Recombinant Humanized Type I Collagen
Based on 1 publication(s) in Google Scholar
Recombinant Humanized Type I Collagen is a recombinant humanized type I collagen. Recombinant Humanized Type I Collagen primarily serves as a tissue engineering scaffold and exhibits activity in promoting cell attachment, proliferation, and differentiation. Recombinant Humanized Type I Collagen specifically binds to integrins (α1β1/α2β1) and receptors (DDR1/DDR2) on the cell surface, activates intracellular signaling to regulate cytoskeletal rearrangement and gene expression, thereby achieving repair and regeneration of tissues such as bone and cartilage. Recombinant Humanized Type I Collagen can be used in tissue engineering and regenerative medicine research, including bone graft substitutes, dental guided tissue regeneration, cartilage reconstruction, and skin substitutes.
For research use only. We do not sell to patients.
- Purity : 95.00%
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications Citing Use of MedChemExpress (MCE) Recombinant Humanized Type I Collagen
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Biological Activity
Description
IC50 & Target
[1]|
DDR1 |
DDR2 |
α1β1 |
α2β1 |
Collagen I |
In Vitro
Recombinant Humanized Type I Collagen exhibits significantly higher resistance to bacterial collagenase degradation than animal-derived collagen membranes in in vitro degradation experiments[1].
Recombinant Humanized Type I Collagen (8 weeks) fabricated into a porous sponge scaffold supports chondrocyte attachment, maintains chondrocyte phenotype, and stimulates cartilage-specific extracellular matrix deposition in rabbit chondrocytes[1].
Recombinant Humanized Type I Collagen (prepared as a collagen/fibroblast gel; cultured to 2 days) supports cell growth in human fibroblasts and interacts with cells to induce gel contraction (simulating the dermal layer formation process)[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:Human decidual stromal cells (DSCs)
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Concentration:25 μg/mL (coating)
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Incubation Time:2 h (coating); 24 h (migration)
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Result:Migration ability of human DSCs was significantly enhanced compared with the 0.2% fetal bovine serum control.
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Cell Line:Human peripheral blood naïve CD4+ T cells
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Concentration:10 μg/mL (rhCOLI); 2 μg/mL (T cell TransAct); 20 μg/mL (human TGF-β1); 50 μg/mL (human IL-2)
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Incubation Time:3 days (differentiation culture)
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Result:Foxp3 expression was upregulated in Treg cells, with the most significant effect at 10 μg/mL: 46.21% versus 24.73% in the control.
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Cell Line:Human peripheral blood T cells
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Concentration:10 μg/mL
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Incubation Time:72 h
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Result:Secretion of IL-10 and TGF-β was induced at 10 μg/mL.
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Cell Line:H9C2
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Concentration:1 and 4 mg/mL (hydrogel)
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Incubation Time:72 h (extract conditioning); 24 and 72 h (H9C2 exposure)
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Result:At 72 h, H9C2 cell viability was 134.4% in the 1 mg/mL hydrogel group and 132.3% in the 4 mg/mL hydrogel group.
More live H9C2 cells were observed in the 1 mg/mL and 4 mg/mL groups than in the pH 5.0 control and hydrogel-only groups at 24 and 72 h.
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Cell Line:HUVEC
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Concentration:1 and 4 mg/mL (hydrogel)
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Incubation Time:72 h (extract conditioning); 24 and 72 h (HUVEC exposure)
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Result:At 72 h, HUVEC viability was 121.5% in the 1 mg/mL hydrogel group and 120.1% in the 4 mg/mL hydrogel group.
More live HUVECs were observed in the 1 mg/mL and 4 mg/mL groups, with almost no dead cells.
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Cell Line:HUVEC
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Concentration:1 and 4 mg/mL
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Incubation Time:0, 12, 24, and 48 h
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Result:At 24 h, the scratch areas of HUVECs co-cultured with 1 mg/mL and 4 mg/mL hydrogels were 30.7% and 35.7% of the initial area, respectively.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Sprague Dawley (male)[1]
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Dosage:Single precut rhCI matrix
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Administration:implantation into the right cranial defect; single implantation; 28 days post-surgery
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Result:Produced radiographic healing at 28 days compared with untreated contralateral defects.
New bone was observed emanating from the original cut ends of the defect and following the contours of the implant.
Continuing bone formation occurred at the periphery in the center region of the defects, with active osteoblast surfaces visible under high power.
Untreated contralateral control defects showed minimal new bone formation from the cut ends and were bridged with a thin rim of predominately fibrous connective tissue.
Chemical Information
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Appearance Solid
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Color White to off-white
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SMILES
[Recombinant Humanized Type I Collagen]
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (1)
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Journal Impact Factor
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Most Recent
Purity & Documentation
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Data Sheet (275 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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Handling Instructions (2659 KB)
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)