39 results about "RHOA Protein" patented technology

The invention provides the construction for a farnesyl pyrophosphoric acid synthetase RNA (Ribonucleic Acid) interference recombinant lentivirus vector, which comprises the following steps of: sieving the most effective target sequence of an FDS (farnesyl diphosphate synthase) gene RNAi (RNA interference) in a tool cell 293T cell, synthesizing the double-stranded DNA of the most effective target sequence, connecting to a pGCSIL-GFP vector and successfully constructing the recombinant vector through enzyme cutting, sequencing and identification. Researches indicate that the constructed RNA interference vector LV-sh-FDS can downwards modulate the expression of an FDS mRNA (Messenger RNA) level in a neonatal rat cardiac myocyte, simultaneously can downwards modulate the expression of myocardial hypertrophy markers such as cell areas and marker genes beta-MHC (Myosin Heavy Chain) and BNP (Brain Natriuretic Peptide), additionally can effectively inhabit the activity of RhoA while downwards modulating the FDS, can be applied in preparing medicaments for treating myocardial hypertrophy diseases and also can be applied in preparing medicaments for cholesterol metabolic control.

The present invention relates to the use of short interfering nucleic acid molecules (siNA, such as siRNA) that modulate the expression of VEGF-C and/or RhoA involved in neovascular angiogenesis. In the present invention, inhibition of VEGF-C and/or RhoA gene expression results in decreased expression of VEGF-A, which is required for the initiation and persistence of angiogenesis. Furthermore, the present invention also relates to the inhibition of RhoA expression levels and VEGF-C expression levels to gain the benefit of downregulating two different targets required for angiogenesis. The present invention describes compounds, compositions and methods for the inhibition of neovascularization. In certain embodiments, the present invention relates to methods for inhibiting neovascularization, and compounds for treating ocular diseases such as age-related macular degeneration (AMD), diabetic retinopathy, glaucoma, and other neovascular diseases , such as VEGF-C siRNA and RhoAsiRNA.

Inhibitors of RhoA kinase production and/or activation are suited for relaxing the features and/or for decontracting the skin and thus are useful for preventing and/or combating the signs of aging of the skin, in particular wrinkles and notably expression wrinkles.

This invention provides a stent for implantation in a blood vessel or other tissue, wherein the stent is coated with or contains C3 exoenzyme, a chimeric version thereof or an inhibitor of RhoA. This invention also provides a method for treating or inhibiting the onset of restenosis in a subject which comprises implanting one of the instant stents in the subject's blood vessel.

The invention mainly relates to an N,N-double substituted benzoazacyclo-2-amide compound and an application thereof. The N,N-double substituted benzoazacyclo-2-amide compound is a compound shown as formula I or a salt formed by a medical acid or alkali. The compound provided by the invention has strong inhibition activity on RhoA protease which is tightly related with cardiovascular and cerebrovascular diseases. The compound provided by the invention is hopeful to be developed into a RhoA protease small-molecule inhibitor type cardiovascular and cerebrovascular disease treatment medicine.

Cells within liver tumour mass comprise a unique set of proteins/tumour antigens when compared to the normal liver tissues epithelial cells juxtaposed to the tumour. The presence of tumour antigens couples the production of auto-antibodies against these tumour antigens. The present invention relates to the identification and elucidation of a protein set that can act as a novel marker set for liver cancer diagnosis and prognosis. Specifically, it relates to a kit that enables diagnostic and prognostic measurement of auto-antibodies in serum of liver cancer patients. The present invention provides a non-invasive, specific, sensitive, and cost effective detection and quantification method by evaluating a set of validated liver cancer proteins/tumour antigens, which includes Bmi-1, VCC1, SUMO-4, RhoA, TXN, ET-1, UBE2C, HDGF2, FGF21, LECT2, SOD1, STMN4, Midkine, IL-17A or IL26, to complement the conventional diagnostic methods.

The present disclosure relates to methods, compositions, and kits for the inhibition of signaling by members of the Rho GTPase family. Specifically, the disclosure relates to methods, compositions and kits for the inhibition of RhoA and/or RhoC transcriptional signaling and action of the transcription co-factors MRTF-A and/or MRTF-B. The disclosure finds use in treatment of Rho-mediated disease states (e.g., tumor metastasis and fibrosis), Rho-mediated biological conditions, and in cell signaling research.

The present invention discloses a drug for treating glaucoma. According to the drug, a RNA interference sequence RhoA siRNA is adopted as an active ingredient, wherein a sense strand of the RhoA siRNA is 5'GAAGUCAAGCAUUUCUGUCdTdT3', an antisense strand is 3'dTdTCUUCAGUUCGUAAAGACAG5'. With the RhoA siRNA prepared according to a RNA interference target sequence 5'-GAAGTCAAGCATTTCTGTC-3' of the RhoA in the present invention, an expression level of RhoA mRNA can be effectively reduced, an expression level of RhoA protein in anterior chamber tissue can be efficiently down-regulated, stress fiber formation is affected so as to affect changes of cytoskeleton structures and distributions of actin of trabecular meshwork cells, such that trabecular meshwork cell channel configuration is changed, aqueous humor discharge resistance is changed, and intraocular pressure is affected so as to achieve a purpose of treatment of glaucoma.

Disclosed are compositions and methods for slowing, preventing, or reversing platelet damage, particularly as may occur during blood banking or during refrigeration of platelets. The composition may include one or more of a RAC inhibitor, a CDC42 inhibitor, a RHOA inhibitor, or a combination thereof. The compositions may further include a pharmaceutically acceptable carrier.

The present invention relates to the identification of the cytosolic phosphoprotein CRMP4b as a protein that physically and functionally interacts with RhoA to mediate neurite outgrowth inhibition. siRNA-mediated knockdown of CRMP4 promotes neurite outgrowth on myelin substrates indicating a critical role for CRMP4 in neurite outgrowth inhibition. Disruption of CRMP4b-RhoA binding with a competitive inhibitor attenuates neurite outgrowth inhibition on myelin and aggrecan substrates. Stimulation of neuronal growth cones with Nogo leads to co-localization of CRMP4b and RhoA at discrete regions within the actin-rich central and peripheral domains of the growth cone indicative of a potential function in cytoskeletal rearrangements during neurite outgrowth inhibition. Together these data indicate that a RhoA-CRMP4b complex forms in response to inhibitory challenges in the growth cone environment and regulate cytoskeletal dynamics at distinct sites necessary for axon outgrowth inhibition. Competitive inhibition of CRMP4b-RhoA binding suggests a novel, highly specific therapeutic avenue for promoting regeneration following CNS injury.

Cells are genetically modified to express a luminophore, e.g., a modified (F64L, S65T, Y66H) Green Fluorescent Protein (GFP, EGFP) coupled to a component of an intracellular signalling pathway such as a transcription factor, a cGMP- or cAMP-dependent protein kinase, a cyclin-, calmodulin- or phospholipid-dependent or mitogen-activated serine/threonin protein kinase, a tyrosine protein kinase, or a protein phosphatase (e.g. PKA, PKC, Erk, Smad, VASP, actin, p38, Jnk1, PKG, IkappaB, CDK2, Grk5, Zap70, p85, protein-tyrosine phosphatase 1C, Stat5, NFAT, NFkappaB, RhoA, PKB). An influence modulates the intracellular signalling pathway in such a way that the luminophore is being redistributed or translocated with the component in living cells in a manner experimentally determined to be correlated to the degree of the influence. Measurement of redistribution is performed by recording of light intensity, fluorescence lifetime, polarization, wavelength shift, resonance energy transfer, or other properties by an apparatus consisting of e.g. a fluorescence microscope and a CCD camera. Data stored as digital images are processed to numbers representing the degree of redistribution. The method can be used as a screening program for identifying a compound that modulates a component and is capable of treating a disease related to the function of the component.

The invention provides an evaluation gene group for prognosis prediction of gastric cancer and a corresponding kit. The evaluation gene group is obtained by screening genes comprised in a RhoA proteinactivity regulation pathway for regulating RhoA protein activity, wherein, the evaluation gene group comprises the following genes: RHOA, ARHGAP32, ARHGAP4, ARHGAP6, ARHGAP9, ARHGEF17, ARHGEF2, ARHGEF3, BCR, CDC42, CDKN1B, DLEC1, FARP1, NET1, NGEF, OBSCN, PRPF38B, SLC6A5, TSPAN1, VAV2, and VAV3.