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Study finds new targets for triple-negative breast cancer treatment

Posted by star on 2018-10-08 18:43:12
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    A new study analyzes the transcriptome characteristics of triple-negative breast cancer (TNBC) patients, and identifies and confirms the novel inhibitor Wwox protein of JAK2/STAT3 signaling in breast cancer, elucidating abnormal attenuation of Wwox and abnormal activation of JAK2/STAT3 Such a negative correlation is an important cause of the metastasis of highly malignant TNBC. The study of Loss of Wwox drives metastasis in triple-negative breast cancer by JAK2/STAT3 axis is published online in Nature-Communication.

    In recent years, the incidence of breast cancer in China has continued to rise. TNBC is a type with a high degree of malignancy. Its invasiveness is extremely strong, the risk of distant metastasis is large, and the prognosis is extremely poor. At present, its treatment is relatively simple, mainly chemotherapy, and it is easy to relapse and metastasize. Endocrine therapy and molecular targeted therapy are ineffective against TNBC compared to other types of breast cancer.

    The researchers screened transcriptomic analysis of TNBC cells and normal breast cells to obtain abnormal expression of multiple signals in the IL6/JAK2/STAT3 pathway, demonstrating the high abnormal expression of IL6 in TNBC cells and the persistence of JAK2/STAT3 activation. Activation may be an important factor in the distal metastasis of TNBC. The study also found that SOCS3, the main inhibitor of JAK2/STAT3, was not inhibited in TNBC; the newly discovered fragile site gene Wwox persisted in the IL6/JAK2/STAT3 signaling pathway in breast cancer. Specific inhibition occurs during activation. The researchers demonstrated the inhibitory effect of Wwox on sustained phosphorylation of STAT3 signaling and sustained activa......

Removal of aging glial cells is expected to treat Alzheimer disease

Posted by star on 2018-10-07 23:19:45
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    In a new study, aging cells accumulate in their brains before cognitive loss in the mouse model of brain disease. By preventing the accumulation of these aging cells, they are able to reduce tau protein aggregation, neuronal death and memory loss. The relevant research results are published online in Nature, and the title of the paper is "Clearance of senescent glial cells preventing tau-dependent pathology and cognitive decline".

    It is known that senescent cells accumulate in sites associated with aging diseases (including osteoarthritis and atherosclerosis) and neurodegenerative diseases (including Alzheimer's disease and Parkinson's disease) as the natural age grows. In previous studies, we have found that clearing senescent cells from naturally aged mice prolongs their healthy lifespan.

    In this new study, the mouse model of Alzheimer's disease produces sticky, spider-like tau tangles in their neurons, and their genetically modified senescent cells can be eliminated. When senescent cells were removed, the researchers found that the diseased mice maintained the ability to form memory and eliminate signs of inflammation, did not produce neurofibrillary tangles, and maintained normal brain quality. They also reported that drug interventions that remove senescent cells can regulate the accumulation of tau.

    In addition, the research team was able to identify specific cell types that are senescent. When the brain tissue was observed under a microscope, they found two different types of brain cells called microglia and astrocytes to age. These cells are important proponents of neuronal health and signaling, so it makes sense that aging of any of these cells can have a negativ......


    In a new study, it is reported that in a mouse model of brain disease, senescent cells accumulate in their brains before cognitive loss. By preventing the accumulation of these aging cells, they are able to reduce tau protein accumulation, neuronal death and memory loss. The results of the study were published on September 19, 2018 in the Nature, entitled "Aging glial cells prevent tau-dependent pathology and cognitive decline."

    It is known that senescent cells accumulate in sites associated with aging diseases (including osteoarthritis and atherosclerosis) and neurodegenerative diseases (including Alzheimer and Parkinson) as they age. In previous studies, the researchers have found that removing senescent cells from naturally aged mice prolongs their healthy lifespan.

    The new study used a mouse model that mimicked Alzheimer. They produce sticky, spider-like tau protein tangles in their neurons and after gene was modified, their senescent cells can be cleared.When senescent cells were removed, they found that the diseased mice maintained the ability to form memory and eliminate signs of inflammation, did not produce neurofibrillary tangles, and maintained normal brain quality. They also reported that drug intervention to remove senescent cells can regulate the accumulation of tau protein.

    In addition, the researchers was able to identify specific cell types that are senescent. When the brain tissue was observed under a microscope, they found two different types of brain cells called microglia and astrocytes to age. These cells are important proponents of neuronal health and signaling, so it makes sense that aging of any of these cells can have a negative impact on neuronal health.


New drug therapy restores partial hearing in deaf mice

Posted by star on 2018-09-10 00:44:03
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Deafness is a genetically dominant feature of the LMG2 family, which means that a child inherits a defective copy of the gene from his parents and experiences progressive hearing loss. The mutation of the deafness is located in the region of DFNA27 on chromosome 4. This area contains more than a dozen genes. However, the precise location of this mutation has been unknown.

Most of the previous studies ignored the fourth exon in the Rest gene,because this small exon was not edited into the Rest mRNA of most cells. The normal function of REST proteins is to shut down genes that are only active in a few cell types.

On June 28, a study published Defects in the Alternative Splicing-Dependent Regulation of REST Cause Deafness in Cell showed that exon 4 of mouse Rest was deleted, and ear hair cells died, resulting in a deaf mouse phenotype. The researchers found that many genes that should have been active were shut down before hair cells died. Thus, they reanalyzed the deafness mutations in the LMG2 family and found that the mutations were close to exon 4, altering the boundaries of exon 4, while the REST of hair cells was inactivated.

Integrating exon 4 into REST mRNA is equivalent to a switch that senses hair cells, which shuts down REST and opens up many gene expressions. Activation of these genes is important for hair cell survival and hearing.

Using an exon 4-deficient mouse model, the researchers found that REST inhibits gene expression primarily through a process called histone deacetylation. As a result, they used small molecule drugs that inhibited this process, down-regulating the effects of REST, and successfully restored the mice to partial hearing.

Wuhan EIAab Science Co., Ltd has developed REST protein, antibody and ELISA kit.

Welcome scientific research workers to choose and purchase.



Research Found Key Substances in the Pathogenesis of Psoriasis

Posted by star on 2018-09-06 18:53:36
Hits:35

    A new study in Japan found that in the pathogenesis of psoriasis, a signaling molecule in skin cells plays a key role, and on this basis, it is expected to develop new therapeutic methods.

    Psoriasis is a skin disease associated with immune abnormalities, manifested by erythema, silver shavings and itching on the skin. According to the researchers, psoriasis patients account for about 3% of the global population. In recent years, injection antibody therapy has a good effect, but the cost of treatment is high, and some patients may have antibody failure.

    In a new issue of Epithelial TRAF6 drives IL-17–mediated psoriatic inflammation on the Journal of JCI Insight, the researchers reported that a signal molecule "TRAF6" in skin cells plays a key role in the pathogenesis of psoriasis.

    In mice, mice lacking this signaling molecule do not develop psoriasis. Even when these mice were injected with immunomodulatory factors, immune abnormalities that could have caused psoriasis were induced, and psoriasis was still suppressed.

    Researchers therefore believe that new treatments for psoriasis can be developed for this signaling molecule to address the challenges of previous related therapies.

    Wuhan EIAab Science Co., Ltd has developed several related kits such as E8869h, E8869m, E0063h and E2103h etc. Welcome scientific research workers to choose and purchase.



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