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gfp eyfp fitc  (Novus Biologicals)


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    Structured Review

    Novus Biologicals gfp eyfp fitc
    Gfp Eyfp Fitc, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 94/100, based on 13 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/gfp+eyfp+fitc/GFP+Antibody+%5BFITC%5D/pmc10950302-874-49-51
    Average 94 stars, based on 13 article reviews
    gfp eyfp fitc - by Bioz Stars, 2026-10
    94/100 stars

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    Related Articles

    Incubation:

    Article Title: Autophagy enables microglia to engage amyloid plaques and prevents microglial senescence
    Article Snippet: A series of coronal sections (30 μm) were obtained with a cryostat (Leica). .. Coronal sections were incubated with blocking/permeabilization buffer (5% goat serum and 0.25% Triton X-100 in PBS) at room temperature for 60 min and incubated with antibodies including p-ACC (#3661, Cell Signaling Technology, 1:100), APP-Alexa594 (6E10 clone, #803019, BioLegend, 1:250), CD11b (MCA711, Bio-Rad, 1:200), Clec7a (R1–8g7 clone, #mabg-mdect, InvivoGen, 1:10), GFP/EYFP-FITC (NB100–1771, Novus Biologicals, 1:250), γH2A.X (ab81299, Abcam, 1:250), HMGB1 (ab79823, Abcam, 1:250), Iba-1 (#019–19741, Wako, Japan, 1:500), Ki67 (MA5–14520, ThermoFisher, 1:100), Lamin B1 (ab16048, Abcam, 1:100), LAMP1 (ab24170, Abcam, 1:100), MMP-12 (#22989–1-AP, Proteintech, 1:100), p16 Ink4a (ab211542, Abcam, 1:100), p21 Cip1 (ab188224, Abcam, 1:100), p62 (#GP62-C, Progen, 1:250) and VGLUT2 (#135–404, Synaptic System) at 4 °C overnight followed by secondary antibodies conjugated with Alexa-fluorescein if necessary. .. For sorted microglia, cells were fixed with 4% paraformaldehyde at 4 °C for 15 min, incubated with blocking/permeabilization buffer (1% bovine serum albumin and 0.1% Triton X-100 in PBS) at room temperature for 30 min, and incubated with LC3A/B (#12741, Cell Signaling Technology, 1:100) at 4 °C overnight followed by secondary antibodies conjugated with fluorescein (#A-11070, #A-11072 and #A-21245 for primary antibodies raised from rabbit; #A-11007 and #A-11006 for primary antibodies raised from rat, ThermoFisher, 1:500; #A-11076 and #A-21450 for p62 antibody).

    Article Title: Autophagy enables microglia to engage amyloid plaques and prevents microglial senescence.
    Article Snippet: Dysfunctional autophagy has been implicated in the pathogenesis of Alzheimer’s disease (AD).. Previous evidence suggested disruptions of multiple stages of the autophagy-lysosomal pathway in affected neurons.. However, whether and how deregulated autophagy in microglia, a cell type with an important link to AD, contributes to AD progression remains elusive.

    Blocking Assay:

    Article Title: Autophagy enables microglia to engage amyloid plaques and prevents microglial senescence
    Article Snippet: A series of coronal sections (30 μm) were obtained with a cryostat (Leica). .. Coronal sections were incubated with blocking/permeabilization buffer (5% goat serum and 0.25% Triton X-100 in PBS) at room temperature for 60 min and incubated with antibodies including p-ACC (#3661, Cell Signaling Technology, 1:100), APP-Alexa594 (6E10 clone, #803019, BioLegend, 1:250), CD11b (MCA711, Bio-Rad, 1:200), Clec7a (R1–8g7 clone, #mabg-mdect, InvivoGen, 1:10), GFP/EYFP-FITC (NB100–1771, Novus Biologicals, 1:250), γH2A.X (ab81299, Abcam, 1:250), HMGB1 (ab79823, Abcam, 1:250), Iba-1 (#019–19741, Wako, Japan, 1:500), Ki67 (MA5–14520, ThermoFisher, 1:100), Lamin B1 (ab16048, Abcam, 1:100), LAMP1 (ab24170, Abcam, 1:100), MMP-12 (#22989–1-AP, Proteintech, 1:100), p16 Ink4a (ab211542, Abcam, 1:100), p21 Cip1 (ab188224, Abcam, 1:100), p62 (#GP62-C, Progen, 1:250) and VGLUT2 (#135–404, Synaptic System) at 4 °C overnight followed by secondary antibodies conjugated with Alexa-fluorescein if necessary. .. For sorted microglia, cells were fixed with 4% paraformaldehyde at 4 °C for 15 min, incubated with blocking/permeabilization buffer (1% bovine serum albumin and 0.1% Triton X-100 in PBS) at room temperature for 30 min, and incubated with LC3A/B (#12741, Cell Signaling Technology, 1:100) at 4 °C overnight followed by secondary antibodies conjugated with fluorescein (#A-11070, #A-11072 and #A-21245 for primary antibodies raised from rabbit; #A-11007 and #A-11006 for primary antibodies raised from rat, ThermoFisher, 1:500; #A-11076 and #A-21450 for p62 antibody).

    Article Title: Autophagy enables microglia to engage amyloid plaques and prevents microglial senescence.
    Article Snippet: Dysfunctional autophagy has been implicated in the pathogenesis of Alzheimer’s disease (AD).. Previous evidence suggested disruptions of multiple stages of the autophagy-lysosomal pathway in affected neurons.. However, whether and how deregulated autophagy in microglia, a cell type with an important link to AD, contributes to AD progression remains elusive.



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    fitc-conjugated anti-gfp cross-reacts eyfp  (Rockland Immunochemicals)
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    Characterization of Ksp/CreERT2 transgenic mice. Transgenic mice expressing tamoxifen-inducible Cre recombinase (CreERT2) under the control of the Ksp-cadherin promoter (Ksp) were generated. (A) Ksp/CreERT2 mice were crossed with <t>R26R-EYFP</t> reporter mice, and the bitransgenic progeny were administered tamoxifen (right) or vehicle (left). Staining of kidney sections with an Ab against the human estrogen receptor (red) showed nuclear translocation of the CreERT2 fusion protein (arrows) following administration of tamoxifen. Nuclei were counterstained with DAPI. Staining with an Ab against GFP that cross-reacted with EYFP (green) showed that the reporter gene was activated by Cre/loxP recombination only in tamoxifen-treated animals. Scale bars: 20 µm. (B) Immunoblot analysis of tissues from tamoxifen-treated Ksp/CreERT2;R26R-EYFP mice revealed expression of EYFP only in the kidney, indicating that Cre/loxP recombination was tissue-specific (upper panel). Immunoblot analysis of kidneys from Ksp/CreERT2;R26R-EYFP mice that were treated with tamoxifen or vehicle revealed that Cre/loxP recombination was tamoxifen-dependent (lower panel). Ksp/Cre;R26R-EYFP mouse kidneys were used as positive controls (+), and Ksp/Cre mouse kidneys were used as negative controls (−). Immunoblotting with anti-tubulin Ab was used as a loading control. (C) To identify the nephron segments in which Cre/loxP recombination was induced, Ksp/CreERT2;R26R mice were injected with tamoxifen and the kidneys were co-stained with an Ab <t>against</t> <t>β-galactosidase</t> (red) and markers of specific nephron segments (green). Staining with LTA, anti-NKCC2, anti-NCX1 and anti-AQP3 revealed that lacZ was expressed in proximal tubules (pt), thick ascending limbs of loops of Henle (tal), distal convoluted tubule (dt), and collecting duct (cd), respectively. Arrows indicate co-localization. Scale bars: 20 µm. (D) Efficiency of tamoxifen-inducible Cre/loxP recombination in different nephron segments. Adult Ksp/CreERT2;R26R mice (n = 3) were treated with tamoxifen for 5 days, and 2 weeks later the kidneys were removed and co-stained with an Ab to β-galactosidase and markers of specific nephron segments. Histogram shows the percentage of lacZ-positive cells in the proximal tubules (pt), thick ascending limbs of loops of Henle (tal), distal convoluted tubule (dt) and collecting ducts (cd). Error bars indicate SD.
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    Image Search Results


    Characterization of Ksp/CreERT2 transgenic mice. Transgenic mice expressing tamoxifen-inducible Cre recombinase (CreERT2) under the control of the Ksp-cadherin promoter (Ksp) were generated. (A) Ksp/CreERT2 mice were crossed with R26R-EYFP reporter mice, and the bitransgenic progeny were administered tamoxifen (right) or vehicle (left). Staining of kidney sections with an Ab against the human estrogen receptor (red) showed nuclear translocation of the CreERT2 fusion protein (arrows) following administration of tamoxifen. Nuclei were counterstained with DAPI. Staining with an Ab against GFP that cross-reacted with EYFP (green) showed that the reporter gene was activated by Cre/loxP recombination only in tamoxifen-treated animals. Scale bars: 20 µm. (B) Immunoblot analysis of tissues from tamoxifen-treated Ksp/CreERT2;R26R-EYFP mice revealed expression of EYFP only in the kidney, indicating that Cre/loxP recombination was tissue-specific (upper panel). Immunoblot analysis of kidneys from Ksp/CreERT2;R26R-EYFP mice that were treated with tamoxifen or vehicle revealed that Cre/loxP recombination was tamoxifen-dependent (lower panel). Ksp/Cre;R26R-EYFP mouse kidneys were used as positive controls (+), and Ksp/Cre mouse kidneys were used as negative controls (−). Immunoblotting with anti-tubulin Ab was used as a loading control. (C) To identify the nephron segments in which Cre/loxP recombination was induced, Ksp/CreERT2;R26R mice were injected with tamoxifen and the kidneys were co-stained with an Ab against β-galactosidase (red) and markers of specific nephron segments (green). Staining with LTA, anti-NKCC2, anti-NCX1 and anti-AQP3 revealed that lacZ was expressed in proximal tubules (pt), thick ascending limbs of loops of Henle (tal), distal convoluted tubule (dt), and collecting duct (cd), respectively. Arrows indicate co-localization. Scale bars: 20 µm. (D) Efficiency of tamoxifen-inducible Cre/loxP recombination in different nephron segments. Adult Ksp/CreERT2;R26R mice (n = 3) were treated with tamoxifen for 5 days, and 2 weeks later the kidneys were removed and co-stained with an Ab to β-galactosidase and markers of specific nephron segments. Histogram shows the percentage of lacZ-positive cells in the proximal tubules (pt), thick ascending limbs of loops of Henle (tal), distal convoluted tubule (dt) and collecting ducts (cd). Error bars indicate SD.

    Journal: Human Molecular Genetics

    Article Title: Acute kidney injury and aberrant planar cell polarity induce cyst formation in mice lacking renal cilia

    doi: 10.1093/hmg/ddn045

    Figure Lengend Snippet: Characterization of Ksp/CreERT2 transgenic mice. Transgenic mice expressing tamoxifen-inducible Cre recombinase (CreERT2) under the control of the Ksp-cadherin promoter (Ksp) were generated. (A) Ksp/CreERT2 mice were crossed with R26R-EYFP reporter mice, and the bitransgenic progeny were administered tamoxifen (right) or vehicle (left). Staining of kidney sections with an Ab against the human estrogen receptor (red) showed nuclear translocation of the CreERT2 fusion protein (arrows) following administration of tamoxifen. Nuclei were counterstained with DAPI. Staining with an Ab against GFP that cross-reacted with EYFP (green) showed that the reporter gene was activated by Cre/loxP recombination only in tamoxifen-treated animals. Scale bars: 20 µm. (B) Immunoblot analysis of tissues from tamoxifen-treated Ksp/CreERT2;R26R-EYFP mice revealed expression of EYFP only in the kidney, indicating that Cre/loxP recombination was tissue-specific (upper panel). Immunoblot analysis of kidneys from Ksp/CreERT2;R26R-EYFP mice that were treated with tamoxifen or vehicle revealed that Cre/loxP recombination was tamoxifen-dependent (lower panel). Ksp/Cre;R26R-EYFP mouse kidneys were used as positive controls (+), and Ksp/Cre mouse kidneys were used as negative controls (−). Immunoblotting with anti-tubulin Ab was used as a loading control. (C) To identify the nephron segments in which Cre/loxP recombination was induced, Ksp/CreERT2;R26R mice were injected with tamoxifen and the kidneys were co-stained with an Ab against β-galactosidase (red) and markers of specific nephron segments (green). Staining with LTA, anti-NKCC2, anti-NCX1 and anti-AQP3 revealed that lacZ was expressed in proximal tubules (pt), thick ascending limbs of loops of Henle (tal), distal convoluted tubule (dt), and collecting duct (cd), respectively. Arrows indicate co-localization. Scale bars: 20 µm. (D) Efficiency of tamoxifen-inducible Cre/loxP recombination in different nephron segments. Adult Ksp/CreERT2;R26R mice (n = 3) were treated with tamoxifen for 5 days, and 2 weeks later the kidneys were removed and co-stained with an Ab to β-galactosidase and markers of specific nephron segments. Histogram shows the percentage of lacZ-positive cells in the proximal tubules (pt), thick ascending limbs of loops of Henle (tal), distal convoluted tubule (dt) and collecting ducts (cd). Error bars indicate SD.

    Article Snippet: The following Abs and dilutions were used in this study: AQP3 (Chemicon International Inc., 1:400), acetylated tubulin (Sigma, 1:1000), entactin (Chemicon, 1:1000), β-galactosidase (Molecular Probes, 1:1000), FITC-conjugated anti-GFP that cross-reacts with EYFP (Rockland, 1:200), histone H3pS10 (Sigma 1:1000), Ki-67 (Novocastra, 1:500), NCX1 (generous gift from K.D.

    Techniques: Transgenic Assay, Expressing, Generated, Staining, Translocation Assay, Western Blot, Injection