PTPσ Inhibitor, ISP
Based on 1 publication(s) in Google Scholar
PTPσ Inhibitor, ISP is a PTPσ intracellular wedge domain mimetic peptide containing a TAT cell-penetrating domain, which acts as a PTPσ inhibitor. PTPσ Inhibitor, ISP binds to and inhibits PTPσ, thereby relieving CSPG-mediated axonal growth inhibition. PTPσ Inhibitor, ISP enhances CSPG degradation by promoting the secretion of Cathepsin B or MMP-2, and promotes DRG axonal growth, OPC migration and remyelination. PTPσ Inhibitor, ISP promotes nerve regeneration and improves sensory, motor and urinary functions in animal models of spinal cord injury, dorsal root injury and multiple sclerosis. PTPσ Inhibitor, ISP also increases the phosphorylation of ERK and AKT in colorectal cancer cells. PTPσ Inhibitor, ISP can be used in studies related to PTPσ/CSPG signaling, nerve regeneration, demyelinating diseases and RAS/ERK signaling.
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- Pureté: 97.31%
- Formule: C177H306N66O54S3
- Masse moléculaire:4318.93
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Stockage:
Sealed storage, away from moisture.
Powder -80°C, 2 years , -20°C, 1 year* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
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Activité biologique
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Chemical Information
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Solvant et solubilité
- Pureté et documentation
- Références
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Help & FAQs
Publications Citing Use of MedChemExpress (MCE) PTPσ Inhibitor, ISP
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Activité biologique
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PTPσ |
The PTPσ inhibitor ISP (2.5 μM) induces oligodendrocyte precursor cells (OPCs) to secrete factors that degrade chondroitin sulfate proteoglycans (CSPG), and specifically reduces aggrecan levels under in vitro conditions without affecting laminin[2].
The PTPσ inhibitor ISP (2.5 μM) significantly increases the MMP-2 secretion level and gelatinolytic activity of oligodendrocyte precursor cells (OPCs) cultured in vitro[2].
Degradation of chondroitin sulfate proteoglycan (CSPG) by oligodendrocyte precursor cells (OPCs) induced by the PTPσ inhibitor ISP (2.5 μM) in vitro relies on exocytosis and is mainly mediated by MMP-2 activity[2].
The PTPσ inhibitor ISP (2.5 μM) significantly increases the total protease activity in the conditioned medium of oligodendrocyte precursor cells (OPCs) in vitro[2].
Migration of O4+ oligodendrocyte precursor cells (OPCs) induced by the PTPσ inhibitor ISP (2.5 μM) across the chondroitin sulfate proteoglycan (CSPG) barrier in vitro depends on the activity of MMP-2[2].
Protein Tyrosine Phosphatase σ Inhibitor, ISP (2.5 μM; 8-14 days) accelerates remyelination in cerebellar slices from LPC-induced demyelinated mice in vitro, and this effect depends on the activity of matrix metalloproteinase-2[2].
ISP, a PTPσ inhibitor (2.5 μM), reverses CSPG-induced defects in oligodendrocyte precursor cell (OPC) process outgrowth and maturation in vitro[2].
PTPσ Inhibitor, ISP (2.5 μM; 72-96 h) reverses the inhibitory effect of aggrecan on neurite outgrowth of adult rat DRG neurons[4].
PTPσ Inhibitor, ISP (2.5 μM; 1-4 days) enhances protease activity in cultured DRG systems of adult rats, and increases Cathepsin B secretion in a time-dependent manner[6].
Conditioned medium from DRG treated with the PTPσ inhibitor ISP (2.5 μM) degrades GAG-CSPG and promotes axon crossing of the aggrecan gradient, while CSTB attenuates these effects[6].
PTPσ inhibitor ISP (250 pM-10 μM; 5 days) dose-dependently promotes axons of adult rat DRG to cross the aggrecan/laminin CSPG gradient, and 2.5 μM ISP enables the reformation and continuous migration of collapsed growth cones[1].
PTPσ Inhibitor, ISP (2.5 μM; 2 days, 2 h) increases the survival rate of oligodendrocyte precursor cells (OPCs) cultured on inhibitory chondroitin sulfate proteoglycan (CSPG) substrates and protects them from lysophosphatidylcholine (LPC)-induced death under in vitro conditions[2].
PTPσ Inhibitor, ISP (10 μM; 24 h) activates ERK and AKT in HCT116, SW620 and KM12L4A colorectal cancer cell lines, which is verified by the increased phosphorylation levels of these proteins[3].
The PTPσ inhibitor ISP (10 μM) reverses the PTPRS-mediated reduction in ERK nuclear localization and restores ERK nuclear accumulation in PTPRS-knockout colorectal cancer cells HCT116 and KM12L4A[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:SH-SY5Y neuronal cells
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Concentration:2.5 μM
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Incubation Time:30 min (pre-incubation); 4 days (post-plating incubation)
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Result:Restored phosphorylated Erk1/2 (pErk1/2) to total Erk1/2 (tErk1/2) ratios comparable to those in cells grown on laminin-only substrates, reversing the decrease caused by CSPG exposure.
PTPσ Inhibitor, ISP (11 μg/day; subcutaneous injection; once daily starting at 24 h post-injury for 4 consecutive weeks) promotes NF200+, CGRP+ and IB4+ sensory axons to cross the DREZ in rats with C5-T1 dorsal root crush injury, and restores mechanical and thermal sensation[4].
PTPσ Inhibitor, ISP (44 μg/day, i.p., or 500 μg/day, s.c.; once daily for 7 consecutive weeks) improves motor, sensory and bladder functions in rats with severe thoracic spinal cord compression injury, and increases 5-HT-positive nerve fibers in the preserved tissue bridge at the injury site[5].
PTPσ Inhibitor, ISP (22 μg/mL; subcutaneous injection; once daily starting at 24 h post-injury for 49 consecutive days) increases Cathepsin B expression in sprouting 5-HTergic axons within the injured spinal cord, and this correlates with reduced CSPG staining[6].
ISP, a PTPσ inhibitor (22 μg/mL; subcutaneous injection; once daily for 14 consecutive days), increases activated Cathepsin B in the spinal cord tissue of rats with T8 spinal cord contusion[6].
PTPσ Inhibitor, ISP (20 μg/mouse; i.p.; once daily for 41 consecutive days) improves clinical scores in MOG35-55-induced EAE mice, reduces demyelinating lesions, and increases MBP expression and remyelinated axons, with a stronger effect when administered at the disease onset phase than at the disease peak phase[2].
PTPσ Inhibitor, ISP (20 μg/day; subcutaneous injection; once daily starting at 24 h post-LPC injection) reduces CSPG accumulation and promotes remyelination in a focal spinal cord demyelination model[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Sprague-Dawley (adult female, 230-250 g, contusive SCI induced via 250 kdyn impact to the T8 spinal cord segment)[1]
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Dosage:11 μg/day
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Administration:s.c.; once daily for 7 weeks; started 24 h after injury
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Result:Improved locomotor and urinary function and increased serotonergic innervation below the lesion.
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Animal Model:C57BL6/J (young adult, chronic progressive experimental autoimmune encephalomyelitis induced via MOG35-55 immunization)[2]
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Dosage:20 μg/mouse
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Administration:i.p.; daily; 41 days
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Result:Improved clinical scores, reduced demyelinated lesions and increased MBP expression and remyelination.
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Animal Model:C57BL6/J (young adult, acute focal demyelination induced via lysolecithin (LPC) injection into the dorsal column white matter)[2]
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Dosage:20 μg/mouse
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Administration:s.c.; once daily; started 24 h after LPC injection
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Result:Reduced CSPG accumulation and promoted remyelination.
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Animal Model:Sprague Dawley (adult female, 200-250g, spinal cord dorsal root injury model)[4]
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Dosage:11 µg per day
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Administration:s.c.; once daily for 4 weeks; started 24 h after injury
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Result:Promoted sensory axon regeneration across the DREZ and restored mechanical and thermal sensation.
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Animal Model:HsdCpb:WU (adult female, 175-200 g, spinal cord compression injury model)[5]
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Dosage:44 μg/day; 500 μg/day
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Administration:s.c.; once daily for 7 weeks
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Result:Improved locomotor, sensory and bladder recovery and increased preserved serotonergic fibers.
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Animal Model:Sprague Dawley (female, 225-250 g, thoracic T8 contusive injury induced with 250k dyne force using an Infinite Horizon Impact Device)[6]
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Dosage:22 µg/mL (49-day cohort)
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Administration:s.c.; daily; 49 days (first cohort)
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Result:Increased Cathepsin B in sprouting serotonergic axons and was associated with reduced CSPG staining.
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Animal Model:Sprague Dawley (female, 225-250 g, thoracic T8 contusive injury induced with 250k dyne force using an Infinite Horizon Impact Device)[6]
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Dosage:22 µg/mL (14-day cohort)
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Administration:s.c.; daily; 14 days (second cohort)
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Result:Increased active Cathepsin B in injured spinal cord tissue.
Chemical Information
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Appearance Solid
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Masse moléculaire 4318.93
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Formule C177H306N66O54S3
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Color White to off-white
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Sequence
Gly-Arg-Lys-Lys-Arg-Arg-Gln-Arg-Arg-Arg-Cys-Asp-Met-Ala-Glu-His-Met-Glu-Arg-Leu-Lys-Ala-Asn-Asp-Ser-Leu-Lys-Leu-Ser-Gln-Glu-Tyr-Glu-Ser-Ile-NH2
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Sequence Shortening
GRKKRRQRRRCDMAEHMERLKANDSLKLSQEYESI-NH2
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Sealed storage, away from moisture
Powder -80°C 2 years -20°C 1 year * In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Publications (1)
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Journal Impact Factor
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Most Recent
Solvant et solubilité
H2O : 50 mg/mL (11.58 mM; Need ultrasonic)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Pureté et documentation
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Fiche technique (300 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Instruction de manipulation (2659 KB)
Références
[1]. Lang BT, et al. Modulation of the proteoglycan receptor PTPσ promotes recovery after spinal cord injury. Nature. 2015 Feb 19;518(7539):404-8. [Content Brief]
[2]. Luo F, et al. Modulation of proteoglycan receptor PTPσ enhances MMP-2 activity to promote recovery from multiple sclerosis. Nature communications. 2018 Oct 08;9(1):4126. [Content Brief]
[3]. Davis TB, et al. PTPRS Regulates Colorectal Cancer RAS Pathway Activity by Inactivating Erk and Preventing Its Nuclear Translocation. Scientific reports. 2018 Jun 18;8(1):9296. [Content Brief]
[4]. Yao M et al. Targeting proteoglycan receptor PTPσ restores sensory function after spinal cord dorsal root injury by activation of Erks/CREB signaling pathway. Neuropharmacology. 2019 Jan;144:208-218. [Content Brief]
[5]. Rink S, et al. Recovery after spinal cord injury by modulation of the proteoglycan receptor PTPσ. Experimental neurology. 2018 Nov;309:148-159. [Content Brief]
[6]. Tran AP, et al. Modulation of Receptor Protein Tyrosine Phosphatase Sigma Increases Chondroitin Sulfate Proteoglycan Degradation through Cathepsin B Secretion to Enhance Axon Outgrowth. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2018 Jun 06;38(23):5399-5414. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| H2O | 1 mM | 0.2315 mL | 1.1577 mL | 2.3154 mL | 5.7885 mL |
| 5 mM | 0.0463 mL | 0.2315 mL | 0.4631 mL | 1.1577 mL | |
| 10 mM | 0.0232 mL | 0.1158 mL | 0.2315 mL | 0.5788 mL |
* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.
PTPσ Inhibitor, ISP Related Classifications
HY-P5982 Related Classifications
Powered by Bioz
- PTPσ Inhibitor, ISP
- Phosphatase
- Transmembrane Glycoprotein
- MMP
- ERK
- Akt
- Cathepsin
- AKT
- spinal cord injury
- chondroitin sulfate proteoglycan
- dorsal root ganglion neurons
- Erk/CREB signaling
- colorectal cancer
- multiple sclerosis
- Protein tyrosine phosphatase sigma
- oligodendrocyte progenitor cell
- Erk1/2
- Inhibitor
- inhibitor
- inhibit