-1 was performed on reverse-transcribed RNA harvested from U87MG tumors (T1) and U87:U87/VEGF tumors grown in mice (T2, T3) and compared to PV-1 expression levels in normal mouse brain (NL). Reactions were normalized using primers to the mouse endothelial gene, flk-1 . B. Quantitative RT-PCR analysis of PV-1 expression. Reactions were normalized to flk-1 . Numerical values for the fold increase are indicated. *Statistically significant difference between the levels of PV-1 expression in NL vs. T2 and NL vs. T3 (p = 0.05).
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    Developmental Studies Hybridoma Bank anti pv 1 mab meca 32
    (A-C) Whole-mount images of vasculature in the uvea (A), diaphragm (B), and trachea (C). Mice were intravenously injected with Alexa Fluor 594-conjugated anti-nepmucin mAb (red) and Alexa Fluor 647-conjugated <t>anti-PV-1</t> mAb (blue), and transcardially perfused with 4% PFA. Collected tissues were observed using a laser-scanning confocal microscope, and Z-series images of each tissue were projected into one plane to show the vascular structures. (D, E) Mice were intravenously injected with Alexa Fluor 647-conjugated anti-nepmucin mAb (blue). After fixation, collected tissues were stained with Cy3-conjugated anti-α-smooth muscle actin mAb (red). The arterioles (D) and venules (E) were identified by the wrapping morphology of α-smooth muscle actin-expressing perivascular cells. Nepmucin-expressing vascular fragments enwrapped by α-smooth muscle actin + cells are indicated by arrows. (F) A frozen section of tissue containing the ventral aorta and inferior vena cava was stained with Alexa Fluor 594-conjugated anti-nepmucin mAb (red) and FITC-conjugated anti-CD31 mAb (green). Note that nepmucin staining was absent in the aorta (AO) and vena cava (VC), whereas it was detectable in the capillaries of the surrounding adipose tissues. Ar: arteriole, Ve: venule. Scale bars, 100 µm.
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    Zhermack Inc elite double 32 pvs
    (A-C) Whole-mount images of vasculature in the uvea (A), diaphragm (B), and trachea (C). Mice were intravenously injected with Alexa Fluor 594-conjugated anti-nepmucin mAb (red) and Alexa Fluor 647-conjugated <t>anti-PV-1</t> mAb (blue), and transcardially perfused with 4% PFA. Collected tissues were observed using a laser-scanning confocal microscope, and Z-series images of each tissue were projected into one plane to show the vascular structures. (D, E) Mice were intravenously injected with Alexa Fluor 647-conjugated anti-nepmucin mAb (blue). After fixation, collected tissues were stained with Cy3-conjugated anti-α-smooth muscle actin mAb (red). The arterioles (D) and venules (E) were identified by the wrapping morphology of α-smooth muscle actin-expressing perivascular cells. Nepmucin-expressing vascular fragments enwrapped by α-smooth muscle actin + cells are indicated by arrows. (F) A frozen section of tissue containing the ventral aorta and inferior vena cava was stained with Alexa Fluor 594-conjugated anti-nepmucin mAb (red) and FITC-conjugated anti-CD31 mAb (green). Note that nepmucin staining was absent in the aorta (AO) and vena cava (VC), whereas it was detectable in the capillaries of the surrounding adipose tissues. Ar: arteriole, Ve: venule. Scale bars, 100 µm.
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    (A-C) Whole-mount images of vasculature in the uvea (A), diaphragm (B), and trachea (C). Mice were intravenously injected with Alexa Fluor 594-conjugated anti-nepmucin mAb (red) and Alexa Fluor 647-conjugated <t>anti-PV-1</t> mAb (blue), and transcardially perfused with 4% PFA. Collected tissues were observed using a laser-scanning confocal microscope, and Z-series images of each tissue were projected into one plane to show the vascular structures. (D, E) Mice were intravenously injected with Alexa Fluor 647-conjugated anti-nepmucin mAb (blue). After fixation, collected tissues were stained with Cy3-conjugated anti-α-smooth muscle actin mAb (red). The arterioles (D) and venules (E) were identified by the wrapping morphology of α-smooth muscle actin-expressing perivascular cells. Nepmucin-expressing vascular fragments enwrapped by α-smooth muscle actin + cells are indicated by arrows. (F) A frozen section of tissue containing the ventral aorta and inferior vena cava was stained with Alexa Fluor 594-conjugated anti-nepmucin mAb (red) and FITC-conjugated anti-CD31 mAb (green). Note that nepmucin staining was absent in the aorta (AO) and vena cava (VC), whereas it was detectable in the capillaries of the surrounding adipose tissues. Ar: arteriole, Ve: venule. Scale bars, 100 µm.
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    (A-C) Whole-mount images of vasculature in the uvea (A), diaphragm (B), and trachea (C). Mice were intravenously injected with Alexa Fluor 594-conjugated anti-nepmucin mAb (red) and Alexa Fluor 647-conjugated <t>anti-PV-1</t> mAb (blue), and transcardially perfused with 4% PFA. Collected tissues were observed using a laser-scanning confocal microscope, and Z-series images of each tissue were projected into one plane to show the vascular structures. (D, E) Mice were intravenously injected with Alexa Fluor 647-conjugated anti-nepmucin mAb (blue). After fixation, collected tissues were stained with Cy3-conjugated anti-α-smooth muscle actin mAb (red). The arterioles (D) and venules (E) were identified by the wrapping morphology of α-smooth muscle actin-expressing perivascular cells. Nepmucin-expressing vascular fragments enwrapped by α-smooth muscle actin + cells are indicated by arrows. (F) A frozen section of tissue containing the ventral aorta and inferior vena cava was stained with Alexa Fluor 594-conjugated anti-nepmucin mAb (red) and FITC-conjugated anti-CD31 mAb (green). Note that nepmucin staining was absent in the aorta (AO) and vena cava (VC), whereas it was detectable in the capillaries of the surrounding adipose tissues. Ar: arteriole, Ve: venule. Scale bars, 100 µm.
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    Chemie GmbH x pv asv n 28 x siiv geiv n 32
    (A-C) Whole-mount images of vasculature in the uvea (A), diaphragm (B), and trachea (C). Mice were intravenously injected with Alexa Fluor 594-conjugated anti-nepmucin mAb (red) and Alexa Fluor 647-conjugated <t>anti-PV-1</t> mAb (blue), and transcardially perfused with 4% PFA. Collected tissues were observed using a laser-scanning confocal microscope, and Z-series images of each tissue were projected into one plane to show the vascular structures. (D, E) Mice were intravenously injected with Alexa Fluor 647-conjugated anti-nepmucin mAb (blue). After fixation, collected tissues were stained with Cy3-conjugated anti-α-smooth muscle actin mAb (red). The arterioles (D) and venules (E) were identified by the wrapping morphology of α-smooth muscle actin-expressing perivascular cells. Nepmucin-expressing vascular fragments enwrapped by α-smooth muscle actin + cells are indicated by arrows. (F) A frozen section of tissue containing the ventral aorta and inferior vena cava was stained with Alexa Fluor 594-conjugated anti-nepmucin mAb (red) and FITC-conjugated anti-CD31 mAb (green). Note that nepmucin staining was absent in the aorta (AO) and vena cava (VC), whereas it was detectable in the capillaries of the surrounding adipose tissues. Ar: arteriole, Ve: venule. Scale bars, 100 µm.
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    ATCC maculicola 90 32 a0928 g01980 g01981 pseudomonas syringae pv
    (A-C) Whole-mount images of vasculature in the uvea (A), diaphragm (B), and trachea (C). Mice were intravenously injected with Alexa Fluor 594-conjugated anti-nepmucin mAb (red) and Alexa Fluor 647-conjugated <t>anti-PV-1</t> mAb (blue), and transcardially perfused with 4% PFA. Collected tissues were observed using a laser-scanning confocal microscope, and Z-series images of each tissue were projected into one plane to show the vascular structures. (D, E) Mice were intravenously injected with Alexa Fluor 647-conjugated anti-nepmucin mAb (blue). After fixation, collected tissues were stained with Cy3-conjugated anti-α-smooth muscle actin mAb (red). The arterioles (D) and venules (E) were identified by the wrapping morphology of α-smooth muscle actin-expressing perivascular cells. Nepmucin-expressing vascular fragments enwrapped by α-smooth muscle actin + cells are indicated by arrows. (F) A frozen section of tissue containing the ventral aorta and inferior vena cava was stained with Alexa Fluor 594-conjugated anti-nepmucin mAb (red) and FITC-conjugated anti-CD31 mAb (green). Note that nepmucin staining was absent in the aorta (AO) and vena cava (VC), whereas it was detectable in the capillaries of the surrounding adipose tissues. Ar: arteriole, Ve: venule. Scale bars, 100 µm.
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    Image Search Results


    A: We used PV-Cre x Ai-32 mice (n = 18, 9 female) with surgically affixed headbars on their skulls, and craniotomies over the striatum. These mice expressed ChR2 (EYFP) in PV+ neurons across the brain including the striatum, as visualized in a representative brain slice under fluorescence microscopy (inset). During each recording session, we lowered an optrode into a craniotomy targeting either the dorsal striatum (dStr) or the ventral striatum (vStr) for simultaneous electrophysiological recording and optical stimulation with blue light. B: Recording locations were determined based on a combination of craniotomy coordinates, recording depths, and histology, and classified as either from dorsal striatum (dStr, green square,depth: 2.5 ‒ 3.5 mm), or ventral striatum (vStr, red square, 3.5 ‒ 4.5 mm deep).

    Journal: bioRxiv

    Article Title: Optogenetic mapping of rhythmic phase-dependent excitability in the mouse striatum

    doi: 10.1101/2024.02.01.578473

    Figure Lengend Snippet: A: We used PV-Cre x Ai-32 mice (n = 18, 9 female) with surgically affixed headbars on their skulls, and craniotomies over the striatum. These mice expressed ChR2 (EYFP) in PV+ neurons across the brain including the striatum, as visualized in a representative brain slice under fluorescence microscopy (inset). During each recording session, we lowered an optrode into a craniotomy targeting either the dorsal striatum (dStr) or the ventral striatum (vStr) for simultaneous electrophysiological recording and optical stimulation with blue light. B: Recording locations were determined based on a combination of craniotomy coordinates, recording depths, and histology, and classified as either from dorsal striatum (dStr, green square,depth: 2.5 ‒ 3.5 mm), or ventral striatum (vStr, red square, 3.5 ‒ 4.5 mm deep).

    Article Snippet: PV-Cre female mice were bred with Ai-32 (ChR2(H134R)-EYFP) males (Jackson Labs), to produce offspring PV-Cre:Ai-32 mice expressing ChR2 in parvalbumin-positive (PV+) interneurons throughout the brain, including the striatum ( ).

    Techniques: Slice Preparation, Fluorescence, Microscopy

    PV-1 mRNA expression in intracranial glioma xenografts. A. RT-PCR for PV-1 was performed on reverse-transcribed RNA harvested from U87MG tumors (T1) and U87:U87/VEGF tumors grown in mice (T2, T3) and compared to PV-1 expression levels in normal mouse brain (NL). Reactions were normalized using primers to the mouse endothelial gene, flk-1 . B. Quantitative RT-PCR analysis of PV-1 expression. Reactions were normalized to flk-1 . Numerical values for the fold increase are indicated. *Statistically significant difference between the levels of PV-1 expression in NL vs. T2 and NL vs. T3 (p = 0.05).

    Journal: BMC Neuroscience

    Article Title: Plasmalemmal Vesicle Associated Protein-1 (PV-1) is a marker of blood-brain barrier disruption in rodent models

    doi: 10.1186/1471-2202-9-29

    Figure Lengend Snippet: PV-1 mRNA expression in intracranial glioma xenografts. A. RT-PCR for PV-1 was performed on reverse-transcribed RNA harvested from U87MG tumors (T1) and U87:U87/VEGF tumors grown in mice (T2, T3) and compared to PV-1 expression levels in normal mouse brain (NL). Reactions were normalized using primers to the mouse endothelial gene, flk-1 . B. Quantitative RT-PCR analysis of PV-1 expression. Reactions were normalized to flk-1 . Numerical values for the fold increase are indicated. *Statistically significant difference between the levels of PV-1 expression in NL vs. T2 and NL vs. T3 (p = 0.05).

    Article Snippet: Anti-PV-1 (meca-32) rat polyclonal antibody and anti-CD31 rat polyclonal antibody were from BD Biosciences Pharmingen (San Jose, CA).

    Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction, Quantitative RT-PCR

    PV-1 protein expression in intracranial glioma xenografts. A. Immunohistochemistry for PV-1 was performed on frozen brain sections containing U87:U87/VEGF tumors (T1, T2) or normal brain (NL); 100×. PV-1 expression was detected solely on the microvessels within the tumors and showed a comparable staining pattern to that of the endothelial control marker, CD31. PV-1 expression was not detected in normal brain as compared to CD31. B. The interface between normal brain (NL) and brain tumor (T) demonstrated that PV-1 expression was tightly restricted to the tumor; overview 40×, detail 100×.

    Journal: BMC Neuroscience

    Article Title: Plasmalemmal Vesicle Associated Protein-1 (PV-1) is a marker of blood-brain barrier disruption in rodent models

    doi: 10.1186/1471-2202-9-29

    Figure Lengend Snippet: PV-1 protein expression in intracranial glioma xenografts. A. Immunohistochemistry for PV-1 was performed on frozen brain sections containing U87:U87/VEGF tumors (T1, T2) or normal brain (NL); 100×. PV-1 expression was detected solely on the microvessels within the tumors and showed a comparable staining pattern to that of the endothelial control marker, CD31. PV-1 expression was not detected in normal brain as compared to CD31. B. The interface between normal brain (NL) and brain tumor (T) demonstrated that PV-1 expression was tightly restricted to the tumor; overview 40×, detail 100×.

    Article Snippet: Anti-PV-1 (meca-32) rat polyclonal antibody and anti-CD31 rat polyclonal antibody were from BD Biosciences Pharmingen (San Jose, CA).

    Techniques: Expressing, Immunohistochemistry, Staining, Marker

    PV-1 protein expression after ischemic insult. A. Top row, PV-1; bottom row, CD31; 100×. PV-1 is not detected 8 or 24 hours after ischemia, unlike the endothelial control marker, CD31. PV-1 expression is detectable in a small number of vessels in the affected tissue 48 hours after injury. PV-1 protein is expressed in a majority of the vessels and is comparable to CD31 staining levels in the injured region by 7 days after injury. Sham (uninjured brain) shows no expression of PV-1. B. Overview of PV-1 expression within the ischemic region 48 h and 7d after injury. PV-1 is induced throughout the affected brain tissue at 48 h (see arrows) and remains evenly distributed by 7d.

    Journal: BMC Neuroscience

    Article Title: Plasmalemmal Vesicle Associated Protein-1 (PV-1) is a marker of blood-brain barrier disruption in rodent models

    doi: 10.1186/1471-2202-9-29

    Figure Lengend Snippet: PV-1 protein expression after ischemic insult. A. Top row, PV-1; bottom row, CD31; 100×. PV-1 is not detected 8 or 24 hours after ischemia, unlike the endothelial control marker, CD31. PV-1 expression is detectable in a small number of vessels in the affected tissue 48 hours after injury. PV-1 protein is expressed in a majority of the vessels and is comparable to CD31 staining levels in the injured region by 7 days after injury. Sham (uninjured brain) shows no expression of PV-1. B. Overview of PV-1 expression within the ischemic region 48 h and 7d after injury. PV-1 is induced throughout the affected brain tissue at 48 h (see arrows) and remains evenly distributed by 7d.

    Article Snippet: Anti-PV-1 (meca-32) rat polyclonal antibody and anti-CD31 rat polyclonal antibody were from BD Biosciences Pharmingen (San Jose, CA).

    Techniques: Expressing, Marker, Staining

    Vessel quantitation after ischemic insult. Dark bars, PV-1; open bars, CD31. Five high power fields were counted per mouse brain. Data are expressed as mean +/- standard error of the mean. *Statistically significant difference between the number of PV-1 positive and CD31 positive vessel (p < 0.001, 95% CI). **No statistically significant difference between number of PV-1 vessels and CD31 vessels (p > 0.05).

    Journal: BMC Neuroscience

    Article Title: Plasmalemmal Vesicle Associated Protein-1 (PV-1) is a marker of blood-brain barrier disruption in rodent models

    doi: 10.1186/1471-2202-9-29

    Figure Lengend Snippet: Vessel quantitation after ischemic insult. Dark bars, PV-1; open bars, CD31. Five high power fields were counted per mouse brain. Data are expressed as mean +/- standard error of the mean. *Statistically significant difference between the number of PV-1 positive and CD31 positive vessel (p < 0.001, 95% CI). **No statistically significant difference between number of PV-1 vessels and CD31 vessels (p > 0.05).

    Article Snippet: Anti-PV-1 (meca-32) rat polyclonal antibody and anti-CD31 rat polyclonal antibody were from BD Biosciences Pharmingen (San Jose, CA).

    Techniques: Quantitation Assay

    (A-C) Whole-mount images of vasculature in the uvea (A), diaphragm (B), and trachea (C). Mice were intravenously injected with Alexa Fluor 594-conjugated anti-nepmucin mAb (red) and Alexa Fluor 647-conjugated anti-PV-1 mAb (blue), and transcardially perfused with 4% PFA. Collected tissues were observed using a laser-scanning confocal microscope, and Z-series images of each tissue were projected into one plane to show the vascular structures. (D, E) Mice were intravenously injected with Alexa Fluor 647-conjugated anti-nepmucin mAb (blue). After fixation, collected tissues were stained with Cy3-conjugated anti-α-smooth muscle actin mAb (red). The arterioles (D) and venules (E) were identified by the wrapping morphology of α-smooth muscle actin-expressing perivascular cells. Nepmucin-expressing vascular fragments enwrapped by α-smooth muscle actin + cells are indicated by arrows. (F) A frozen section of tissue containing the ventral aorta and inferior vena cava was stained with Alexa Fluor 594-conjugated anti-nepmucin mAb (red) and FITC-conjugated anti-CD31 mAb (green). Note that nepmucin staining was absent in the aorta (AO) and vena cava (VC), whereas it was detectable in the capillaries of the surrounding adipose tissues. Ar: arteriole, Ve: venule. Scale bars, 100 µm.

    Journal: PLoS ONE

    Article Title: Dynamic Changes in Endothelial Cell Adhesion Molecule Nepmucin/CD300LG Expression under Physiological and Pathological Conditions

    doi: 10.1371/journal.pone.0083681

    Figure Lengend Snippet: (A-C) Whole-mount images of vasculature in the uvea (A), diaphragm (B), and trachea (C). Mice were intravenously injected with Alexa Fluor 594-conjugated anti-nepmucin mAb (red) and Alexa Fluor 647-conjugated anti-PV-1 mAb (blue), and transcardially perfused with 4% PFA. Collected tissues were observed using a laser-scanning confocal microscope, and Z-series images of each tissue were projected into one plane to show the vascular structures. (D, E) Mice were intravenously injected with Alexa Fluor 647-conjugated anti-nepmucin mAb (blue). After fixation, collected tissues were stained with Cy3-conjugated anti-α-smooth muscle actin mAb (red). The arterioles (D) and venules (E) were identified by the wrapping morphology of α-smooth muscle actin-expressing perivascular cells. Nepmucin-expressing vascular fragments enwrapped by α-smooth muscle actin + cells are indicated by arrows. (F) A frozen section of tissue containing the ventral aorta and inferior vena cava was stained with Alexa Fluor 594-conjugated anti-nepmucin mAb (red) and FITC-conjugated anti-CD31 mAb (green). Note that nepmucin staining was absent in the aorta (AO) and vena cava (VC), whereas it was detectable in the capillaries of the surrounding adipose tissues. Ar: arteriole, Ve: venule. Scale bars, 100 µm.

    Article Snippet: Anti-PV-1 mAb (MECA-32) was from the Developmental Studies Hybridoma Bank (the University of Iowa).

    Techniques: Injection, Microscopy, Staining, Expressing

    (A-E) Frozen sections of thymus (A), spleen (B), liver (C), kidney (D), and small intestine (E) were stained with an anti-nepmucin mAb (Alexa Fluor 594; red) and anti-PV-1 mAb (Alexa Fluor 647; blue). Cryosections of the thymus (A) and small intestine (E) were further incubated with Hoechst 33342 (white). In the thymus (A), the cortico-medullary junction is indicated by a dotted line. Med: medulla, Cor: Cortex, CA: central artery, WP: white pulp, RP: red pulp, CV: central vein, GL: glomerulus. Scale Bars, 100 µm.

    Journal: PLoS ONE

    Article Title: Dynamic Changes in Endothelial Cell Adhesion Molecule Nepmucin/CD300LG Expression under Physiological and Pathological Conditions

    doi: 10.1371/journal.pone.0083681

    Figure Lengend Snippet: (A-E) Frozen sections of thymus (A), spleen (B), liver (C), kidney (D), and small intestine (E) were stained with an anti-nepmucin mAb (Alexa Fluor 594; red) and anti-PV-1 mAb (Alexa Fluor 647; blue). Cryosections of the thymus (A) and small intestine (E) were further incubated with Hoechst 33342 (white). In the thymus (A), the cortico-medullary junction is indicated by a dotted line. Med: medulla, Cor: Cortex, CA: central artery, WP: white pulp, RP: red pulp, CV: central vein, GL: glomerulus. Scale Bars, 100 µm.

    Article Snippet: Anti-PV-1 mAb (MECA-32) was from the Developmental Studies Hybridoma Bank (the University of Iowa).

    Techniques: Staining, Incubation

    The thymus was collected on P0.5 (A) and spleens were collected on P0.5, 7.5, 10.5, and 14.5, as well as from adult mice (B). Tissue sections were stained with an anti-MAdCAM-1 mAb (Alexa Fluor 488; green), anti-nepmucin mAb (Alexa Fluor 594; red), and anti-PV-1 mAb (Alexa Fluor 647; blue). In the spleen at P7.5-10.5, nepmucin was detected predominantly in microvessels leading to the marginal sinus (arrows). From P14.5 to adulthood, nepmucin was also found in the marginal sinus ECs (arrowheads). Scale bars, 100 µm.

    Journal: PLoS ONE

    Article Title: Dynamic Changes in Endothelial Cell Adhesion Molecule Nepmucin/CD300LG Expression under Physiological and Pathological Conditions

    doi: 10.1371/journal.pone.0083681

    Figure Lengend Snippet: The thymus was collected on P0.5 (A) and spleens were collected on P0.5, 7.5, 10.5, and 14.5, as well as from adult mice (B). Tissue sections were stained with an anti-MAdCAM-1 mAb (Alexa Fluor 488; green), anti-nepmucin mAb (Alexa Fluor 594; red), and anti-PV-1 mAb (Alexa Fluor 647; blue). In the spleen at P7.5-10.5, nepmucin was detected predominantly in microvessels leading to the marginal sinus (arrows). From P14.5 to adulthood, nepmucin was also found in the marginal sinus ECs (arrowheads). Scale bars, 100 µm.

    Article Snippet: Anti-PV-1 mAb (MECA-32) was from the Developmental Studies Hybridoma Bank (the University of Iowa).

    Techniques: Staining

    (A) The pancreas was collected from 13-week-old female NOD mice and ICR mice. Tissue sections were stained with anti-nepmucin mAb (green), anti-PV-1 mAb (blue), anti-PNAd mAb (red), and Hoechst 33432 (white). Alternatively, a frozen section was stained with anti-CD4 mAb (green), anti-PNAd mAb (red), and Hoechst 33432 (white). The Langerhans’s islets are delineated with dotted lines. Scale bars, 100 µm. (B, C) Lymphocytes prepared from the indicated tissues of NOD or ICR mice (15–19 weeks old) were incubated with admixed nepmucin-human IgG Fc chimeras and PE-conjugated F(ab’) 2 anti-human IgG. The proportion of CD4 + T cells bound to full-length nepmucin (FL) is shown in (B), and representative histograms for the binding of nepmucin FL and its mutant (Δmucin; nepmucin mutant lacking the mucin-like domain, and ΔIg; nepmucin mutant lacking the Ig domain) are shown in (C). Data represent the mean ± SD (n = 6 mice per group) from two independent experiments. *** p <0.005.

    Journal: PLoS ONE

    Article Title: Dynamic Changes in Endothelial Cell Adhesion Molecule Nepmucin/CD300LG Expression under Physiological and Pathological Conditions

    doi: 10.1371/journal.pone.0083681

    Figure Lengend Snippet: (A) The pancreas was collected from 13-week-old female NOD mice and ICR mice. Tissue sections were stained with anti-nepmucin mAb (green), anti-PV-1 mAb (blue), anti-PNAd mAb (red), and Hoechst 33432 (white). Alternatively, a frozen section was stained with anti-CD4 mAb (green), anti-PNAd mAb (red), and Hoechst 33432 (white). The Langerhans’s islets are delineated with dotted lines. Scale bars, 100 µm. (B, C) Lymphocytes prepared from the indicated tissues of NOD or ICR mice (15–19 weeks old) were incubated with admixed nepmucin-human IgG Fc chimeras and PE-conjugated F(ab’) 2 anti-human IgG. The proportion of CD4 + T cells bound to full-length nepmucin (FL) is shown in (B), and representative histograms for the binding of nepmucin FL and its mutant (Δmucin; nepmucin mutant lacking the mucin-like domain, and ΔIg; nepmucin mutant lacking the Ig domain) are shown in (C). Data represent the mean ± SD (n = 6 mice per group) from two independent experiments. *** p <0.005.

    Article Snippet: Anti-PV-1 mAb (MECA-32) was from the Developmental Studies Hybridoma Bank (the University of Iowa).

    Techniques: Staining, Incubation, Binding Assay, Mutagenesis