
PrP 106-126
CAS No. 148439-49-0
PrP 106-126( —— )
Catalog No. M30148 CAS No. 148439-49-0
PrP106-126 is a fragment of human prion protein that is present in biological samples. It has been shown to act as an agonist at the human FPR2/ALX GPCR.
Purity : >98% (HPLC)






Size | Price / USD | Stock | Quantity |
100MG | Get Quote | Get Quote |
![]() ![]() |
200MG | Get Quote | Get Quote |
![]() ![]() |
500MG | Get Quote | Get Quote |
![]() ![]() |
Biological Information
-
Product NamePrP 106-126
-
NoteResearch use only, not for human use.
-
Brief DescriptionPrP106-126 is a fragment of human prion protein that is present in biological samples. It has been shown to act as an agonist at the human FPR2/ALX GPCR.
-
DescriptionPrP106-126 is a fragment of human prion protein that is present in biological samples. It has been shown to act as an agonist at the human FPR2/ALX GPCR.(In Vitro):PrP (106-126) (100 μM) induces mTOR phosphorylation over time in N2a cells. PrP (106-126)-treated cells show significantly increased ROS production in comparison with that of PBS-treated control cells. Knockdown of PRAS40 enhances PrP (106-126)-induced apoptosis. PRAS40 alleviates PrP (106-126)-induced neuronal apoptosis via mTOR-AKT activation. PrP (106-126) interacts selectively with porcine brain endothelial cells (PBEC) via their luminal side, and causes cumulative cell death, as shown by lactate dehydrogenase release, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide reduction, Caspase 3 induction and direct cell counting. In addition, PrP (106-126), but not its corresponding scrambled peptide, produces a 50% reduction of the trans-endothelial electrical resistance, while the PBEC maintained confluency.
-
In VitroPrP (106-126) (100 μM) induces mTOR phosphorylation over time in N2a cells. PrP (106-126)-treated cells show significantly increased ROS production in comparison with that of PBS-treated control cells. Knockdown of PRAS40 enhances PrP (106-126)-induced apoptosis. PRAS40 alleviates PrP (106-126)-induced neuronal apoptosis via mTOR-AKT activation. PrP (106-126) interacts selectively with porcine brain endothelial cells (PBEC) via their luminal side, and causes cumulative cell death, as shown by lactate dehydrogenase release, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide reduction, Caspase 3 induction and direct cell counting. In addition, PrP (106-126), but not its corresponding scrambled peptide, produces a 50% reduction of the trans-endothelial electrical resistance, while the PBEC maintained confluency.
-
In Vivo——
-
Synonyms——
-
PathwayOthers
-
TargetOther Targets
-
Recptor——
-
Research Area——
-
Indication——
Chemical Information
-
CAS Number148439-49-0
-
Formula Weight1912.3
-
Molecular FormulaC80H138N26O24S2
-
Purity>98% (HPLC)
-
SolubilityH2O : 1 mg/mL (0.52 mM; Need ultrasonic and warming)
-
SMILES——
-
Chemical NameSequence:Lys-Thr-Asn-Met-Lys-His-Met-Ala-Gly-Ala-Ala-Ala-Ala-Gly-Ala-Val-Val-Gly-Gly-Leu-Gly
Shipping & Storage Information
-
Storage(-20℃)
-
ShippingWith Ice Pack
-
Stability≥ 2 years
Reference
Yang W, et al. PRAS40 alleviates neurotoxic prion peptide-induced apoptosis via mTOR-AKT signaling. CNS Neurosci Ther. 2017 May;23(5):416-427.
molnova catalog



related products
-
Dihydroxyfumaric aci...
Dihydroxyfumaric acid is a known generator of superoxide anions and by hydroxyl free radicals. Dihydroxyfumarate exposure can cause insulin inhibitory effects. It can spontaneously convert to hydroxypyruvate or to oxaloglycolate.
-
Sodium carbonate
Sodium Carbonate, also named as Disodium carbonate, Soda Ash, Carbonic acid disodium salt, is the disodium salt of carbonic acid with alkalinizing property.
-
N20C hydrochloride
NMDA receptor antagonist.