MOUSE ANTI RAT RECA-1【科瑞奥博】

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MOUSE ANTI RAT RECA-1

货号： MCA970GA 基本售价： 1954.0 元规格： 0.1 mg

产品信息

概述
货号	MCA970GA
克隆号	HIS52
同种亚型	IgG1
反应种属	Rat
来源宿主	Mouse
应用	C, IF

性能
供应商	Bio-Rad Antibodies
运输条件
存放说明	Store at +4^oC or at -20^oC if preferred. This product should be stored undiluted. Storage in frost free freezers is not recommended. Avoid repeated freezing and thawing as this may denature the antibody. Should this product contain a precipitate we recommend microcentrifugation before use.Store at +4^oC or at -20^oC if preferred. This product should be stored undiluted. Storage in frost free freezers is not recommended. Avoid repeated freezing and thawing as this may denature the antibody. Should this product contain a precipitate we recommend microcentrifugation before use.

声明
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参考图片

Published customer image:
Mouse anti Rat RECA-1 antibody, clone HIS52 used for the detection of RECA-1 expressing cells by immunofluorescence.
Image caption
Transduction of AdV-eGFP/AdV-ZFP-VEGF into the spinal cord. (A) Photomicrographs showing a transverse section of rat spinal cord obtained adjacent to the injury site 10 days after spinal cord injury and AdV-eGFP injection. eGFP signal was detected in both the gray matter and white matter. (B) High-power (63X) confocal images show that the AdV-eGFP vector (green) transfected neurons (NeuN), astrocytes (GFAP), oligodendrocytes (CC1) and endothelial cells (RECA-1). Cells have been counter-stained with DAPI (blue) as nuclear marker. (C) Bar graph displays quantification of transduced cell types ± SEM, as identified by the cell-specific markers NeuN, GFAP, RECA-1 and CC1. (D) Evaluation of AdV-ZFP-VEGF gene transfer. Western blot showed that the NFκB p65 rabbit polyclonal antibody recognizes the p65 activation domain in the AdV-ZFP-VEGF treated animals. The higher molecular weight bands are endogenous NFκBp65 fragments, which are also recognized by the antibody; however, these bands are present in both the control and treatment groups. The lower band (arrow) corresponds to the AdV-ZFP-VEGF and was only present in the treated animals. Lower panel shows actin expression as a protein control. Scale bar: 1000 μm for A; 100 μm for B.

From: Figley SA, Liu Y, Karadimas SK, Satkunendrarajah K, Fettes P, et al. (2014) Delayed Administration of a Bio-Engineered Zinc-Finger VEGF-A Gene Therapy Is Neuroprotective and Attenuates Allodynia Following Traumatic Spinal Cord Injury. PLoS ONE 9(5): e96137.

Published customer image:
Mouse anti Rat RECA-1 antibody, clone HIS52 used for the detection of RECA-1 expressing cells by immunofluorescence.
Image caption
AdV-ZFP-VEGF results in increased vessel counts and angiogenesis. (A) Left panel: Illustration of the area of spinal cord areas used for RECA-1 counting (2 grey matter areas, 2 white matter areas). (B) Representative sections taken 2 mm rostral to the epicenter from a AdV-ZFP-VEGF treated and AdV-eGFP control animal respectively immunostained with RECA-1 at 10 days after SCI; scale 100 μm. An increased number of vessels were observed in the AdV-ZFP-VEGF treated group. (C) Bar graph illustrating the RECA-1 positive cell counts 10 days after SCI. AdV-ZFP-VEGF administration resulted in a significant increase in vascular counts (2 mm and 4 mm away from the epicenter) as compared with the control group. (D) Representative confocal image from an ADV-ZFP-VEGF treated animal at 5 days post-injury. Image was taken at 2 mm rostral from the epicenter, and shows double-labeled cells. Cells were stained for endothelial cells (RECA-1, green) and proliferation (Ki67, red). Scale bar = 50 μm (30 μm for magnified panel). (E) Angiogenesis was assessed by quantifying Ki67/RECA-1 co-labeled vessels. Data is presented at the percentage of RECA-1+ vessels that were also Ki67+, with an overall average increase of 10% vascular proliferation observed in the animals receiving AdV-ZFP-VEGF administration. All data are presented as mean ± SEM, and was analyzed by Two-way ANOVA (Holm-Sidak post-hoc). Angiogenesis data were analyzed by performing an arcsine transformation of the values, prior to Two-way ANOVA and post-hoc testing. *p<0.01, **p<0.001. n = 4/sham and injured control groups, n = 5/AdV-eGFP and AdV-ZFP-VEGF groups.

From: Figley SA, Liu Y, Karadimas SK, Satkunendrarajah K, Fettes P, et al. (2014) Delayed Administration of a Bio-Engineered Zinc-Finger VEGF-A Gene Therapy Is Neuroprotective and Attenuates Allodynia Following Traumatic Spinal Cord Injury. PLoS ONE 9(5): e96137.

Published customer image:
Mouse anti Rat RECA-1 antibody, clone HIS52 used for the detection of RECA-1 expressing cells by immunofluorescence.
Image caption
Increased vascular coverage and neuronal projections by angiogenic factors. (A, B) CT treatment of organotypic slice cultures (every 4 days for 2 weeks) retains the vasculature (confocal projection for the pan-endothelial marker RECA-1 and TH), (C) increases the thickness of the striatal portion of the slice, (D,E) promotes the sprouting of TH+ fibers from the S. Nigra section to the striatal section (2-weeks after control (BSA) and CT treatment). [Size bars: 20 μm].

From: Androutsellis-Theotokis A, Rueger MA, Park DM, Boyd JD, Padmanabhan R, et al. (2010) Angiogenic Factors Stimulate Growth of Adult Neural Stem Cells. PLoS ONE 5(2): e9414.

Published customer image:
Mouse anti Rat RECA-1 antibody, clone HIS52 used for the detection of RECA-1 expressing cells by immunofluorescence.
Image caption
Significant increase in ipsilateral gray matter vasculature rostral and at the epicenter of the injury. bpV(pic)-treated animals demonstrated significantly increased vascular (RECA-1)-positive area in the ipsilateral gray matter 2 mm rostral and at the epicenter of the lesion 6 weeks post-SCI. * = central canal in photomicrographs. No significant difference was observed 2 mm caudal to the epicenter. **, p<0.01; *, p<0.05. n = 4-5. Error bars = SEM. Scale bar (Rostral & Caudal) = 100 μm; (Epicenter) = 150 μm.

From: Walker CL, Walker MJ, Liu N-K, Risberg EC, Gao X, et al. (2012) Systemic Bisperoxovanadium Activates Akt/mTOR, Reduces Autophagy, and Enhances Recovery following Cervical Spinal Cord Injury. PLoS ONE 7(1): e30012.

Published customer image:
Mouse anti Rat RECA-1 antibody, clone HIS52 used for the detection of RECA-1 expressing cells by immunofluorescence.
Image caption
CXCR1(A) and CXCR2 (B) mRNA in left and right bronchi, and (C) co-localization of CXCR2 with RECA-1+ subepithelial blood vessel. Significant changes in CXCR2 were measured only in the left bronchus (*P<0.05 from 0 h and ##P<0.01 from right bronchus). Frozen sections of left bronchus 6 h after LPAL show co-localization of anti-CXCR2 (red) with RECA-1+ subepithelial blood vessels (green: 100× original magnification, and inset 600× original magnification).

From: Perino MG, Moldobaeva A, Jenkins J, Wagner EM (2013) Chemokine Localization in Bronchial Angiogenesis. PLoS ONE 8(6): e66432.

Published customer image:
Mouse anti Rat RECA-1 antibody, clone HIS52 used for the detection of RECA-1 expressing cells by immunohistochemistry.
Image caption
Double immunostaining for ED1 or RECA-1 with IL-1β in the study groups. Kidney sections were stained using two-color immunohistochemistry with ED1 or RECA-1 stained red and IL-1β stained brown in an HBSS-treated rat with nephritis (a,c) and an MSC-treated rat with nephritis (b,d). A large number of ED1+ macrophages shows double staining for IL-1β in the WKY-HBSS rats (circles) (a). RECA-1 is partially double-stained with IL-1β in both the WKY-HBSS rats and the WKY-MSC rats (squares) (c,d). Original magnifications, x1000.

From: Suzuki T, Iyoda M, Shibata T, Ohtaki H, Matsumoto K, et al. (2013) Therapeutic Effects of Human Mesenchymal Stem Cells in Wistar-Kyoto Rats with Anti-Glomerular Basement Membrane Glomerulonephritis. PLoS ONE 8(6): e67475.

Published customer image:
Mouse anti Rat RECA-1 antibody, clone HIS52 used for the detection of RECA-1 expressing cells by immunohistochemistry.
Image caption
Pyruvate reduces R/M hypoglycemia-induced cortical blood vessel loss. (A) Bright field photomicrographs from coronal sections of cortex demonstrate loss of blood vessels at three days after R/M hypoglycemia by RECA-1 (rat endothelial cell antigen 1) staining. Panels show the progression of blood vessel changes in the parietal (PT Ctx) and perirhinal (PRh Ctx) cortex. After R/M hypoglycemia, blood vessels showed decreased density compared to sham-operated rats. Intraperitoneal injection of pyruvate as an adjuvant to glucose at ten minutes after R/M hypoglycemia reduced blood vessel disappearance. Scale bar = 100 μm. (B) Graph represents the % area of RECA-1 immunoreactivity in the parietal and perirhinal cortex. Data are means ± s.e.m., n=5-6 from each group, *P<0.05.

From: Choi BY, Kim JH, Kim HJ, Yoo JH, Song HK, et al. (2013) Pyruvate Administration Reduces Recurrent/Moderate Hypoglycemia-Induced Cortical Neuron Death in Diabetic Rats. PLoS ONE 8(11): e81523.

Published customer image:
Mouse anti Rat RECA-1 antibody, clone HIS52 used for the detection of RECA-1 expressing cells by immunofluorescence.
Image caption
ChABC and GF treatments attenuate the proliferation of microglia/macrophages and promote the generation of new endothelial cells after SCI. (A–D) Representative confocal images of BrdU+/NG2+ macrophages/microglia marked with Iba-1 in the injured spinal cord (arrows). (E–F) Under baseline SCI condition, macrophages/microglia comprised about 25% and 17% of BrdU+/NG2+ cells in rostral and caudal points to the injury center, respectively. After treatment with ChABC and/or GFs, we found a reduction in the number of BrdU+/NG2+/IbA-1+ cells that was statistically significant for ChABC and ChABC+GFs treatment groups relative to the vehicle group. (G–J) Representative confocal images show newly generated endothelial cells marked by Reca-1 and NG2 among BrdU+ cells. Reca-1 positive endothelial cells comprised a subpopulation of proliferating NG2+ cells after SCI (J). (K–L) Quantification of BrdU+/NG2+/Reca-1+ cells showed a significant number of newly generated endothelial cells after treatment with ChABC and/or GFs at both rostral and caudal points to the injury center compared to the vehicle group. *p<0.05, n = 6/group.

From: Karimi-Abdolrezaee S, Schut D, Wang J, Fehlings MG (2012) Chondroitinase and Growth Factors Enhance Activation and Oligodendrocyte Differentiation of Endogenous Neural Precursor Cells after Spinal Cord Injury. PLoS ONE 7(5): e37589.

Published customer image:
Mouse anti Rat RECA-1 antibody, clone HIS52 used for the detection of RECA-1 expressing cells by immunofluorescence.
Image caption
Increased density of blood vessels at perilesional regions with increased d14 vasoreactivity. RECA-1 immunofluorescence staining (red) with DAPI nuclear staining (green) compared in animals without (No VR+) and with (VR+) increased vasoreactivity on d14 (n = 4 per group). Corresponding subcortical regions close to the infarct on d14 showed a higher density of RECA-1 signal. One example per group is shown on the right. White arrows point to the lesion. White line indicates 100 μm.

From: Wegener S, Artmann J, Luft AR, Buxton RB, Weller M, et al. (2013) The Time of Maximum Post-Ischemic Hyperperfusion Indicates Infarct Growth Following Transient Experimental Ischemia. PLoS ONE 8(5): e65322.

Published customer image:
Mouse anti Rat RECA-1 antibody, clone HIS52 used for the detection of RECA-1 expressing cells by immunofluorescence.
Image caption
Effect of clustered ephrin-A1-Fc on vascular formation in the rat striatum. (A) Distribution of BrdU(+) endothelial cells. Brain of the unilaterally lesioned rats 6 weeks after infusion of clustered ephrin-A1-Fc were sectioned coronally and stained for BrdU and Rat Endothelial Cell Antigen-1 (RECA-1). Numbers of the BrdU(+) cells and BrdU(+)& RECA-1(+) cells were counted as described in the Materials and Methods. Total numbers of BrdU(+) cells in 8 animals are shown on the top, and percentages of RECA-1(+) cells among BrdU(+) cells are shown on the bottom. Error bars represent SD. *p<0.01 (n = 8) compared to control (IgG[Fc]). (B) Magnified confocal micrographs of insets in Fig S5. Scale bar: 50 μm. (C) Quantification of endothelial cell area. Coronal sections of striatum were stained for RECA-1 as in Fig S5, and the RECA-1 stained area was quantified using an ImageJ computer program (NIH). The areas taken for measurements were as described in the Materials and Methods. The values from 6 animals were analyzed statistically. *p<0.01 (n = 6). Error bars represent SD. (D) Co-localization of BrdU, CM-DiI, and RECA-1 in endothelial cells of the striatum. Sections taken from the rats treated as in Fig. 5B with intraventricular CM-DiI injection were stained for BrdU and RECA-1 and subjected to 3D confocal microscopy. Micrographs are the all-in-focus compilation of 12 confocal micrographs at 0.5 μm intervals.

From: Jing X, Miwa H, Sawada T, Nakanishi I, Kondo T, et al. (2012) Ephrin-A1-Mediated Dopaminergic Neurogenesis and Angiogenesis in a Rat Model of Parkinson's Disease. PLoS ONE 7(2): e32019.

Published customer image:
Mouse anti Rat RECA-1 antibody, clone HIS52 used for the detection of RECA-1 expressing cells by immunofluorescence.
Image caption
hADSCs led to the appearance of perivascular spaces in between endothelial and astrocytic basement membranes one week after injection. A–D) Confocal images of horizontal sections immunostained with anti-pan-laminin antibody (red) one week after injury. Note that in DMEM animals (A,B) there is no separation between the two membranes whereas in hADSCs–treated animals (C,D) these membranes are separated (arrows in D). E) Confocal images of a horizontal section immunostained with anti-pan-laminin (green) and RECA-1(red). F–F”) Confocal imagens of sequential optical sections immunostained with anti-pan-laminin (green) and DAPI (blue) showing the extravasation of cells from the blood vessels. Bars: C, F = 50 μm B, D, E = 25 μm.

From: Menezes K, Nascimento MA, Gonçalves JP, Cruz AS, Lopes DV, et al. (2014) Human Mesenchymal Cells from Adipose Tissue Deposit Laminin and Promote Regeneration of Injured Spinal Cord in Rats. PLoS ONE 9(5): e96020.

Published customer image:
Mouse anti Rat RECA-1 antibody, clone HIS52 used for the detection of RECA-1 expressing cells by immunofluorescence.
Image caption
Endothelial cell number and capillary length post radiation. (A) Representative images of sections from the corpus callosum immunostained for rat endothelial cell antigen (RECA) at various time points post radiation. RECA expression declines immediately post radiation but is restored and maintained through 15 months. Stereological estimates of the number of capillary segments in the cortex (B) and corpus callosum (C) and of capillary length in both regions (D, E). (*** p<0.001; ** p<0.01; * p<0.05; ANOVA). Bars = SEM. Scale bar in A corresponds to 100 μm.

From: Panagiotakos G, Alshamy G, Chan B, Abrams R, Greenberg E, et al. (2007) Long-Term Impact of Radiation on the Stem Cell and Oligodendrocyte Precursors in the Brain. PLoS ONE 2(7): e588.

Published customer image:
Mouse anti Rat RECA-1 antibody, clone HIS52 used for the detection of RECA-1 expressing cells by immunofluorescence.
Image caption
Representative patterns of RECA-1 staining in rat hippocampus. (a) Microvessels in control (PBS) injected rat hippocampus (left panel) and microvessels in Aβ1-42-injected hippocampus (right panel). Scale bar is for 70μm. (b) Bar graph for the number of microvessels/mm2 (n = 5 each). (c) Bar graph for microvessel length (n = 5 each). *P = 0.05 for A&β1-42 versus PBS.

From: Jantaratnotai N, Ryu JK, Schwab C, McGeer PL, McLarnon JG.
Comparison of Vascular Perturbations in an Aβ-Injected Animal Model and in AD Brain.
Int J Alzheimers Dis. 2011;2011:918280.

Published customer image:
Mouse anti Rat RECA-1 antibody, clone HIS52 used for the detection of RECA-1 expressing cells by immunofluorescence.
Image caption
Morphology of microvessels stained with RECA-1 in Aβ 1-42-injected hippocampus. Panels show morphological features including fragments, looping microvessels, and vessels with knob-like and uneven diameters. The scale bar represents 40 μm.

From: Jantaratnotai N, Ryu JK, Schwab C, McGeer PL, McLarnon JG.
Comparison of Vascular Perturbations in an Aβ-Injected Animal Model and in AD Brain.
Int J Alzheimers Dis. 2011;2011:918280.