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anti psma antibody  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc anti psma antibody
    Anti Psma Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 27 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti psma antibody/product/Cell Signaling Technology Inc
    Average 93 stars, based on 27 article reviews
    anti psma antibody - by Bioz Stars, 2026-04
    93/100 stars

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    Cell Signaling Technology Inc anti psma antibody
    Widefield fluorescence microscopy images of PC3-PIP, <t>LNCaP</t> and PC3 flu cells after incubation with Cy5-conjugates 8 , 9 and 10 (2.5 μ m or 10 μ m , 37 °C, 2 h) with or without blocking (100-fold excess 2-PMPA). Nuclei were stained with DAPI (cyan). The Cy5 signal is shown in magenta. λ exc (DAPI) = 395 nm; λ exc (Cy5) = 640 nm. Scale bar = 50 μm.
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    Image Search Results


    Composite images of α-bungarotoxin (red) targeting postsynaptic neuromuscular junctions (i.e., motor endplates), anti-neurofilament H (purple) targeting the axonal cytoskeletons, and anti-GCPII (green) demonstrating muscle innervation after nerve transection with or without repair; arrowheads emphasize axons. (A) Healthy muscle after sham surgery demonstrating a normal innervated neuromuscular junction with surrounding GCPII expression. Contrast this with the appearance of neuromuscular junctions at (B) 4 weeks, (C) 8 weeks, and (D) 16 weeks after sciatic nerve transection with repair; note progressive flattening and fragmentation of endplates consistent with chronic denervation, the absence of axons, and lack of GCPII expression. Nerve transection with immediate repair demonstrates infiltration of axons and neuromuscular junction reinnervation between (E) 4 weeks and (F) 8 weeks. Also note recovery of GCPII expression near the reinnervated neuromuscular junction, which persists at (G) 16 weeks after nerve repair. Panels are 20× magnification, scale bar: 20 μm.

    Journal: medRxiv

    Article Title: Glutamate Carboxypeptidase II (GCPII)-Targeted PET to Identify Muscle Denervation in Peripheral Nervous System Injuries

    doi: 10.64898/2026.03.18.26348533

    Figure Lengend Snippet: Composite images of α-bungarotoxin (red) targeting postsynaptic neuromuscular junctions (i.e., motor endplates), anti-neurofilament H (purple) targeting the axonal cytoskeletons, and anti-GCPII (green) demonstrating muscle innervation after nerve transection with or without repair; arrowheads emphasize axons. (A) Healthy muscle after sham surgery demonstrating a normal innervated neuromuscular junction with surrounding GCPII expression. Contrast this with the appearance of neuromuscular junctions at (B) 4 weeks, (C) 8 weeks, and (D) 16 weeks after sciatic nerve transection with repair; note progressive flattening and fragmentation of endplates consistent with chronic denervation, the absence of axons, and lack of GCPII expression. Nerve transection with immediate repair demonstrates infiltration of axons and neuromuscular junction reinnervation between (E) 4 weeks and (F) 8 weeks. Also note recovery of GCPII expression near the reinnervated neuromuscular junction, which persists at (G) 16 weeks after nerve repair. Panels are 20× magnification, scale bar: 20 μm.

    Article Snippet: For GCPII content, primary antibody was rabbit anti-GCPII polyclonal antibody (Proteintech, 13163-1-AP, 1:50), secondary antibody was anti-rabbit CoraLite488-conjugated IgG (H+L) (Proteintech, SA00013-2, 1:200).

    Techniques: Expressing

    Images of anti-GCPII (green), anti-cytochrome C (red) targeting mitochondria, and DAPI (blue) targeting nuclei at 12 weeks after nerve transection with or without repair. White boxes around key area of each image. Panel D (sham surgery) is a composite of Panels A-C; Panel H (sciatic nerve transection without repair) is a composite of Panels E-G; Panel L (nerve transection with repair) is a composite of Panels I-K. Note localization of GCPII staining near clusters of subsarcolemmal mitochondria overlying myocyte nuclei, irrespective of denervation. A similar staining pattern was present at all tested timepoints between two and 16 weeks after nerve transection with or without repair. Panels are 63× magnification, scale bar: 10 μm.

    Journal: medRxiv

    Article Title: Glutamate Carboxypeptidase II (GCPII)-Targeted PET to Identify Muscle Denervation in Peripheral Nervous System Injuries

    doi: 10.64898/2026.03.18.26348533

    Figure Lengend Snippet: Images of anti-GCPII (green), anti-cytochrome C (red) targeting mitochondria, and DAPI (blue) targeting nuclei at 12 weeks after nerve transection with or without repair. White boxes around key area of each image. Panel D (sham surgery) is a composite of Panels A-C; Panel H (sciatic nerve transection without repair) is a composite of Panels E-G; Panel L (nerve transection with repair) is a composite of Panels I-K. Note localization of GCPII staining near clusters of subsarcolemmal mitochondria overlying myocyte nuclei, irrespective of denervation. A similar staining pattern was present at all tested timepoints between two and 16 weeks after nerve transection with or without repair. Panels are 63× magnification, scale bar: 10 μm.

    Article Snippet: For GCPII content, primary antibody was rabbit anti-GCPII polyclonal antibody (Proteintech, 13163-1-AP, 1:50), secondary antibody was anti-rabbit CoraLite488-conjugated IgG (H+L) (Proteintech, SA00013-2, 1:200).

    Techniques: Staining

    (A) Representative Western blot and corresponding densitometric analysis (n=2–3 per group) show increased GCPII band intensity in denervated samples at 2-, 8-, 12-, and 24-weeks post-denervation, compared to low baseline expression in naïve muscle (i.e., control). Band intensities were normalized to denervation-duration-matched controls and plotted as relative expression. Statistical analysis was not performed due to the limited sample size. (B) GCPII enzymatic assay demonstrating significantly increased GCPII activity at 8-, 12-, and 24-week timepoints. Activity is expressed in femtomoles of N-acetyl-aspartyl-glutamate (NAAG) hydrolysis per mg GCPII per hour (fmol/mg/h).

    Journal: medRxiv

    Article Title: Glutamate Carboxypeptidase II (GCPII)-Targeted PET to Identify Muscle Denervation in Peripheral Nervous System Injuries

    doi: 10.64898/2026.03.18.26348533

    Figure Lengend Snippet: (A) Representative Western blot and corresponding densitometric analysis (n=2–3 per group) show increased GCPII band intensity in denervated samples at 2-, 8-, 12-, and 24-weeks post-denervation, compared to low baseline expression in naïve muscle (i.e., control). Band intensities were normalized to denervation-duration-matched controls and plotted as relative expression. Statistical analysis was not performed due to the limited sample size. (B) GCPII enzymatic assay demonstrating significantly increased GCPII activity at 8-, 12-, and 24-week timepoints. Activity is expressed in femtomoles of N-acetyl-aspartyl-glutamate (NAAG) hydrolysis per mg GCPII per hour (fmol/mg/h).

    Article Snippet: For GCPII content, primary antibody was rabbit anti-GCPII polyclonal antibody (Proteintech, 13163-1-AP, 1:50), secondary antibody was anti-rabbit CoraLite488-conjugated IgG (H+L) (Proteintech, SA00013-2, 1:200).

    Techniques: Western Blot, Expressing, Control, Enzymatic Assay, Activity Assay

    (A) Mean gastrocnemius muscle uptake administration 2, 4, and 16 weeks after injury. White: sham surgery (uninjured nerve); Gray: repaired nerve; Black: unrepaired nerve; n = 5-6 per group per timepoint. Note persistent muscle uptake in the unrepaired group over time (B) Tissue [ 18 F]DCFPyL uptake after blocking GCPII binding with ZJ-43 coadministration; White: sham surgery (uninjured nerve), pooled across all timepoints; Gray: unrepaired nerve, pooled across all timepoints; Black: ZJ-43 co-administration, 4 weeks after sciatic nerve transection without repair. One outlier in biceps muscle unrepaired group (1.2 % ID/g) was excluded in the plot for improved visibility of remaining data; the outlier was included in statistical comparisons. Groupwise comparisons performed using Kruskal-Wallis test. %ID/g: percent injected dose per gram.

    Journal: medRxiv

    Article Title: Glutamate Carboxypeptidase II (GCPII)-Targeted PET to Identify Muscle Denervation in Peripheral Nervous System Injuries

    doi: 10.64898/2026.03.18.26348533

    Figure Lengend Snippet: (A) Mean gastrocnemius muscle uptake administration 2, 4, and 16 weeks after injury. White: sham surgery (uninjured nerve); Gray: repaired nerve; Black: unrepaired nerve; n = 5-6 per group per timepoint. Note persistent muscle uptake in the unrepaired group over time (B) Tissue [ 18 F]DCFPyL uptake after blocking GCPII binding with ZJ-43 coadministration; White: sham surgery (uninjured nerve), pooled across all timepoints; Gray: unrepaired nerve, pooled across all timepoints; Black: ZJ-43 co-administration, 4 weeks after sciatic nerve transection without repair. One outlier in biceps muscle unrepaired group (1.2 % ID/g) was excluded in the plot for improved visibility of remaining data; the outlier was included in statistical comparisons. Groupwise comparisons performed using Kruskal-Wallis test. %ID/g: percent injected dose per gram.

    Article Snippet: For GCPII content, primary antibody was rabbit anti-GCPII polyclonal antibody (Proteintech, 13163-1-AP, 1:50), secondary antibody was anti-rabbit CoraLite488-conjugated IgG (H+L) (Proteintech, SA00013-2, 1:200).

    Techniques: Blocking Assay, Binding Assay, Injection

    Widefield fluorescence microscopy images of PC3-PIP, LNCaP and PC3 flu cells after incubation with Cy5-conjugates 8 , 9 and 10 (2.5 μ m or 10 μ m , 37 °C, 2 h) with or without blocking (100-fold excess 2-PMPA). Nuclei were stained with DAPI (cyan). The Cy5 signal is shown in magenta. λ exc (DAPI) = 395 nm; λ exc (Cy5) = 640 nm. Scale bar = 50 μm.

    Journal: Journal of Medicinal Chemistry

    Article Title: Zwitterionic Modification of PSMA Ligands Reduces Off-Target Binding and Tissue Retention

    doi: 10.1021/acs.jmedchem.5c03849

    Figure Lengend Snippet: Widefield fluorescence microscopy images of PC3-PIP, LNCaP and PC3 flu cells after incubation with Cy5-conjugates 8 , 9 and 10 (2.5 μ m or 10 μ m , 37 °C, 2 h) with or without blocking (100-fold excess 2-PMPA). Nuclei were stained with DAPI (cyan). The Cy5 signal is shown in magenta. λ exc (DAPI) = 395 nm; λ exc (Cy5) = 640 nm. Scale bar = 50 μm.

    Article Snippet: The PSMA-positive cell line LNCaP was obtained from DSMZ (Deutsche Sammlung von Mikroorganismen and Zelllinien #ACC 256).

    Techniques: Fluorescence, Microscopy, Incubation, Blocking Assay, Staining

    Representative confocal microscopy images of (A) PC3-PIP and LNCaP cells after incubation with Cy5 conjugates 8 , 9 and 10 (10 μ m , 2 h, 37 °C) and (B) ZW800−617 13 (10 μ m , 2 h, 37 °C). Nuclei were stained with DAPI (cyan). The Cy5 signal is shown in magenta and the ZW800 signal in yellow. Images are shown as maximum intensity projections of z-stacks acquired with a 63x oil immersion objective. λ exc (DAPI) = 405 nm; λ exc (Cy5) = 653 nm, λ exc (ZW800) = 770 nm. Scale bar = 20 μm.

    Journal: Journal of Medicinal Chemistry

    Article Title: Zwitterionic Modification of PSMA Ligands Reduces Off-Target Binding and Tissue Retention

    doi: 10.1021/acs.jmedchem.5c03849

    Figure Lengend Snippet: Representative confocal microscopy images of (A) PC3-PIP and LNCaP cells after incubation with Cy5 conjugates 8 , 9 and 10 (10 μ m , 2 h, 37 °C) and (B) ZW800−617 13 (10 μ m , 2 h, 37 °C). Nuclei were stained with DAPI (cyan). The Cy5 signal is shown in magenta and the ZW800 signal in yellow. Images are shown as maximum intensity projections of z-stacks acquired with a 63x oil immersion objective. λ exc (DAPI) = 405 nm; λ exc (Cy5) = 653 nm, λ exc (ZW800) = 770 nm. Scale bar = 20 μm.

    Article Snippet: The PSMA-positive cell line LNCaP was obtained from DSMZ (Deutsche Sammlung von Mikroorganismen and Zelllinien #ACC 256).

    Techniques: Confocal Microscopy, Incubation, Staining

    Full body cryo-fluorescence tomography images (maximum intensity projection) of PC3-PIP and PC3 flu tumor-bearing xenograft mice obtained 4 h p.i. of 20 nmol dose of Cy5 conjugates 8 , 9 , 10 and ZW800 conjugate 13 . Selected organs are marked with the following abbreviations: PC3-PIP = PSMA-positive tumor xenograft; PC3 flu = PSMA-negative tumor xenograft; LG = lacrimal glands; Bl = bladder; GI = gastrointestinal tract, K i = kidney. Images were captured at 45 μm/pixel resolution with the following set ups: Cy5 channel = 640 nm excitation laser and 680/13 nm emission filter; ZW800 channel = 780 nm excitation laser and 840/70 nm emission filter.

    Journal: Journal of Medicinal Chemistry

    Article Title: Zwitterionic Modification of PSMA Ligands Reduces Off-Target Binding and Tissue Retention

    doi: 10.1021/acs.jmedchem.5c03849

    Figure Lengend Snippet: Full body cryo-fluorescence tomography images (maximum intensity projection) of PC3-PIP and PC3 flu tumor-bearing xenograft mice obtained 4 h p.i. of 20 nmol dose of Cy5 conjugates 8 , 9 , 10 and ZW800 conjugate 13 . Selected organs are marked with the following abbreviations: PC3-PIP = PSMA-positive tumor xenograft; PC3 flu = PSMA-negative tumor xenograft; LG = lacrimal glands; Bl = bladder; GI = gastrointestinal tract, K i = kidney. Images were captured at 45 μm/pixel resolution with the following set ups: Cy5 channel = 640 nm excitation laser and 680/13 nm emission filter; ZW800 channel = 780 nm excitation laser and 840/70 nm emission filter.

    Article Snippet: The PSMA-positive cell line LNCaP was obtained from DSMZ (Deutsche Sammlung von Mikroorganismen and Zelllinien #ACC 256).

    Techniques: Fluorescence, Tomography