JNK
JNKs are a part of the superfamily of mitogen-activated protein kinases that heavily influence both cell proliferation and apoptosis, where the activation of JNKs can result in either proliferation or apoptosis, depending on the type of stimuli and/or cell type. One route through which JNKs influence extrinsic apoptosis initiation is through TNF interactions. Specifically, JNKs have been shown to be activated by TNFα, and JNKs can also contribute to TNF-induced apoptosis. JNK is also involved in intrinsic apoptosis initiation, where for instance, JNKs have been shown to induce the transcription of proapoptotic genes through direct transcriptional activity or through specific transcription factors, such as c-Jun. Additionally, JNK can mediate the expression of Bcl-2 family members. The JNK pathway therefore plays a large role in the regulation of both extrinsic and intrinsic apoptosis initiation pathways.
MAPK/ERK Signaling
JNK
-
c-JUN peptide
catalog no : M30827
cas no: 610273-01-3
Peptide comprising residues 33 - 57 of the JNK binding (δ) domain of human c-Jun. Disrupts JNK/c-Jun interaction leading to inhibition of serum-induced c-Jun phosphorylation, up-regulation of p21cip/waf and modulation of inflammatory gene expression. Specifically induces apoptosis in HeLa tumor cells. -
[D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P
catalog no : M30808
cas no: 96736-12-8
Broad spectrum neuropeptide inverse agonist and antagonist. Potent full inverse agonist for the ghrelin receptor (EC50 = 5.2 nM); diminishes constitutive ghrelin receptor signaling. Also antagonist at tachykinin, bradykinin, CCK and bombesin receptors. Induces apoptosis and inhibits cancer cell growth in vitro. -
JIP-1 (153-163)
catalog no : M30659
cas no: 438567-88-5
Peptide inhibitor of c-Jun N-terminal kinase (JNK), based on residues 153-163 of JNK-interacting protein-1 (JIP-1). Binds to JNK with affinity in the micromolar range and minimally inhibits p38 and ERK. -
d-Epigalbacin
catalog no : M29497
cas no: 84709-25-1
d-Epigalbacin is a naturally occurring lignin. d-Epigalbacin is a potent, selective JNKs inhibitor, with IC50s of 1.7 μM, 2.9 μM and 1.74 μM for JNK1, JNK2 and JNK3, respectively. -
CC-90001
catalog no : M28833
cas no: 1403859-14-2
CC-90001 is an orally administered c-Jun N-terminal kinase (JNK) inhibitor with bias for JNK1 over JNK2.