32 results about "C-Jun N-terminal kinases" patented technology

The present invention relates to compounds that are inhibitors of c-jun N-terminal kinase 1, 2, or 3 (JNK1, JNK2, or JNK3), compositions containing the compounds and the use of the compounds in the prevention or treatment of disorders regulated by the activation of JNK1, JNK2 and JNK3.

The invention relates to novel polynucleotides and their encoded gene products that are expressed in skin cells, particularly keratinocytes, and methods of using the same. Specifically, the present invention provides polynucleotides encoding several novel protein kinases that are c-Jun N-terminal kinase kinase kinases, i.e., MLK4, PAK4, PAK5 and YSK2. In addition, the invention provides methods of using the disclosed polynucleotides and their gene products in drug discovery, particularly in screening for drugs that can reduce ultraviolet light-induced damage of the skin, inflammation and psoriasis, and drugs that can enhance wound healing.

Methods of reducing Wallerian degeneration are disclosed. These methods comprise inhibiting expression or activity of a mixed lineage kinase such as a dual leucine-zipper-bearing kinase (DLK), inhibiting expression or activity of a molecule acting downstream from DLK, such as a c-Jun N-terminal kinase (JNK), or a combination thereof. Further disclosed are methods of screening candidate compounds for DLK inhibition activity. These methods comprise providing a neuronal culture comprising a plurality of axons; contacting the culture with a candidate compound and with an axon degeneration-triggering agent; and comparing axonal degeneration in the culture to a control culture comprising the axon degeneration-triggering agent but not the candidate compound.

The intravitreal administration of a JNK-inhibiting peptide which comprises (a) at least either one of the JNK-inhibiting sequences depicted in SEQ ID NO:1 and SEQ ID NO:2 and (b) at least either one of the transfer sequences depicted in SEQ ID NO:3 and SEQ ID NO:4 and has a length shorter than 150 amino acid residues wherein at least one amino acid residue is a D-amino acid residue can prevent the occurrence of spermidine-induced damage of retinal pigment epitheliums, tunicamycin-induced visual cell injury, and laser-induced choroidal neovascularization. Therefore, the JNK-inhibiting peptide is useful for the prevention or treatment of retinal diseases. By using the JNK-inhibiting peptide, it becomes possible to provide a medicinal agent and a method both of which can prevent or treat retinal diseases through topical administration in eyes. It also becomes possible to provide use of the JNK-inhibiting peptide for the production of the medicinal agent.

The present invention relates to sulfonamide derivatives of formula (I) notably for use as pharmaceutically active compounds, as well as to pharmaceutical formulations containing such sulfonamide derivatives. Said sulfonamide derivatives are useful in the treatment of neuronal disorders, autoimmune diseases, cancer and cardiovascular diseases. Furthermore, said sulfonamide derivatives are efficient modulators of the JNK pathway, they are in particular efficient and selective inhibitors of JNK2 and -3. The present invention is furthermore related to novel sulfonamide derivatives as well as to methods of their preparation. Formula (I) IAr1 is a substituted or unsubstituted aryl or heteroaryl group; X is O or S, preferably O; Ar2 a substituted or unsubstituted arylene or heteroarylene group; R1 and R2 are independently selected from the group consisting of hydrogen and a C1-C6-alkyl group.

The invention relates to the technical field of biology, in particular to a human JNK1 (c-Jun N-terminal kinase) gene targeting small interfering RNA (ribonucleic acid) and application thereof. The small interfering RNA comprises a sense strand and an anti-sense strand, a nucleotide sequence of the sense strand is as shown in SEQ ID NO:2, and a nucleotide sequence of the anti-sense strand is as shown in SEQ ID NO:3. The sequences of the small interfering RNA are not publically reported yet, interference after transcription of the JNK1 gene can be realized to reduce expression of p-JNK in inflamed dental pulp stem cells, apoptosis of the dental pulp stem cells can be specifically reduced, odontoblast differentiation of the dental pulp stem cells is promoted, and a novel treatment scheme is provided for pulpitis.

The present invention is based at least in part on the discovery of a role for the JNK signaling pathway in longevity. In particular, the present inventors have shown that modulation of the c-jun N-terminal kinase (JNK) signaling pathway in an organism, optionally in combination with modulation of the insulin receptor (IR) signaling pathway, can enhance longevity in an organism. Accordingly, the present invention features methods of identifying modulators of longevity in assays featuring organisms and / or cells having either a functional or deregulated JNK signaling pathway and, optionally, a functional or deregulated IR signaling pathway. Also featured is an in vitro method of identifying an agent capable of enhancing longevity featuring an assay composition having a JNK signaling pathway molecule and insulin signaling pathway molecule. Further featured are therapeutic methods for the use of JNK signaling pathway modulators to enhance longevity.

The present invention is based at least in part on the discovery of a role for the JNK signaling pathway in longevity. In particular, the present inventors have shown that overexpression of c-jun N-terminal kinase 1 (jnk-1) extends lifespan and that said extended lifespan is associated with DAF-16 phosphorylation by JNK-1 and the consequent DAF-16 localization to the nucleus. Accordingly, the present invention features methods of identifying modulators of longevity in assays featuring organisms and / or cells having a JNK signaling pathway and, optionally, an IR signaling pathway. Also featured is an in vitro method of identifying an agent capable of enhancing longevity featuring an assay composition having a JNK signaling pathway molecule and insulin signaling pathway molecule. Further featured are therapeutic methods for the use of JNK signaling pathway modulators to enhance longevity, to prevent or reduce obesity and to prevent or treat type II diabetes.

The present invention relates to a system and device for preventing stenosis and / or restenosis after an invasive procedure in a body vessel or cavity having an inner wall surface, the system comprising inserting a device coated with a growth arresting, lipid-derived, bioactive substance at a desired location along the inner wall surface of the body vessel or cavity. The present invention provides for the use of c-Jun aminoterminal kinase inhibitor (''JNK Inhibitor'') and certain analogs as restenosis inhibitors, incorporated into a stent.