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Jnk inhibitor
BML-EI354-0001 1 mg 434.00 USD
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Replaces Prod. #: ALX-159-600

This L-stereoisomer is a cell permeable JNK (c-Jun N-terminal kinase) inhibitor. For increased cell permeability the peptide was covalently linked to the 10 aa recognized by the TAT transporter. Neuroprotective agent for stroke. Inhibits the interaction between JNK (JNK-1, -2 and –3) and its substrate with the same IC50 (in vitro IC50 ~ 1µM), but is degraded more readily than the D-stereoisomer, thus requiring higher treatment concentrations in vitro and in vivo.

Product Details

Alternative Name:JNK inhibitor 1 (L-stereoisomer), c-Jun N-terminal kinase peptide inhibitor 1, L-stereoisomer
Purity:≥95% (HPLC)
Appearance:White to off-white solid.
Solubility:Soluble in water.
Shipping:Blue Ice
Long Term Storage:-20°C
Use/Stability:Stable for at least 2 years after receipt when stored at -20°C. Solutions can be stored at -20°C for up to 3 months.
Handling:Avoid freeze/thaw cycles.
Scientific Background:A protein inhibitor named IB1 has been described that competitively blocks the interaction between JNK and c-Jun, thereby inhibiting the signalling events downstream of JNK like c-Jun, ATF2 and ELK1 phosphorylation. To convert IB1 into cell-permeable inhibitors of JNK (JNKI peptides) the minimal 20 aa inhibitory sequence of IB1 was covalently linked to the 10 amino acids recognized by TAT transporter. The L-JNKI1 and the protease resistant D-JNKI1 peptides represent the only potent inhibitors that are specific for JNK (JNK1, JNK2 and JNK3). Different from chemical inhibitors that directly affect kinase activity e.g. by competing with the ATP-binding site of the protein kinase, JNKI1 rather inhibits the interaction between JNK and its substrate, resulting in a JNK K.O. phenotype. In contrast to pure diffusion the TAT-peptides are actively transported into cells, where they remain until their proteolytic degradation. They can be used for in vitro as well as for in vivo applications (IC50~1µM). D-JNKI1 is the only form found to be active on neuronal cells, probably due to a high level of proteolytic degradation of the L-stereoisomer (T. Borsello and C. Bonny; unpublished data).
Technical Info/Product Notes:As these peptides tend to be toxic in neurons above concentrations of 5µM, it is recommended to use concentrations of ~1µM or less. When interpreting results of c-Jun inhibition, one should also note that a number of other c-Jun kinases are thought to contribute to c-Jun phosphorylation (C. Bonny, personal communication).

For in vivo applications in mice it is suggested to start with 30-50µl of a 1mM stock solution administered intraperitoneally. Cellular uptake of L-JNKI1 peptides can now be confirmed using the FITC-conjugated L-TAT control peptide (Prod. No. ALX-168-009F).

Note: L-TAT control peptides should only be used with L-JNKI1.
Regulatory Status:RUO - Research Use Only

Product Literature References

Endothelial MAPKs Direct ICAM-1 Signaling to Divergent Inflammatory Functions: S. Dragoni, et al.; J. Immunol. 198, 4074 (2017), Abstract; Full Text
Unfolded protein response induced by Brefeldin A increases collagen type I levels in hepatic stellate cells through an IRE1α, p38 MAPK and Smad-dependent pathway: M.R. de Galarreta, et al.; Biochim. Biophys. Acta 1862, 2115 (2016), Application(s): Cell culture, Abstract;
Inhibition of c-Jun NH2-terminal kinase activity improves ischemia/reperfusion injury in rat lungs: M. Ishii, et al.; J. Immunol. 172, 2569 (2004), Abstract;
A peptide inhibitor of c-Jun N-terminal kinase protects against excitotoxicity and cerebral ischemia: T. Borsello, et al.; Nat. Med. 9, 1180 (2003), Abstract;
Activation of JNK in sensory neurons protects against sensory neuron cell death in diabetes and on exposure to glucose/oxidative stress in vitro: S.A. Price, et al.; Ann. N. Y. Acad. Sci. 1010, 95 (2003), Abstract;
Hyperosmolarity and CD95L trigger CD95/EGF receptor association and tyrosine phosphorylation of CD95 as prerequisites for CD95 membrane trafficking and DISC formation: R. Reinehr, et al.; FASEB J. 17, 731 (2003), Abstract;
Insulin-secreting beta-cell dysfunction induced by human lipoproteins: M.E. Roehrich, et al.; J. Biol. Chem. 278, 18368 (2003), Abstract; Full Text
Translation inhibitors sensitize prostate cancer cells to TRAIL-induced apoptosis by activating c-Jun N-terminal kinase: N.K. Sah, et al.; J. Biol. Chem. 278, 20593 (2003), Abstract; Full Text
Transduction of full-length TAT fusion proteins into mammalian cells: TAT-p27Kip1 induces cell migration: H. Nagahara, et al.; Nat. Med. 4, 1449 (1998), Abstract;

General Literature References

Use of cell-permeable peptides to prevent neuronal degeneration: T. Borsello & C. Bonny; Trends Mol. Med. 10, 239 (2004), Abstract;
Cell-permeable peptide inhibitors of JNK: novel blockers of beta-cell death: C. Bonny, et al.; Diabetes 50, 77 (2001), Abstract; Full Text
In vivo protein transduction: delivery of a biologically active protein into the mouse: S.R. Schwarze, et al.; Science 285, 1569 (1999), Abstract;
IB1, a JIP-1-related nuclear protein present in insulin-secreting cells: C. Bonny, et al.; J. Biol. Chem. 273, 1843 (1998), Abstract; Full Text
A cytoplasmic inhibitor of the JNK signal transduction pathway: M. Dickens, et al.; Science 277, 693 (1997), Abstract;

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L-TAT control peptide (FITC conjugate) 

Control peptide for L-JNKI
≥90% (HPLC) | Print as PDF
ALX-168-009F-R050 50 µl FITC 112.00 USD
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