GrTx1
GrTx1 is a peptide toxin originally isolated from the venom of the spider Grammostola rosea. GrTx1 blocks sodium channel, with IC50s of 0.63 μM, 0.23 μM, 0.77 μM, 1.29 μM, 0.63 μM and 0.37 μM for Nav1.1, Nav1.2, Nav1.3, Nav1.4, Nav1.6 and Nav1.7, repectively. GrTx1 can be used for neurological disease research.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- Formel: C159H243N45O41S8
- Molecular Weight:3697.43
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biologische Aktivität
Beschreibung
In Vitro
GrTx1 (0-100 μΜ, 3 min) blocks Na+ currents of neuroblastoma F-11 cells with an IC50 of 2.8 μM[1]. GrTx1 (10 μΜ, 3 min) blocks about 85% Na+ currents of neuroblastoma F-11 cells with no effects on common K+ channels, such as Kv1.1 and 1.4[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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Molecular Weight 3697.43
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Formel C159H243N45O41S8
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Sequence
Tyr-Cys-Gln-Lys-Trp-Met-Trp-Thr-Cys-Asp-Ser-Lys-Arg-Lys-Cys-Cys-Glu-Asp-Met-Val-Cys-Gln-Leu-Trp-Cys-Lys-Lys-Arg-Leu (Disulfide bonds: Cys2-Cys16, Cys9-Cys21, Cys15-Cys25)
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Sequence Shortening
YCQKWMWTCDSKRKCCEDMVCQLWCKKRL (Disulfide bonds: Cys2-Cys16, Cys9-Cys21, Cys15-Cys25)
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Initial Source
Grammostola rosea
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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Research Protocol for Neurological Diseases
PINK1/Parkin-mediated mitophagy pathway is a mitochondrial quality-control signaling axis in which mitochondrial depolarization stabilizes PINK1 on damaged mitochondria, activates Parkin recruitment and E3 ubiquitin ligase activity, promotes ubiquitination of outer mitochondrial membrane proteins, recruits selective autophagy adaptors, and drives lysosomal degradation of damaged mitochondria. In neurological disease research, this pathway is experimentally important because neurons, especially dopaminergic neurons, are highly dependent on mitochondrial integrity, and defective mitochondrial turnover can lead to mitochondrial dysfunction, oxidative stress, impaired neuronal survival, α-synuclein accumulation, and neuroinflammatory damage-associated signals. The genetic disease link is strongest in Parkinson’s disease because mutations in PRKN/parkin cause autosomal recessive juvenile parkinsonism, mutations in PINK1 cause hereditary early-onset Parkinson’s disease, and Drosophila studie
Reinheit & Dokumentation
Verweise
[1]. Clement H,et.al. Isolation and characterization of a novel toxin from the venom of the spider Grammostola rosea that blocks sodium channels. Toxicon. 2007 Jul;50(1):65-74. [Content Brief]
[2]. Redaelli E, et.al. Target promiscuity and heterogeneous effects of tarantula venom peptides affecting Na+ and K+ ion channels. J Biol Chem. 2010 Feb 5;285(6):4130-4142. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)