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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
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gcpii content - by Bioz Stars, 2026-09
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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