16 results about "Erk signaling" patented technology

This invention discloses a method for inducing pluripotent stem cells to differentiate into skin keratinocytes and its culture medium, solving problems such as long differentiation cycles, low yields, insufficient purity, and animal-derived contamination in existing technologies. The first stage uses medium I containing FGF2 and tanshinone IIA to promote mesodermal differentiation. The second stage uses medium II containing BMP4, EGF, dexamethasone, and PVA to regulate and synergistically induce the BMP / ERK signaling pathway. The final stage uses medium III for expansion culture, obtaining fibroblasts with a purity >99% within 20 days. This method is non-invasive, simple, and low-cost, with potential for large-scale production. The obtained cells can be used for skin regeneration, disease modeling, drug screening, and clinical treatment, demonstrating significant medical application and industrial transformation value.

Methods are provided for differentiating human pluripotent stem cells into dorsal neuroectodermal progenitor cells and further into glial progenitor cells and oligodendrocyte progenitor cells (OPCs) using inhibitors of BMP signaling and MAPK / ERK signaling. Also provided are cells and cell compositions obtained by such methods, and uses of such cells. Further provided are methods and protocols for effectively differentiating human pluripotent stem cells into OPCs in the absence of the ventral morphogen SHH or an activator of SHH signaling. The methods of the present disclosure reproducibly generate dorsal neuroectodermal progenitor cells at day 7 of the differentiation process, glial progenitor cells at day 21 of the differentiation process, and OPCs at day 42 of the differentiation process.

The invention belongs to the technical field of medicines, and particularly relates to application of TPHP in bone metabolism. According to the application disclosed by the invention, the TPHP is found to have a remarkable inhibition effect on proliferation and invasion and migration of bone cells, and the TPHP damages proliferation, migration and invasion functions of MC3T3-E1 osteoblasts by inhibiting an MAPK / ERK signal channel and down-regulating related gene expression. The action effect of the TPHP is remarkable, and subsequent scientific research is facilitated. In addition, TPHP is easy to obtain and low in cost, related preparations and biological models are easy to prepare, the process is mature, industrialized production can be achieved, and the market acceptance degree is high.

The invention discloses an anti-aging two-factor composition based on epigenetic reprogramming and application thereof, and belongs to the technical field of biological medicine. The composition comprises a Wnt pathway small molecule activator Laduvilliub and an ERK pathway activator bFGF, and through synergistic activation of Wnt and ERK signal pathways, epigenetic reprogramming of senescent cells is induced, and senescence-related chromatin open change, histone modification imbalance and DNA methylation clock drift are significantly reversed. At the cellular level, the composition can reverse various senescence phenotypes, namely restoring multiplication capacity, down-regulating expression of senescence-related secretory phenotype factors, relieving DNA damage, improving telomerase activity and telomere length and increasing nucleofibrin. At an individual level (an old mouse model), the composition is injected in the intraperitoneal cavity, so that the cognitive ability and the exercise ability are remarkably improved, the aging pathological characteristics of multiple organs are reduced, and the aging-related gene expression profiles of the organs such as the liver and muscles are reversed. The double-factor composition can be applied to anti-aging drugs, health care products or cosmetics.

The present invention relates to anti-GREM1 antagonists for use in methods of treating or preventing cancer in combination with inhibitors of Ras-Raf-MEK-ERK signaling.

The invention relates to application of HAX1 in diagnosis or treatment of tongue squamous cell carcinoma, and belongs to the field of bioengineering. Key prognosis genes are screened by screening differentially expressed genes of genes related to tongue squamous cell carcinoma in a GEO database and associating the screened genes with survival data of patients and using COX and LASSO regression algorithms; and carrying out visual analysis on the expression conditions of the screened DEGs in TSCC patients with different clinical grades, and determining the significant correlation between the HAX1 and the TSCC. By constructing a HAX1 differential expression TSCC cell line, the influence of HAX1 on TSCC in the aspects of promoting TSCC cell proliferation, enhancing TSCC cell migration and invasion ability, inhibiting TSCC cell apoptosis, enhancing TSCC cell dryness, promoting TSCC related angiogenesis ability and the like is proved, and the effect of inhibiting HAX1 expression in TSCC treatment is further proved; the molecular mechanism research of the HAX1 for regulating and controlling the TSCC proves that the HAX1 remarkably regulates and controls the downstream gene expression in the TSCC; the gene is closely related to the MAPK / ERK signal pathway, and the RAF / MEK / ERK pathway is regulated and controlled through the interaction with the RAF family.

The present invention relates to an anti-GREM1 antagonist in combination with a Ras-Raf-MEK-ERK signaling inhibitor for use in a method of treating or preventing cancer.

The invention relates to the technical field of ERK signal pathways, in particular to an ERK signal pathway inhibitor, a breast cancer drug, a method and application. The ERK signal channel inhibitor provided by the embodiment of the invention not only can knock down CKAP4 protein expression, but also can knock down various protein expressions in an ERK signal channel, so that the ERK signal channel is inhibited. By inhibiting the ERK signal pathway, the inhibitors can inhibit proliferation, migration and invasion, can block breast cancer cells in the G1 phase and promote apoptosis of the breast cancer cells, and have application prospects as breast cancer drugs.

The invention discloses a method and a culture medium for inducing pluripotent stem cells to efficiently differentiate into fibroblasts, and solves the problems of long differentiation period, low yield, insufficient purity, animal source pollution and the like in the prior art. In the first stage, a culture medium I containing FGF2 and tanshinone IIA is used for promoting mesoderm differentiation, in the second stage, a culture medium II containing BMP4, EGF, dexamethasone and PVA is used for regulating and controlling a BMP / ERK signal channel and conducting synergistic induction, in the final stage, a culture medium III is used for multiplication culture, and fibroblasts with the purity larger than 99% are obtained within 17 days. The method is noninvasive, simple and convenient in process and low in cost and has large-scale production potential, and the obtained cells can be used for skin regeneration, disease modeling, drug screening and clinical treatment and have remarkable medical application and industrial transformation value.

The invention discloses a process for affinity separation of active components in inonotus obliquus by using a VEGFR2 extracellular domain and application, and relates to the technical field of active component extraction.The process comprises the steps that eight active components including echinacoside, trilliin, typhaenoside, hederagenin, asiaticoside, lanosterol, betulin and aster ketone are selected; the inhibition effect of the compound on cervical cancer cells is studied. The method comprises the following steps: taking a sample to be detected, taking a detection solution, carrying out lauryl sodium sulfate-polyacrylamide gel electrophoresis and Western blot analysis, determining the protein expression quantity of VEGFR-2 related pathways, and researching the regulating effects of trillioside, betulin, hederagenin and lanosterol on a PI3K / AKT signal pathway, a PLC gamma / ERK signal pathway, Bad protein, Caspase-9 protein and Cleaved Caspase-9 protein of SiHa cells.

The invention relates to the technical field of traditional Chinese medicine research, in particular to a method for analyzing chemical components of a Shuganning injection and a method for screening acute liver injury resistant pharmacodynamic substances of the Shuganning injection. According to the invention, UHPLC Q-Exactive Plus Orbitrap HRMS component analysis, network pharmacology, biofilm interference technology, cell thermal displacement and molecular docking are applied for the first time to screen an active component group of the Shuganning injection for treating acute liver injury, and screen a potential active component group of the Shuganning injection for treating acute liver injury combined with core targets ERK and p38; and preparing a mixture according to the content ratio of the active ingredient group in the Shuganning injection. Acetaminophen is adopted to induce and establish an acute liver injury rat model, and the pharmacological action of active ingredients is evaluated from plasma biochemical analysis and liver tissue pathology; western blot, real-time fluorescent quantitative PCR (polymerase chain reaction) and immunofluorescence are applied to investigate the influence of active components on p38 and ERK signal channels.

In various aspects and embodiments, the present disclosure provides compositions and methods for treating pancreatic cancer (e.g., pancreatic ductal adenocarcinoma, i.e., PDAC). According to aspects of the present disclosure, the composition comprises an aptamer that targets accumulation of the composition to pancreatic cancer cells, and an antisense oligonucleotide that inhibits the expression of mRNA associated with important signaling pathways that promote the growth or survival of pancreatic cancer cells, such as the KRAS-RAF-MEK-ERK signaling pathway or the RTK-RAS-ERK cascade. Exemplary antisense oligonucleotides described herein target KRAS, including mutant KRAS. Exemplary antisense oligonucleotides described herein target SOS1 and / or SOS2 transcripts.

The invention provides a tetrahedral framework nucleic acid compound for Braf gene silencing as well as a preparation method and application thereof, and belongs to the technical field of biological medicines. The tetrahedral framework nucleic acid compound disclosed by the invention is tetrahedral framework nucleic acid loaded with siRNA; the forward sequence of the siRNA is shown as SEQ ID NO.8, and the reverse sequence of the siRNA is shown as SEQ ID NO.7. The compound disclosed by the invention can be enriched at a tumor site, is effectively taken by cancer cells, and shows a good synergistic anti-tumor effect by inhibiting Braf expression, inhibiting proliferation and invasion of cancer cells, promoting cell apoptosis, inhibiting activation of an MEK-ERK signal channel and improving the mitochondrial dysfunction and DNA damage level. Meanwhile, the compound disclosed by the invention has good biological safety and biocompatibility. Therefore, the compound disclosed by the invention is suitable for preparing thyroid cancer related medicines and has a good industrial application prospect.

In various aspects and embodiments, the present disclosure provides compositions and methods for treating pancreatic cancer (e.g., pancreatic ductal adenocarcinoma or PDAC). In accordance with aspects of the present disclosure, the composition comprises an aptamer that targets the accumulation of the composition into pancreatic cancer cells, and an antisense oligonucleotide that inhibits the expression of mRNA associated with a key signaling pathway that promotes proliferation or survival in pancreatic cancer cells, such as a KRAS-RAF-MEK-ERK signaling pathway or an RTK-RAS-ERK cascade. The exemplary antisense oligonucleotides described herein target a KRAS, including a mutant KRAS. The exemplary antisense oligonucleotides described herein target a SOS1 transcript and / or a SOS2 transcript.

In the various aspects and embodiments, the present disclosure provides compositions and methods for treating pancreatic cancer (e.g., pancreatic ductal adenocarcinoma, or PDAC). In accordance with aspects of the disclosure, the composition comprises an aptamer that targets accumulation of the composition to pancreatic cancer cells, and an antisense oligonucleotide that inhibits the expression of an mRNA associated with key signaling pathways that promote proliferation or survival in pancreatic cancer cells, such as the KRAS-RAF-MEK-ERK signaling pathway or RTK-RAS-ERK cascade. Exemplary antisense oligonucleotides described herein target KRAS, including mutant KRAS. Exemplary antisense oligonucleotides described herein target SOS1 and / or SOS2 transcripts.

A human 2D patient-derived organoid screening platform to study tissue patterning and kinase pathway dynamics in single cells. With the help of this system, it is discovered that waves of ERK signaling induced by apoptotic cells play a critical role in maintaining tissue patterning and homeostasis.