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JNK/c-Jun

JNKs (c-Jun N-terminal kinases) are a group of mitogen-activated protein kinases (MAPKs), originally called stress activated protein kinases (SAPKs), because they are activated by various environmental stresses. They can also be activated by cytokines and growth factors.

Products
Background
Literature (1)
Pathways (1)
Gene Data

JNK/c-Jun Inhibitors
Cat. No. Product Name / Activity
3314 BI 78D3
Selective, competitive JNK inhibitor
1989 c-JUN peptide
Peptide inhibitor of JNK/c-Jun interaction
6258 CC 401 dihydrochloride
High affinity JNK inhibitor; also inhibits HCMV replication
4924 CEP 1347
Inhibitor of JNK signaling
1496 SP 600125
Selective JNK inhibitor
5044 SR 3576
Highly potent and selective JNK3 inhibitor
3607 SU 3327
Selective JNK inhibitor
2827 TCS JNK 5a
Selective inhibitor of JNK2 and JNK3
3222 TCS JNK 6o
Selective JNK inhibitor

JNK/c-Jun Activators
Cat. No. Product Name / Activity
1290 Anisomycin
JNK, SAPK and p38 activator

Other
Cat. No. Product Name / Activity
6558 CP 43
Inhibits TAOK activation of JNK

Related Targets

JNKs (c-Jun N-terminal kinases) are a group of mitogen-activated protein kinases (MAPKs), originally called stress activated protein kinases (SAPKs), because they are activated by a variety of environmental stresses. They are also activated in response to cytokines such as TNF-α and IL-1, and growth factors.

There are three isoforms of JNK; JNK1, JNK2 and JNK3. JNK1 and JNK2 are ubiquitously expressed, whilst JNK3 expression is limited to the brain, heart and testis. JNK phosphorylates a wide variety of substrates including c-Jun. c-Jun is a component of the AP-1 transcription factor complex and is involved in the control cell proliferation, transformation, survival and death. JNK also phosphorylates p53 and some non-nuclear proteins. JNK-mediated phosphorylation of target proteins is essential for the induction of gene expression of interleukins, VEGF, COX-2, MMP-9, heme oxygenase-1, ICAM-1, NCX1, GnRHR and others.

JNK is critical in processes as divergent as apoptosis, cell survival, proliferation and differentiation. The JNK pathway appears to be involved in inflammatory and autoimmune disorders including rheumatoid arthritis, irritable bowel disease, and atherosclerosis.

External sources of pharmacological information for JNK/c-Jun :

    Literature for JNK/c-Jun

    Tocris offers the following scientific literature for JNK/c-Jun to showcase our products. We invite you to request* your copy today!

    *Please note that Tocris will only send literature to established scientific business / institute addresses.

    MAPK Signaling Scientific Review

    MAPK Signaling Scientific Review

    MAP kinase signaling is integral to the regulation of numerous cellular processes such as proliferation and differentiation, and as a result is an important focus of cancer and immunology research. Updated for 2016, this review discusses the regulation of the MAPK pathway and properties of MAPK cascades. Compounds available from Tocris are listed.

    Pathways for JNK/c-Jun

    MAPK Signaling Pathway

    MAPK Signaling Pathway

    The mitogen-activated protein kinase pathway evokes an intracellular signaling cascade in response to extracellular stimuli such as heat and stress. It can influence cell division, metabolism and survival.

    JNK/c-Jun Gene Data

    Gene Species Gene Symbol Gene Accession No. Protein Accession No.
    JNK1 Human MAPK8 NM_139047 P45983
    Mouse Mapk8 NM_016700 Q91Y86
    Rat Mapk8 XM_341399 P49185
    JNK2 Human MAPK9 NM_139069 P45984
    Mouse Mapk9 NM_016961 Q9WTU6
    Rat Mapk9 NM_017322 P49186
    JNK3 Human MAPK10 NM_002753 P53779
    Mouse Mapk10 NM_009158 Q61831
    Rat Mapk10 NM_012806 P49187
    c-Jun Human JUN NM_002228 P05412
    Mouse Jun NM_010591 P05627
    Rat Jun NM_021835 P17325