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kill zombie cells can help stay young

Posted by star on 2018-05-25 00:54:53
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    There is a special kind of cell in mice that did not divide and wouldn't die but can make the animal accelerate ageing, the researchers found that clear away these 'senescent' cells can alleviate or even prevent certain illnesses and stimulate new tissue production.This year alone, it has been proved that clearing out the cells in mice can regain fitness, fur density and kidney function. It has also improved lung disease and even mended damaged cartilage.

    We know that when a cell becomes mutation or damage it often stops dividing and may be secreting a distress signal to inform the immune system clearing out the abnormal cell,No one is quite sure when or why that happens. It has been suggested that the immune system stops responding to the cells.

    Lacking of universal features as marker to identify the senescent cells lead to the work very laborious . Senescent cells relay on protective mechanisms to stay undead state, different cell may have a unique way to protect itself from wiping out. reserchers identified six signalling pathways that prevent cell death, Then it was just a matter of finding compounds that would disrupt those pathways. 14 senolytics have been described in the literature, a peptide that activates a cell-death pathway and can restore lustrous hair and physical fitness to ageing mice , senolytic drugs just wipe out senescent cells which already exit ,they won't prevent the formation of such cells in the future, which means that senescence can continue to perform its original tumour-suppressing role in the body.

    If eliminating senescent cells in humans does improve age-related illnesses, researchers will aim to create broader anti-ageing therapies.



Tau protein cytotoxicity can be rescued by acetylated microtubules

Posted by star on 2018-05-25 00:44:29
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     Alzheimer's disease (AD), one of the major pathological changes is the neurofibrillary tangles that result from the over-phosphorylation of microtubule-binding protein Tau in the brain cells of patients. In addition to AD, there are also hyper-phosphorylation of Tau and formation of neurofibrillary tangles during the pathogenesis of several other neurodegenerative diseases, collectively referred to as tauopathies. Under normal physiological conditions, Tau protein acts as a stabilizing microtubule, but Tau protein is dysfunctional in the brains of patients with Tauopathies, resulting in destruction of the microtubule structure. Previous studies by Zhang Yongqing, a research team at the Institute of Genetics and Development, showed that in a transgenic Drosophila model of Tauopathy, heterologously expressed Tau is hyper-phosphorylated and results in decreased density of microtubules and destruction of the network. Histone deacetylase family members HDAC6 mutation can be effectively inhibited Tau heterologous expression of microtubule damages, and HDAC6 specific point mutation function analysis and specific inhibition of HDAC6 microtubule deacetylase activity of drug treatment experiments. The results show that HDAC6 mutation and activity destruction probably rescues Tau-induced microtubule destruction by increasing microtubule acetylation level.

    However, HDAC6 has multiple substrates. To further verify the relationship between microtubule acetylation and Tau toxicity, we mutated lysine at position 40 of endogenous a-tubulin in Drosophila to glutamine to mimic the acetylation status of microtubules. The results indicate that mimicking acetylated microtubules can rescue the developmental abnormalities of microtubules and synapses caused by overexpression of Tau. In addition, after the Drosophila......


    Esophageal cancer is a malignant disease caused by abnormal hyperplasia of the esophageal squamous epithelium. The development of the epithelium is atypical hyperplasia, carcinoma in situ, invasive carcinoma, etc. The expression of different proteins in different individuals, or the same individuals in different states, these highly specific protein expressions determined that patients with esophageal cancer had different characteristics.

    In the journal nature published a study from the university of Basel, Switzerland, Michael n. Hall led the research team has discovered a new tumor-suppressor protein LHPP, when this kind of protein expression, can prevent not controlled the growth of cell proliferation, and once they appear defects, will to some extent induce uncontrolled growth of cells, cause cancer. It is also found that LHPP level is also associated with the disease burden and patient prognosis, so the researchers believe that it can be used as a biomarker for diagnosis and prognosis.

    In primary hepatocellular carcinoma, 90% of HCC cells are HCC, while 50% of HCC cells are involved in mTOR signaling pathway. By activating mTOR in mice, the mice developed hepatomegaly at 6 weeks of age, and fully developed liver cells at 20 weeks. The characteristics of liver cancer in mice were almost the same as those of human liver cancer. The mice were named L-dKO mice.

    The researchers analyzed a proteomic analysis of liver tissue in healthy mice at 20 weeks old L-dKO mice and screened out a very different protein -LHPP. This protein is normally expressed in healthy tissue and is rarely expressed in cancer tissues.

    Studies have shown that LHPP is a histidine phosphatase, the enzyme that removes phosphate groups from proteins. The protein expres......


    

     Microtubule-binding proteins (MAPs) mainly include the microtubule positive-terminal binding protein (+TIPs) and the negative-terminal binding protein (+TIPs). These proteins regulate microtubule dynamics and mediate the involvement of microtubules in a variety of cellular biological processes. At present, a variety of + TIPs have been found, whose core members are the EBs protein family. EBs can autonomously bind to the positive end of microtubules, regulate the dynamic changes of microtubules, and can recruit many other + TIPs to the positive end of microtubules, but it is unclear how EBs are regulated. Nowadays, there is still a limited understanding of -TIPs in the studies. The CAMSAPs family of proteins, as a new class of TIPs, binds to the negative end of a dynamically growing microtubule and stabilizes the negative end of the microtubule.

     Recent studies on the relationship between CAMSAPs and EB1 have found that CAMSAP2 has the most significant effect on the positive localization of EB1 in microtubules. CAMSAPs bind to EB1 through the C-terminal domain, while the EB1 linker region inhibits the binding of EB1-specific domains to CAMSAPs. The results show that CAMSAP2-EB1 interaction can be independent of microtubules in the cytoplasm, and the intracellular protein content of CAMSAP2 affects the length of EB1 at the positive end of microtubules. In contrast, EB1 can also help CAMSAP2 stabilize in the microtubule negative end. With live cell imaging, it was observed that EB1 comets at the positive end of the microtubules could target the CAMSAP2 site for transient collisions with CAMSAP2, and knockdown of CAMSAP2 caused the change of the direction of EB1 movement. This implies that non-centrosome microtubules are likely to be end-to-end connected with other microtubules to par......

mTOR signaling pathway is associated with tumor potential

Posted by star on 2018-05-21 19:58:49
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     Mammalian target protein (mTOR) is an atypical serine/threonine kinase, which is a member of the protein family of the PIKKs kinase associated with phosphatidyl inositol kinase. MTOR evolution is relatively conservative, but integration of nutrition, energy, and growth factors and other extracellular signals, participate in gene transcription, protein translation, biological processes such as ribosome synthesis and cell apoptosis, also play a very important role in cell growth. Studies have shown that mice are more likely to die after mTOR knockout. Studying the relationship between mTOR and related diseases can provide a potential target for disease treatment.

    The mTOR signaling pathway is diverse and determines its key role in the development of disease. Studies on mTOR pathway regulation may be helpful for future treatment.

    MTOR pathway mainly affects mRNA translation and protein synthesis. If the pathway is maladjusted, it may lead to abnormal cell proliferation, indicating that it is closely related to the development of tumor. The scientists found a linear relationship between tumor recurrence rate and mTOR expression in metastatic lymph nodes in pT2b gastric cancer. The expression of mTOR phosphorylation was significantly correlated with metastatic lymph nodes, while the expression of p-mtor in metastatic lymph nodes was also associated with the low survival rate after the disease. The researchers showed that in prostate cancer, the specific therapy targeted at mTOR was significantly increased in anti-tumor effect compared to single measures after combined with anti-androgen therapy. The precursors of cerebellar granulocytes may develop into neuroblastoma in pediatric brain tumors. In addition, the study found that lovastatin, a statin, can obviously inhibit the mouse neurobla......

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