product summary
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company name :
Alomone Labs
product type :
chemical
product name :
µ-Conotoxin GIIIB
catalog :
C-270
more info or order :
citations: 23
Reference
Zanetti G, Negro S, Megighian A, Mattarei A, Lista F, Fillo S, et al. A CXCR4 receptor agonist strongly stimulates axonal regeneration after damage. Ann Clin Transl Neurol. 2019;6:2395-2402 pubmed publisher
Negro S, Zanetti G, Mattarei A, Valentini A, Megighian A, Tombesi G, et al. An Agonist of the CXCR4 Receptor Strongly Promotes Regeneration of Degenerated Motor Axon Terminals. Cells. 2019;8: pubmed publisher
Benoit E, Couesnon A, Lindovský J, Iorga B, Araoz R, Servent D, et al. Synthetic Pinnatoxins A and G Reversibly Block Mouse Skeletal Neuromuscular Transmission In Vivo and In Vitro. Mar Drugs. 2019;17: pubmed publisher
Rodrigues A, Wang Z, Messi M, Delbono O. Sympathomimetics regulate neuromuscular junction transmission through TRPV1, P/Q- and N-type Ca2+ channels. Mol Cell Neurosci. 2019;95:59-70 pubmed publisher
Zanetti G, Duregotti E, Locatelli C, Giampreti A, Lonati D, Rossetto O, et al. Variability in venom composition of European viper subspecies limits the cross-effectiveness of antivenoms. Sci Rep. 2018;8:9818 pubmed publisher
Bradford A, Machamer J, Russo T, McNutt P. 3,4-diaminopyridine reverses paralysis in botulinum neurotoxin-intoxicated diaphragms through two functionally distinct mechanisms. Toxicol Appl Pharmacol. 2018;341:77-86 pubmed publisher
Wang X, McIntosh J, Rich M. Muscle Nicotinic Acetylcholine Receptors May Mediate Trans-Synaptic Signaling at the Mouse Neuromuscular Junction. J Neurosci. 2018;38:1725-1736 pubmed publisher
Chand K, Lee K, Lee J, Qiu H, Willis E, Lavidis N, et al. Defects in synaptic transmission at the neuromuscular junction precede motor deficits in a TDP-43Q331K transgenic mouse model of amyotrophic lateral sclerosis. FASEB J. 2018;32:2676-2689 pubmed publisher
Wu M, White H, Boehm B, Meriney C, Kerrigan K, Frasso M, et al. New Cav2 calcium channel gating modifiers with agonist activity and therapeutic potential to treat neuromuscular disease. Neuropharmacology. 2018;131:176-189 pubmed publisher
Hurtado E, Cilleros V, Just L, Simó A, Nadal L, Tomas M, et al. Synaptic Activity and Muscle Contraction Increases PDK1 and PKC?I Phosphorylation in the Presynaptic Membrane of the Neuromuscular Junction. Front Mol Neurosci. 2017;10:270 pubmed publisher
Hurtado E, Cilleros V, Nadal L, Simó A, Obis T, Garcia N, et al. Muscle Contraction Regulates BDNF/TrkB Signaling to Modulate Synaptic Function through Presynaptic cPKC? and cPKC?I. Front Mol Neurosci. 2017;10:147 pubmed publisher
Jones R, Reich C, Dissanayake K, Kristmundsdottir F, Findlater G, Ribchester R, et al. NMJ-morph reveals principal components of synaptic morphology influencing structure-function relationships at the neuromuscular junction. Open Biol. 2016;6: pubmed
Xu Y, Halievski K, Henley C, Atchison W, Katsuno M, Adachi H, et al. Defects in Neuromuscular Transmission May Underlie Motor Dysfunction in Spinal and Bulbar Muscular Atrophy. J Neurosci. 2016;36:5094-106 pubmed publisher
Spaulding E, Sleigh J, Morelli K, Pinter M, Burgess R, Seburn K. Synaptic Deficits at Neuromuscular Junctions in Two Mouse Models of Charcot-Marie-Tooth Type 2d. J Neurosci. 2016;36:3254-67 pubmed publisher
Magown P, Shettar B, Zhang Y, Rafuse V. Direct optical activation of skeletal muscle fibres efficiently controls muscle contraction and attenuates denervation atrophy. Nat Commun. 2015;6:8506 pubmed publisher
Wu Y, Tejero R, Arancillo M, Vardar G, Korotkova T, Kintscher M, et al. Syntaxin 1B is important for mouse postnatal survival and proper synaptic function at the mouse neuromuscular junctions. J Neurophysiol. 2015;114:2404-17 pubmed publisher
Duregotti E, Negro S, Scorzeto M, Zornetta I, Dickinson B, Chang C, et al. Mitochondrial alarmins released by degenerating motor axon terminals activate perisynaptic Schwann cells. Proc Natl Acad Sci U S A. 2015;112:E497-505 pubmed publisher
Thyagarajan B, Potian J, Baskaran P, McArdle J. Capsaicin modulates acetylcholine release at the myoneural junction. Eur J Pharmacol. 2014;744:211-9 pubmed publisher
Rodrigues H, Fonseca M, Camargo W, Lima P, Martinelli P, Naves L, et al. Reduced expression of the vesicular acetylcholine transporter and neurotransmitter content affects synaptic vesicle distribution and shape in mouse neuromuscular junction. PLoS ONE. 2013;8:e78342 pubmed publisher
Ruiz R, Biea I, Tabares L. ?-Synuclein A30P decreases neurodegeneration and increases synaptic vesicle release probability in CSP?-null mice. Neuropharmacology. 2014;76 Pt A:106-17 pubmed publisher
Krieger F, Elflein N, Ruiz R, Guerra J, Serrano A, Asan E, et al. Fast motor axon loss in SMARD1 does not correspond to morphological and functional alterations of the NMJ. Neurobiol Dis. 2013;54:169-82 pubmed publisher
Ackermann B, Kröber S, Torres Benito L, Borgmann A, Peters M, Hosseini Barkooie S, et al. Plastin 3 ameliorates spinal muscular atrophy via delayed axon pruning and improves neuromuscular junction functionality. Hum Mol Genet. 2013;22:1328-47 pubmed publisher
Torres Benito L, Neher M, Cano R, Ruiz R, Tabares L. SMN requirement for synaptic vesicle, active zone and microtubule postnatal organization in motor nerve terminals. PLoS ONE. 2011;6:e26164 pubmed publisher
product information
cat :
C-270
SKU :
C-270_0.1 mg
Product Name :
µ-Conotoxin GIIIB
Group Type :
Non Antibodies
Product Type :
Proteins
Accession :
P01524
Accession Number :
https://www.uniprot.org/uniprotkb/P01524/entry
Applications :
Electrophysiology
Formulation :
Lyophilized from double distilled water (ddH2O). May contain TFA as a residual counter ion.
Storage After Reconstitution :
The reconstituted solution can be stored at 4°C for up to 1 week. For longer periods (up to 6 months), small aliquots should be stored at -20°C. We do not recommend storing the product in working solutions for longer than a few days. Avoid multiple freeze-thaw cycles.
Reconstitution and Solubility :
Centrifuge the vial (10,000 × g for 5 minutes) before adding solvent to spin down all the powder to the bottom of the vial. The lyophilized product may be difficult to visualize. Add solvent directly to the centrifuged vial. Gently tap, tilt, and roll the vial to aid dissolution. Avoid vigorous vortexing; light vortexing for up to 3 seconds is acceptable if needed. The product is soluble in pure water at high micromolar concentrations (100 µM - 1 mM). For long-term storage in solution, we recommend preparing a stock solution by dissolving the product in double-distilled water (ddH2O) at a concentration between 100-1000x of the final working concentration. Divide the stock solution into small aliquots and store at -20°C. Before use, thaw the relevant vial(s) and dilute to the desired working concentration in your working buffer. Centrifuge all product preparations before use. It is recommended to prepare fresh solutions in working buffers just before use. Avoid multiple freeze-thaw cycles to maintain biological activity.
Solubility :
Centrifuge the vial before adding solvent (10,000 x g for 5 minutes) to spin down all the powder to the bottom of the vial. The lyophilized product may be difficult to visualize. Add solvent directly to the centrifuged vial. Tap the vial to aid in dissolving the lyophilized product. Tilt and gently roll the liquid over the walls of the vial. Avoid vigorous vortexing. Light vortexing for up to 3 seconds is acceptable if needed. The product is soluble in pure water at high micromolar concentrations (100 µM - 1 mM). For long-term storage in solution, we recommend preparing a stock solution by dissolving the product in double-distilled water (ddH2O) at a concentration between 100-1000x of the final working concentration. Divide the stock solution into small aliquots and store at -20°C. Before use, thaw the relevant vial(s) and dilute to the desired working concentration in your working buffer. Centrifuge all product preparations before use. It is recommended to prepare fresh solutions in working buffers just before use. Avoid multiple freeze-thaw cycles to maintain biological activity.
Storage Before Reconstitution :
The product is shipped as a lyophilized powder at room temperature. Upon receipt, store the product at -20°C. Protect from moisture.
Origin :
Conus geographus (Geography cone) (Nubecula geographus)
Source :
Synthetic peptide
Gene ID :
SCN4A
Product Page - Scientific background :
µ-Conotoxin GIIIB was originally isolated from the marine snail Conus geographus. The peptide toxin selectively blocks NaV1.4 channels, which are expressed predominantly in skeletal muscle.1,2 It is a potent blocker and 600 nM completely blocked NaV1.4-related currents in rat skeletal muscle.3
Supplier :
Alomone Labs
Target :
NaV1.4 Na+ channels
Long Description :
A Selective Blocker of Skeletal Muscle NaV1.4 Channels
Short Description :
A Selective Blocker of Skeletal Muscle NaV1.4 Channels
MW :
2640 Da
Synonyms :
Myotoxin II, Geographutoxin II, GTx-II
Modifications :
Disulfide bonds between: Cys3-Cys15, Cys4-Cys20, and Cys10-Cys21 X = 4-Hydroxyproline Ala22 - C-terminal amidation
Molecular formula :
C101H175N39O30S7
Effective Concentration :
100 - 600 nM
Activity :
μ-Conotoxin GIIIB binds and blocks site 1 of voltage-gated Na+ channels1.
Storage of solutions :
The reconstituted solution can be stored at 4°C for up to 1 week. For longer periods (up to 6 months), small aliquots should be stored at -20°C. We do not recommend storing the product in working solutions for longer than a few days. Avoid multiple freeze-thaw cycles.
Lead Time :
1-2 Business Days
Country of origin :
Israel/IL
Purity :
≥99% (HPLC)
CAS No :
140678-12-2
Form :
Lyophilized
Comment :
Contact Alomone Labs for technical support and product customization
Sequence :
RDCCTXXRKCKDRRCKXMKCCA-NH2
Is Toxin :
Yes
UNSPSC :
12352202
Bioassay Tested :
yes
Steril endotoxin free :
no
Cited Application :
Electrophysiology
more info or order :
company information
Alomone Labs
Jerusalem BioPark (JBP), Hadassah Ein Kerem
P.O. Box 4287
Jerusalem 9104201
info@alomone.com
http://www.alomone.com
972 2 531 8002
headquarters: Israel