46 results about "C-jun" patented technology

This invention relates to compounds, compositions, and methods useful for modulating mitogen activated protein kinase (MAP kinase) gene expression using short interfering nucleic acid (siNA) molecules. This invention also relates to compounds, compositions, and methods useful for modulating the expression and activity of other genes involved in pathways of MAP kinase gene expression and / or activity by RNA interference (RNAi) using small nucleic acid molecules. In particular, the instant invention features small nucleic acid molecules, such as short interfering nucleic acid (siNA), short interfering RNA (siRNA), double-stranded RNA (dsRNA), micro-RNA (miRNA), and short hairpin RNA (shRNA) molecules and methods used to modulate the expression of MAP kinase genes, such as Jun amino-terminal kinase (e.g., JNK-1, JNK-2), p38 (MAPK 14), ERK (e.g., ERK-1, ERK-2) and / or c-Jun.

Methods of diagnosing and prognosticating the development of human cancers, such as breast cancer, colon cancer, and pancreatic cancer, are provided. The diagnostic and prognostic methods include the detection and / or quantifying of the amount of expression of JAB1 in human cells, particularly in relation to the amount of p27 or c-Jun. In addition, methods for reducing the expression of JAB1 protein in cells and inhibiting its interaction with p27 or c-Jun, for example, are provided.

Methods for producing nucleic acid fragment libraries that express highly diverse peptide domains, wherein the nucleic acid fragments are derived form microorganisms or eukaryotes with compact genomes. Also peptides derived form the libraries wherein the peptides are selected on the basis of their abilities to bind selected target proteins, including c-jun and antibodies raised against dust mite allergens.

Compositions and methods for the treatment and diagnosis of diseases or disorders amenable to treatment through modulation of Activating Protein 1 (AP-1) expression are provided. In accordance with various embodiments of the present invention, oligonucleotides are provided which are specifically hybridizable with c-fos or c-jun, the genes encoding c-Fos or c-Jun, respectively. In a preferred embodiment, a method of modulating the metastasis of malignant tumors via modulation of one or more of the AP-1 subunits is provided; this method can be effected using the oligonucleotides of the invention or any other agent which modulates AP-1 or AP-1-mediated transcription.

Compositions and methods are provided for ameliorating various effects of UVA and UVB radiation, especially from the sun. The compositions include an ingredient that prevents photoaging from MED and subMED radiation, namely an MMP (matrix metalloproteinase) inhibitor, especially formulated for oral administration, and more especially formulated for controlled-release so as to provide the MMP inhibitor when MMP induction (including upstream signalling molecules like c-JUN, and / or MMPs like stromelysin) is most prevalent.

The present invention provides a method for the screening of nucleic acid fragment expression libraries and selecting encoded peptides based upon their ability to modulate the activity of a target protein or nucleic acid and assume conserved conformations compatible with albeit not reiterative of the target protein or nucleic acid. The present invention also provides methods for the diagnosis and treatment of ischemia. The present invention also provides c-Jun dimerization inhibitory peptides and analogues thereof that are useful for treatment of ischemia.

This invention is related to the use of at least one oligonucleotide with a length of from about 8 to about 30 nucleotide building blocks for manufacturing a pharmaceutical preparation for the prophylaxis and / or the treatment of diseases, that are modulated by TGF-beta2, TGF-beta1, TGF-beta3, VEGF, interleukin-10, c-jun, c-fos, and / or prostaglandin E2 in a mammal, wherein said oligonucleotide hybridizes with a messenger RNA of a TGF-beta2, TGF-beta1, TGF-beta3, VEGF, interleukin-10, c-jun, c-fos and / or prostaglandin E2 gene and wherein said preparation comprises said oligonucleotide in a concentration of about 1 microM to about 25 microM.

The present invention provides a method of preventing or reducing restenosis, neointima formation, graft failure, atherosclerosis, angiogenesis and / or solid tumour growth in a subject The method comprises administering to the subject a prophylactically effective dose of a nucleic acid which decreases the level of c-Jun mRNA, c-Jun mRNA translation or nuclear accumulation or activity of c-Jun. It is preferred that the nucleic acid is a DNAzyme that targets c-Jun mRNA.

The disclosure provides methods for inhibiting the activity of a miRNA cluster in a cell, and also for screening a cell for a phenotype(s) of interest resulting from inhibition of a miRNA cluster. The methods use a cluster pool which comprises at least one miRNA inhibitor specific for each miRNA in the miRNA cluster. MiRNA inhibitors are described that induce apoptosis in breast cancer cells and hence are useful in the treatment of breast cancer. The disclosure also provides pharmaceutical compositions which are useful for the treatment of breast cancer; methods for inducing the nuclear translocation of NF-κB in a breast cancer cell; methods for inducing the nuclear translocation of c-Jun in a breast cancer cell; method for inhibiting the nuclear translocation of NF-κB in a breast cancer cell; and methods for providing prognostic medical information relating to breast cancer progression.

The invention provides a method for preparing induced pluripotent stem cells and a composition used in the method. The method comprises the following step: introducing a composition of promoting induced pluripotent stem cells to form into a body cell, wherein the composition comprises (i) a c-Jun antagonist, and a group of factors selected from the following seven groups of factors (1) Sox2, Klf-4 and c-Myc, (2) Klf4 and c-Myc, (3) Oct3 / 4, Klf4 and c-Myc, (4) Sox2, Nanog and Lin28, (5) Oct3 / 4, Nanog and Lin28, (6) Oct3 / 4, Klf and Sox2 and (7) Klf4 and Sox2; or (ii) a c-Jun antagonist, Jhdm1b and Id1, and at least one of Glis1, Sall4 or Lrh1; or (iii) a c-Jun antagonist, Jhdm1b and Id1, and at least one of Oct4, Klf4, Sox2, Lin28, Esrrb, Lef1, Utf1 or miRNA C. Through the method disclosed by the invention, the induced pluripotent stem cells can be successfully prepared; the obtained induced pluripotent stem cells are good in quality; and no abnormal chromosome is generated.

The invention relates to the technical field of biomedical engineering. Liver transplantation is the only effective means that can be employed for treating liver diseases in late stage at present and is greatly limited in clinic use due to lack of liver sources. Hepatic stem cells have a self-updating capacity and a bidirectional differentiation capacity of differentiating into hepatocytes and cholangiocytes and therefore can provide an infinite number of donor cells for hepatocyte transplantation treatment in theory. The method for the transdifferentiation of fibroblasts into hepatic stem cells, which is provided by the invention, is to reprogram fibroblasts into hepatic stem cells which have the unique self-updating and bidirectional differentiation capacities of hepatic stem cells by using three transcription factors, namely c-Jun, Foxa2 and Hnf1beta. The inducible hepatic stem cells prepared by the method can be used as ideal cell sources for cell treatment of acute hepatic failure and liver diseases in medium and late stages, can be used as seed cells for medicine screening and tissue engineering livers and can provide an ideal research platform for researching cell biological characteristics of hepatic stem cells, liver development and the like.

Comprehensive analysis of transcription control factor complexes in a mouse brain cDNA library with c-Jun as a bait by using the cotranslation selection and screening of in vitro virus (IVV) and the C-terminal labeling method are conducted, thereby to provide known and unknown proteins which are unknown to form a complex with the c-Jun protein, whereby proteins that interact with c-Jun, nucleic acids encoding them and inhibitors utilizing them as well as methods for detecting an interaction and screening methods are provided.

The invention belongs to the field of biotechnology, and in particular relates to a method for regulating expression, quantity and activity of a heat shock protein 70 and application thereof. The method provided by the invention can also regulate tumor tissue, activity of a transcription factor NF-kB, expression and activity of a death receptor DR4 and DR5, phosphorylation and activity of JNK and c-Jun, expression and activity of a p53 protein, expression and proapoptotic activity of proapoptotic molecules Bax, Bid, t-Bid, capsase 3, capsase 8 and capsase 9, and expression and activity of c-FLIP and Bcl-2, and promote apoptosis of tumor tissues and cells. The invention also relates to application of the above method to preparation of drugs cooperatively applied with cell apoptosis induced drug.

Exposure of human skin to ultraviolet (UV) radiation from the sun not only induces the production of enzymes (matrix metalloproteinases) that degrade collagen, but also inhibits the synthesis of new collagen by inhibiting the synthesis of procollagen. This UV-induced inhibition of the synthesis of collagen can be prevented by the topical application of a retinoid or c-JUN inhibitor to the skin prior to exposure to UV radiation.

The invention relates to the stem cell research in the biological technology field, in particular to a method of inducing pluripotent stem cells throuhg the c-Jun N terminal deletion and applications. The technical scheme aims to provide an application of combined utilization of the c-Jun N terminal deletion and pluripotent stem cell inducing factors in a luripotent stem cell inducing process, and the c-Jun N terminal deletion is a series of clipped amino acid sequences or corresponding nucleotide sequences of amino acids from 170 bits to 334 bits of the c-Jun N protein of AP-1 family protein. According to the method and applications, during the process of pluripotent stem cell inducing, N terminal cut truncated type of the c-Jun N protein of the AP-1 family protein is used, an efficient reprogramming induction system is provided, micro molecules or genes of core reprogramming factors are replaced, and a promoting role of revealing core reprogramming factors in the reprogramming is played.

A mouse that is deficient for c-Jun and JunB in the epidermis or in which deletion of c-Jun and JunB can be specifically induced in the epidermis, and methods for obtaining such mice. The mice and keratinocytes derived therefrom are useful as an animal model for psoriasis and psoriatic arthritis.

The present invention relates to a genetically modified pig as a model for studying psoriasis. The modified pig model displays one or more phenotypes associated with psoriasis. Disclosed is also a modified pig comprising a mutation in the endogenous ILK-I Ra, JunB / cJun, CD18, IKK2, and / or LIG1 gene, and / or a human, porcine and / or murine PPARs, PPAR-δ, lκB-α, STAT3c, Integrin beta 1, Integrin alpha 2, MEK1, Amphiregulin, BMP-6, VEGF, JunBΔec-JunΔep, IL-I a, TGF.beta 1, CD18 hypo, Cre / lkk2FL / FL, Dsg1, SCCE, TGF-a, TNF-a, IL-20, IFN-g, LIG1 KO, KGF, IL-6, PAFR1 Cre / lkk2FL / FL, IL1 R, Dsg3, IFN-gamma, p40, ILI Ra, IKK2, JunB / c-Jun, and / or LIG1 gene, transcriptional and / or translational product or part thereof. The invention further relates to methods for producing the modified pig; and methods for evaluating the effect of a therapeutical treatment of psoriasis, for screening the efficacy of a pharmaceutical composition, and a method for treatment of human being suffering from psoriasis are disclosed.

The present invention provides a method for treating or inhibiting rheumatoid arthritis in a subject, the method comprising administering to the subject a therapeutically effective amount of a nucleic acid which decreases the level of c-Jun mRNA, c-Jun mRNA translation or nuclear accumulation or activity of c-Jun protein.

The invention discloses application of kaempferol to drugs for treating osteoarthritis. Kaempferol decreases expression of anti-galectin-1 in sensory neurone by inhibiting NF-kappa B and MAPK signal pathway activated in the inflammatory environment, reducing expression of c-Fos, c-Jun and delta FosB in sensory neurone and inhibiting combination activity of transcription factor activator protein-1(AP-1) and DNA, expression of anti-galectin-1 in nerve cell is reduced, and accordingly development of osteoarthritis is relieved. The invention provides a new drug for clinic treatment of osteoarthritis, and meanwhile states the mechanism of the novel treatment drug. New thought and experiences are provided for better understanding the pathological process of osteoarthritis and developing the drugs for treating osteoarthritis in the future.

The disclosure provides methods for inhibiting the activity of a miRNA cluster in a cell, and also for screening a cell for a phenotype(s) of interest resulting from inhibition of a miRNA cluster. The methods use a cluster pool which comprises at least one miRNA inhibitor specific for each miRNA in the miRNA cluster. MiRNA inhibitors are described that induce apoptosis in breast cancer cells and hence are useful in the treatment of breast cancer. The disclosure also provides pharmaceutical compositions which are useful for the treatment of breast cancer; methods for inducing the nuclear translocation of NF-κB in a breast cancer cell; methods for inducing the nuclear translocation of c-Jun in a breast cancer cell; method for inhibiting the nuclear translocation of NF-κB in a breast cancer cell; and methods for providing prognostic medical information relating to breast cancer progression.

An isolated polypeptide (JNK) characterized by having a molecular weight of 46 kD as determined by reducing SDS-PAGE, having serine and threonine kinase activity, phosphorylating the c-Jun N-terminal activation domain and polynucleotide sequences and method of detection of JNK are provided herein. JNK phosphorylates c-Jun N-terminal activation domain which affects gene expression from AP-1 sites.

The invention discloses application of a RhoGDI inhibitor to the preparation of drugs for treating nasopharynx cancer. The invention further discloses application of a RhoGDI inhibitor to the preparation of nasopharynx cancer radiotherapy sensitizer. The invention further discloses a drug for treating nasopharynx cancer, which adopts a preparation prepared from the RhoGDI inhibitor taken as an active component and pharmaceutically acceptable auxiliary materials. The RhoGDI inhibitor achieves the effects of tumor growth resistance, tumor metastasis resistance and radiotherapy sensitivity through specific inhibition of RhoGDI expression and activation of a JNK-1 pathway at the downstream (namely the activation of the expression of downstream p-JNK-1, c-Jun, inhibition the expression of p-AKT, enhancement the conversion of pro-caspase-3 to cleaved-caspase-3), and has a good clinical application prospect.

An isolated polypeptide (JNK) characterized by having a molecular weight of 46 kD as determined by reducing SDS-PAGE, having serine and threonine kinase activity, phosphorylating the c-Jun N-terminal activation domain and polynucleotide sequences and method of detection of JNK are provided herein. JNK phosphorylates c-Jun N-terminal activation domain which affects gene expression from AP-1 sites.

This invention is related to the use of at least one oligonucleotide with a length of from about 8 to about 30 nucleotide building blocks for manufacturing a pharmaceutical preparation for the prophylaxis and / or the treatment of diseases, that are modulated by TGF-beta2, TGF-beta1, TGF-beta3, VEGF, interleukin-10, c-jun, c-fos, and / or prostaglandin E2 in a mammal, wherein said oligonucleotide hybridizes with a messenger RNA of a TGF-beta2, TGF-beta1, TGF-beta3, VEGF, interleukin-10, c-jun, c-fos and / or prostaglandin E2 gene and wherein said preparation comprises said oligonucleotide in a concentration of about 1 microM to about 25 microM.

Exposure of human skin to ultraviolet (UV) radiation from the sun not only induces the production of enzymes (matrix metalloproteinases) that degrade collagen, but also inhibits the synthesis of new collagen by inhibiting the synthesis of procollagen. This UV-induced inhibition of the synthesis of collagen can be prevented by the topical application of a retinoid or c-JUN inhibitor to the skin prior to its exposure to UV radiation.

A mouse that is deficient for c-Jun and JunB in the epidermis or in which deletion of c-Jun and JunB can be specifically induced in the epidermis, and methods for obtaining such mice. The mice and keratinocytes derived therefrom are useful as an animal model for psoriasis and psoriatic arthritis.

The invention belongs to the technical field of cancer treatment and prevention, and particularly relates to application of quercetin-3-methylether in chemoprophylaxis of esophagus cancer. The quercetin-3-methylether is used for chemoprophylaxis of a canceration process of esophagus cancer. The overall design idea of the invention is as follows: during an esophageal canceration process of a rat induced with NMBA, through influencing the incidence rate and diversity of precancerous lesion and judging the expression situation of KI67,c-Jun indexes by use of an immunohistochemical method, the chemoprophylaxis effect of the quercetin-3-methylether on esophagus cancer is judged. According to the application, through constructing an esophageal canceration model process of the white rat induced with NMBA, the effect of quercetin-3-methylether on esophagus cancer is specifically evaluated. Results indicate that when quercetin-3-methylether with proper concentration has a favorable effect of preventing the canceration process of esophagus cancer and providing a new concept and reference possibility for chemoprophylaxis of esophagus cancer.

The present invention is related to a recombinant adeno associated viral construct comprising at least: a first terminal repeat of an Adeno Associated Virus a strong heterologous promoter an heterologous DNA corresponding to the gene encoding for the c-jun mutant protein TAM67, said gene being under the control of said promoter a polyadenylation signal, and a second terminal repeat of an Adeno Associated Virus