pm26TGF-β1 peptide
Based on 1 publication(s) in Google Scholar
pm26TGF-β1 peptide is a peptide that mimics a portion of the human TGF-β1 molecule. pm26TGF-β1 peptide shows high affinity for the TGF-β1 receptor. pm26TGF-β1 peptide displays potent anti-inflammatory properties and does not exhibit neutrophils’ chemoattraction.
For research use only. We do not sell to patients.
- Formula: C54H93N19O20S2
- Molecular Weight:1392.56
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications Citing Use of MedChemExpress (MCE) pm26TGF-β1 peptide
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Biological Activity
Description
IC50 & Target
In Vitro
The synthetic pm26TGF-β1 peptide (1 μM, 10 μM and 100 μM; 24-48 hours) tested in peripheral blood mononuclear cells (PBMC) significantly down-modulates TNF-α and up-regulates IL-10 responses in an inflammatory microenvironment, leading to regulatory T cells (Treg) phenotype differentiation[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Male C57BL/6 mice (5-7-weeks old; 20-30g) injected with carrageenan[1]
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Dosage:100 µg/kg, 300 µg/kg or 1000 µg/kg
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Administration:Subcutaneous injection; once
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Result:Decreased neutrophils migration during inflammatory process in C57BL/6 mice.
Chemical Information
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Molecular Weight 1392.56
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Formula C54H93N19O20S2
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Sequence
Ala-Cys-Glu-Ser-Pro-Leu-Lys-Arg-Gln-Cys-Gly-Gly-Gly-Ser
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Sequence Shortening
ACESPLKRQCGGGS
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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
Protocols
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)