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Proteintech reca 1
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.
Reca 1, 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
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1) Product Images from "Targeting VEGFR2 inhibition within a spatially-confined conduit promotes nerve self-resolution and alleviates mechanical allodynia"

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

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.03.009

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.
Figure Legend 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.

Techniques Used: Staining, Activation Assay, Marker



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Image Search Results


USP18 aggravates cardiac I/R injury through regulation of mitochondria and inhibition of mitophagy. a Electron microscopy image showing mitophagy in USP18-cKO mouse hearts ( n= 5). Scale bar=3 μm. White arrowheads indicate sites of mitophagy. b Protein levels of PINK1, Parkin, ubiquitinated proteins (Ub), P62, and LC3II in mitochondria from heart tissue in USP18-cKO and WT mice 24 h after I/R injury ( n =4). c Electron microscopy image showing mitophagy in USP18-overexpres (OV) mouse hearts ( n =5). Scale bar=3 μm. White arrowheads indicate sites of mitophagy. d Protein levels of PINK1, Parkin, Ub, P62, and LC3II proteins in mitochondria from the heart tissue of USP18-OV mice 24 h after I/R injury ( n =4). Color shift in mitophagy dye (red) and lysosomal dye (green) in NRVMs showing mitophagy in NRVMs with USP18 siRNA transfection ( e ) or Ad-USP18 infection ( f ) and the quantitative mitophagy index in each group ( n= 5). Scale bar=9 μm. Protein levels of PINK1, Parkin, Ub, P62, and LC3II in mitochondria from NRVMs transfected with USP18 siRNA ( g ) or infected with Ad-USP18 ( h ). ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001 ⁎⁎⁎⁎ P <0.0001. USP18. Ubiquitin-specific protease 18; I/R. Ischemia/reperfusion; WT. Wild-type; KO. Knockout; P62. Sequestosome 1; LC3. Microtubule-associated protein 1 light chain 3; VDAC. Voltage-dependent anion channel.

Journal: Military Medical Research

Article Title: USP18 exacerbates myocardial I/R injury by inhibiting Parkin mitophagy through the deubiquitinase PTEN-L

doi: 10.1016/j.mmr.2026.100004

Figure Lengend Snippet: USP18 aggravates cardiac I/R injury through regulation of mitochondria and inhibition of mitophagy. a Electron microscopy image showing mitophagy in USP18-cKO mouse hearts ( n= 5). Scale bar=3 μm. White arrowheads indicate sites of mitophagy. b Protein levels of PINK1, Parkin, ubiquitinated proteins (Ub), P62, and LC3II in mitochondria from heart tissue in USP18-cKO and WT mice 24 h after I/R injury ( n =4). c Electron microscopy image showing mitophagy in USP18-overexpres (OV) mouse hearts ( n =5). Scale bar=3 μm. White arrowheads indicate sites of mitophagy. d Protein levels of PINK1, Parkin, Ub, P62, and LC3II proteins in mitochondria from the heart tissue of USP18-OV mice 24 h after I/R injury ( n =4). Color shift in mitophagy dye (red) and lysosomal dye (green) in NRVMs showing mitophagy in NRVMs with USP18 siRNA transfection ( e ) or Ad-USP18 infection ( f ) and the quantitative mitophagy index in each group ( n= 5). Scale bar=9 μm. Protein levels of PINK1, Parkin, Ub, P62, and LC3II in mitochondria from NRVMs transfected with USP18 siRNA ( g ) or infected with Ad-USP18 ( h ). ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001 ⁎⁎⁎⁎ P <0.0001. USP18. Ubiquitin-specific protease 18; I/R. Ischemia/reperfusion; WT. Wild-type; KO. Knockout; P62. Sequestosome 1; LC3. Microtubule-associated protein 1 light chain 3; VDAC. Voltage-dependent anion channel.

Article Snippet: To block mitophagy, the selective dynamin-related protein 1 (Drp1) inhibitor Mdivi-1 was used (50 μmol/L, MedChemExpress, USA).

Techniques: Inhibition, Electron Microscopy, Transfection, Infection, Ubiquitin Proteomics, Knock-Out

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

Gel-AgNA/MgGA MN promote mucosal regeneration. (a) HE and Safranin O staining of rabbit tracheal samples harvested at Day 10 post-operation after treated with Gel, Gel-AgNA, Gel-MgGA, and Gel-AgNA/MgGA MN. (b) IF staining of CK14 (marker of basal cells, red) and AC-Tub (marker of cilia cell, green). (c) IF staining of ZO-1 (marker of tight junctions, orange). (d, e) Quantitative analysis of regenerated epithelial coverage and thickness (n = 9). (f) Masson and Sirius Red staining for collagen evaluation after various treatments (n = 5). Quantitative analysis of collagen volume fraction (g) and fiber orientation (h) . The pentagram indicates luminal side of trachea.

Journal: Bioactive Materials

Article Title: Spatiotemporally engineered microneedle for microenvironment remodeling propels mucosal regeneration after tracheal mucosal injury

doi: 10.1016/j.bioactmat.2026.01.026

Figure Lengend Snippet: Gel-AgNA/MgGA MN promote mucosal regeneration. (a) HE and Safranin O staining of rabbit tracheal samples harvested at Day 10 post-operation after treated with Gel, Gel-AgNA, Gel-MgGA, and Gel-AgNA/MgGA MN. (b) IF staining of CK14 (marker of basal cells, red) and AC-Tub (marker of cilia cell, green). (c) IF staining of ZO-1 (marker of tight junctions, orange). (d, e) Quantitative analysis of regenerated epithelial coverage and thickness (n = 9). (f) Masson and Sirius Red staining for collagen evaluation after various treatments (n = 5). Quantitative analysis of collagen volume fraction (g) and fiber orientation (h) . The pentagram indicates luminal side of trachea.

Article Snippet: Immunofluorescence staining of CK14 (Abcam, ab181595), AC-Tub (Proteintech, 66200-1-Ig), ZO-1 (Proteintech, 21773-1-AP), and Immunohistochemical (IHC) staining for CD31 (Servicebio, S1002) were conducted to reveal the conditions of mucosal regeneration, according to previous literature [ ].

Techniques: Staining, Marker

Effect of corn processing on relative mRNA level for mTOR , 4E-BP1 , p70S6K and protein abundances of mTOR, phosphorylated mTOR (p-mTOR), eukaryotic initiation factor 4E-binding protein 1 (4E-BP1), phosphorylated 4E-BP1 (p-4E-BP1), p70 ribosomal protein S6 kinase (p70S6K) and phosphorylated p70S6K (p-p70S6K) in the longissimus thoracis of piglets. Results are presented as means ± standard error of the mean (SEM), n = 4. Data columns with different letters were significantly different ( P ≤ 0.05).

Journal: Animal Nutrition

Article Title: Modulating starch digestion kinetics via feed processing: Implications for growth and metabolism in weaned pigs

doi: 10.1016/j.aninu.2025.08.011

Figure Lengend Snippet: Effect of corn processing on relative mRNA level for mTOR , 4E-BP1 , p70S6K and protein abundances of mTOR, phosphorylated mTOR (p-mTOR), eukaryotic initiation factor 4E-binding protein 1 (4E-BP1), phosphorylated 4E-BP1 (p-4E-BP1), p70 ribosomal protein S6 kinase (p70S6K) and phosphorylated p70S6K (p-p70S6K) in the longissimus thoracis of piglets. Results are presented as means ± standard error of the mean (SEM), n = 4. Data columns with different letters were significantly different ( P ≤ 0.05).

Article Snippet: The membranes were blocked at room temperature, followed by incubation at 4 °C overnight with the following primary antibodies: mammalian target of rapamycin (mTOR, catalog No. 2983, Cell Signaling Technology, Danvers, MA, USA), phosphorylated mTOR (p-mTOR, catalog No. 5536, Cell Signaling Technology, Danvers, MA, USA), eukaryotic initiation factor 4E-binding protein 1 (4E-BP1, catalog No. 9644, Cell Signaling Technology, Danvers, MA, USA), phosphorylated 4E-BP1 (p-4E-BP1, catalog No. 2855, Cell Signaling Technology, Danvers, MA, USA), p70 ribosomal protein S6 kinase (p70S6K, catalog No. 2708, Cell Signaling Technology, Danvers, MA, USA), phosphorylated p70S6K (p-p70S6K, catalog No. 9234, Cell Signaling Technology, Danvers, MA, USA), and glyceraldehyde-3-phosphate dehydrogenase (GAPDH, catalog No. 5174, Cell Signaling Technology, Danvers, MA, USA).

Techniques: Binding Assay