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mouse anti reca 1  (Bio-Rad)


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    Bio-Rad mouse anti reca 1
    Mouse Anti Reca 1, supplied by Bio-Rad, used in various techniques. Bioz Stars score: 94/100, based on 474 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+reca/Mouse+anti+Rat+RECA-1/pmc12811084-87-25-29
    Average 94 stars, based on 474 article reviews
    mouse anti reca 1 - by Bioz Stars, 2026-09
    94/100 stars

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    Related Articles

    Staining:

    Article Title: VASCULAR ENDOTHELIAL GROWTH FACTOR IS UP-REGULATED AFTER STATUS EPILEPTICUS AND PROTECTS AGAINST SEIZURE-INDUCED NEURONAL LOSS IN HIPPOCAMPUS
    Article Snippet: Sections were immunostained as previously described ( Scharfman et al., 2000 ) using a Vectastain Elite ABC kit (Vector Laboratories, Burlingame, CA, USA) and an anti-VEGF (goat polyclonal, 1:1000, R & D Systems) antibody; other sections were additionally double-immunostained with VEGF and a second antibody, glial fibrillary acidic protein (GFAP rabbit polyclonal, 1:60,000, Dako, Carpinteria, CA, USA), an astrocyte marker, to detect co-localization of VEGF protein with GFAP. .. Brains were also stained with an anti-RECA (rat endothelial cell antigen, 1:250, Serotec, Raleigh, NC, USA) antibody to visualize vasculature. ..

    Article Title: Dexamethasone treatment and ICAM-1 deficiency impair VEGF-induced angiogenesis in adult brain.
    Article Snippet: Background: Infusion of exogenous vascular endothelial growth factor (VEGF) into adult brain at doses above 60 ng/ day induces dramatic angiogenesis accompanied by vascular leak and inflammation.. Blood vessels formed by this treatment are dilated and tortuous, exhibiting a pathological morphology.. Pathological VEGF-induced angiogenesis is preceded by vascular leak and inflammation, which have been proposed to mediate subsequent angiogenesis.

    Article Title: Vascular endothelial growth factor is up-regulated after status epilepticus and protects against seizure-induced neuronal loss in hippocampus.
    Article Snippet: Sections were immunostained s previously described (Scharfman et al., 2000) using a Vecastain Elite ABC kit (Vector Laboratories, Burlingame, CA, USA) nd an anti-VEGF (goat polyclonal, 1:1000, R & D Systems) ntibody; other sections were additionally double-immunostained ith VEGF and a second antibody, glial fibrillary acidic protein GFAP rabbit polyclonal, 1:60,000, Dako, Carpinteria, CA, USA), n astrocyte marker, to detect co-localization of VEGF protein with FAP. .. Brains were also stained with an anti-RECA (rat endotheial cell antigen, 1:250, Serotec, Raleigh, NC, USA) antibody to isualize vasculature. ..

    Clinical Proteomics:

    Article Title: Dexamethasone treatment and ICAM-1 deficiency impair VEGF-induced angiogenesis in adult brain.
    Article Snippet: Background: Infusion of exogenous vascular endothelial growth factor (VEGF) into adult brain at doses above 60 ng/ day induces dramatic angiogenesis accompanied by vascular leak and inflammation.. Blood vessels formed by this treatment are dilated and tortuous, exhibiting a pathological morphology.. Pathological VEGF-induced angiogenesis is preceded by vascular leak and inflammation, which have been proposed to mediate subsequent angiogenesis.



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    Prevention of neuroma formation by a spatially confined conduit filled with GelMA MAVP MPS. ( A ) Illustration of 3D-printed GelMA MPs loaded with MAVP and the proposed mechanism of action within the neural conduit. ( B ) Representative images and ( C ) quantitative scores of autotomy behavior over 12 weeks (n = 6). ( D ) Representative gait footprints at 12 weeks post-surgery. ( E ) Quantification of left hindlimb stance duration (n = 6) and ( F ) maximum contact area (n = 6). ( G ) IF staining of p-VEGFR2 activation and ( H ) IF staining of neovascularization marker <t>RECA-1.</t> (I) Quantification of p-VEGFR2-positive area percentage (n = 6). and ( J ) quantification of RECA-1-positive area percentage (n = 6). ( K ) Regenerated nerve length measurements (n = 6). Mean values are shown and error bars represent ± s.d., as analyzed by one-way ANOVA followed by the Tukey-Kramer test in ( C , E , F , I , J and K ). Biological replicates were used for all experiments. ns, p > 0.05, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.
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    Image Search Results


    Prevention of neuroma formation by a spatially confined conduit filled with GelMA MAVP MPS. ( A ) Illustration of 3D-printed GelMA MPs loaded with MAVP and the proposed mechanism of action within the neural conduit. ( B ) Representative images and ( C ) quantitative scores of autotomy behavior over 12 weeks (n = 6). ( D ) Representative gait footprints at 12 weeks post-surgery. ( E ) Quantification of left hindlimb stance duration (n = 6) and ( F ) maximum contact area (n = 6). ( G ) IF staining of p-VEGFR2 activation and ( H ) IF staining of neovascularization marker RECA-1. (I) Quantification of p-VEGFR2-positive area percentage (n = 6). and ( J ) quantification of RECA-1-positive area percentage (n = 6). ( K ) Regenerated nerve length measurements (n = 6). Mean values are shown and error bars represent ± s.d., as analyzed by one-way ANOVA followed by the Tukey-Kramer test in ( C , E , F , I , J and K ). Biological replicates were used for all experiments. ns, p > 0.05, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Journal: Bioactive Materials

    Article Title: Targeting VEGFR2 inhibition within a spatially-confined conduit promotes nerve self-resolution and alleviates mechanical allodynia

    doi: 10.1016/j.bioactmat.2026.03.009

    Figure Lengend Snippet: Prevention of neuroma formation by a spatially confined conduit filled with GelMA MAVP MPS. ( A ) Illustration of 3D-printed GelMA MPs loaded with MAVP and the proposed mechanism of action within the neural conduit. ( B ) Representative images and ( C ) quantitative scores of autotomy behavior over 12 weeks (n = 6). ( D ) Representative gait footprints at 12 weeks post-surgery. ( E ) Quantification of left hindlimb stance duration (n = 6) and ( F ) maximum contact area (n = 6). ( G ) IF staining of p-VEGFR2 activation and ( H ) IF staining of neovascularization marker RECA-1. (I) Quantification of p-VEGFR2-positive area percentage (n = 6). and ( J ) quantification of RECA-1-positive area percentage (n = 6). ( K ) Regenerated nerve length measurements (n = 6). Mean values are shown and error bars represent ± s.d., as analyzed by one-way ANOVA followed by the Tukey-Kramer test in ( C , E , F , I , J and K ). Biological replicates were used for all experiments. ns, p > 0.05, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Article Snippet: The following primary antibodies were used for the subsequent steps: anti-Yap (mouse, 1:200, Santa sc-376830); anti-p-VEGFR2 (rabbit, 1:100 Invitrogen, PA5-105765); α-SMA (rabbit, 1:200, Proteintech 14395-1-AP); Reca-1 (mouse, 1:200, Santa sc-52665); anti-CD31 (mouse, 1:200, Santa sc-13537); anti-Ki67 (rabbit, 1:150, Cell Signaling 9129S); anti-NF-200 (mouse, 1:200, Sigma, SAB4200747); anti-MBP (rabbit, 1:200, Abcam ab218011); anti-F4/80 (mouse, 1:200, Santa sc-377009); Iba-1 (rabbit, 1:150, Abcam ab178846); anti-CGRP (rabbit, 1:400, Abcam ab283568); anti-TRPA1 (mouse, 1:200, Santa sc-376495); anti-CD86 (rabbit, 1:200, Proteintech 30691-1-AP); CD206 (rabbit, 1:200, Proteintech 18704-1-AP).

    Techniques: Staining, Activation Assay, Marker