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gcpii content  (Proteintech)


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    Proteintech gcpii content
    Composite images of α-bungarotoxin (red) targeting postsynaptic neuromuscular junctions (i.e., motor endplates), anti-neurofilament H (purple) targeting the axonal cytoskeletons, <t>and</t> <t>anti-GCPII</t> (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.
    Gcpii Content, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/gcpii+content/FOLH1+Fusion+Protein/med_rxiv__64898__2026__03__18__26348533-189-1-10
    Average 94 stars, based on 2 article reviews
    gcpii content - by Bioz Stars, 2026-09
    94/100 stars

    Images

    1) Product Images from "Glutamate Carboxypeptidase II (GCPII)-Targeted PET to Identify Muscle Denervation in Peripheral Nervous System Injuries"

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

    Journal: medRxiv

    doi: 10.64898/2026.03.18.26348533

    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.
    Figure Legend 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.

    Techniques Used: 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.
    Figure Legend 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.

    Techniques Used: Staining

    Related Articles

    Expressing:

    Article Title: Glutamate Carboxypeptidase II (GCPII)-Targeted PET to Identify Muscle Denervation in Peripheral Nervous System Injuries
    Article Snippet: The Despeckle function was applied to reduce background noise, and contrast enhancement was performed to increase pixel intensity differences between signal and background.The Despeckle function was applied to reduce background noise, and contrast enhancement was performed to increase pixel intensity differences between signal and background.. 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).. For mitochondrial staining, primary antibody was mouse anti-cytochrome C monoclonal antibody (Invitrogen, 45-6100, 1:100), secondary antibody was goat anti-mouse Alexa Fluor 594 IgG1 (Invitrogen, A-21125, 1:200).For mitochondrial staining, primary antibody was mouse anti-cytochrome C monoclonal antibody (Invitrogen, 45-6100, 1:100), secondary antibody was goat anti-mouse Alexa Fluor 594 IgG1 (Invitrogen, A-21125, 1:200).

    Staining:

    Article Title: Glutamate Carboxypeptidase II (GCPII)-Targeted PET to Identify Muscle Denervation in Peripheral Nervous System Injuries
    Article Snippet: The Despeckle function was applied to reduce background noise, and contrast enhancement was performed to increase pixel intensity differences between signal and background.The Despeckle function was applied to reduce background noise, and contrast enhancement was performed to increase pixel intensity differences between signal and background.. 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).. For mitochondrial staining, primary antibody was mouse anti-cytochrome C monoclonal antibody (Invitrogen, 45-6100, 1:100), secondary antibody was goat anti-mouse Alexa Fluor 594 IgG1 (Invitrogen, A-21125, 1:200).For mitochondrial staining, primary antibody was mouse anti-cytochrome C monoclonal antibody (Invitrogen, 45-6100, 1:100), secondary antibody was goat anti-mouse Alexa Fluor 594 IgG1 (Invitrogen, A-21125, 1:200).



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    gcpii content  (Proteintech)
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    Proteintech gcpii content
    Composite images of α-bungarotoxin (red) targeting postsynaptic neuromuscular junctions (i.e., motor endplates), anti-neurofilament H (purple) targeting the axonal cytoskeletons, <t>and</t> <t>anti-GCPII</t> (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.
    Gcpii Content, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/gcpii+content/FOLH1+Fusion+Protein/med_rxiv__64898__2026__03__18__26348533-189-1-10
    Average 94 stars, based on 1 article reviews
    gcpii content - by Bioz Stars, 2026-09
    94/100 stars
    		  Buy from Supplier

    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