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Progress in research on regulation mechanism of glial cells in brain

Posted by star on 2018-05-21 19:27:12
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    Decision-making is one of the most basic cognitive functions of the brain, and many brain diseases can lead to cognitive impairment in decision-making. Clinically, many chronic diseases have been found, such as chronic pain, which can severely damage the brain. Thus, finding the nerve cells and molecular which targets for chronic pain-induced decision-making disorders has been the focus of neuroscience researchers. Glial cells account for more than 90% of the brain nerve cells. Classical theory that glial cells are only the brain "glue", can only play a certain "support" role. In recent years, this traditional view has gradually been subverted with the extensive application of optical genetic technology. Glial cells on the multiple regulations of neurons gradually are discovered by researchers. However, astroglial regulation of decision-making ability and its regulatory mechanism have not been conclusived yet.

    The team found that the decision-making cognitive function of animals in chronic pain model was significantly decreased by means of optical genetic technology and animal behavior combined with electrophysiological techniques in vivo. The intrinsic neural circuit mechanism lies in that the lateral almond (BLA) Synchronicity of cingulate gyrus (ACC) was significantly reduced. The photo-genetics specific stimulation of astrocytes in the cerebral cortex could effectively increase the concentration of L-lactate in the local microcirculation. The synchronization between the two brain regions effectively ameliorates the effect of chronic pain on decision-making in rats. This study proposed a new model for decision-making neurocognitive neural basis from the perspective of basic metabolism of glial cells, and provided a new idea for clinical intervention in the treatment of cognitive impairment of ch......

Bacteriophages may help maintain human health

Posted by star on 2018-05-07 00:21:53
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          Bacteriophages were found to kill bacteria in the wreckage of World War I soldiers. A century later, the virus is drawing new attention because of its potential role in the human body. From the ocean to the soil, bacteriophages are almost ubiquitous. Now, one study shows that humans absorb up to 30 billion phages each day through the gut. Although the exact location of the virus is still unknown, recent data and other studies have prompted scientists to suspect that a large number of phages in the body - the "phage group" - may influence the physiology by regulating the immune system. A study of various animals from corals to humans found that the phage abundance in the mucus layer was more than four times greater than that in the surrounding environment, as was the case for phagosomes that protect human gums and gut. As it turns out, the outer sheath of the bacteriophage binds to mucus that is secreted by the body in large quantities and mucus together with water. Attached to the mucus makes the phage to encounter more bacterial prey. As a result, it has been demonstrated in a series of in vitro studies that these viruses protect the basal cells from possible bacterial pathogens and thus provide an additional immunological layer.



A new mechanism for regulating the activation of NLRP3 inflammasome

Posted by star on 2018-05-03 18:39:28
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        As an important part of natural immunity, NLRP3 inflammasome plays an important role in the development of immune response and disease, and its overactivation can lead to a variety of major human diseases such as alzheimer's disease, inflammatory bowel disease, diabetes and malignancy. Previous studies have found that the Danger signal molecules(Danger Signals) induced mitochondrial damage that leading to excessive activation of NLRP3, but the detailed regulation mechanism that how does the body maintains mitochondrial homeostasis to prevent excessive activation of NLRP3 is rarely reported. Professor Xu Qiang and professor Sun Yang research team's latest work found that protein tyrosine phosphatase SHP2 can be transferred to the mitochondria by the NLRP3 activator ATP, the crystallization of uric acid and the bacteriocin in the NLRP3. In the mitochondrial outer membrane protein Tom20 / Tim23 Tom40 complexes and mitochondrial membrane protein complexes, SHP2 quickly through the outer and inner membrane targeting mitochondrial matrix, combined with mitochondrial membrane protein ANT1, remove its 191 tyrosine phosphorylation, and stability of mitochondrial membrane potential, inhibition of mitochondrial DNA, and the release of reactive oxygen species, cut the resulting excessive activation of NLRP3 inflammatory corpuscle.

 

       The work found an important endogenous fine regulation of NLRP3 inflammatory small body activation new mechanism - activating negative regulation signal to maintain mitochondrial homeostasis shortly after inflammatory response. A negative regulatory mechanism to clarify will help us understand how the body is fine regulation of inflammatory response so as to maintain a stable internal environment......

The phosphorylation of NCOA3 is also a biomarker for many cancers.

Posted by star on 2018-05-01 23:46:28
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         Nuclear receptor coactivator-3 (NCOA3, SRC-3), a 1420-AA nuclear receptor coactivator, does not directly bind to DNA. It is recruited to specific gene promoters by interacting with nuclear hormone receptors such as the progesterone receptor, estrogen receptor, and peroxisome proliferation activated receptor and other transcription factors such as E2F1, PEA3, and AP1.

         It is reported that NCOA3 which is amplified in breast cancer 1 (AIB1) and also plays an important role in lung, ovary, prostate and pancreatic cancer over-expresses in many cancer cells. [1] NCOA3 plays an important role in optimal activation of the PERK–eIF2α–ATF4 pathway. XBP1–NCOA3 axis regulates cell fate decisions in ER-positive breast cancer cells. The PERK–ATF4 arm directly upregulated vascular endothelial growth factor A (VEGFA) and Lysosomal-Associated Membrane Protein 3 (LAMP3), thereby regulating tumour vascularity and invasion.[2] Moreover, the phosphorylation of NCOA3 can further increase the transcriptional activity of NCOA3. So the phosphorylation of NCOA3 is also a biomarker for many cancers. [3]

 

          On April 3, 2018, a heavy study which was done by the team of Bert O'Malley at Baylor College of Medicine was published in the top journal "Nature


On April 3, 2018, Nature published an online article called Metabolic enzyme PFKFB4 activates transcriptional coactivator SRC-3 to drive breast cancer. The article points out that the Warburg pathway enzyme PFKFB4 acts as a molecular fulcrum that couples sugar metabolism to transcriptional activation by stimulating SRC-3 to promote aggressive metastatic tumours.

PFKFB4 also known as 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 4 which in humans is encoded by the PFKFB4 gene is an activator of a key regulatory enzyme of glycolysis and phosphofructokinase. PFKFB4 is a bifunctional enzyme that can increase intracellular F2,6BP and, thus, flux through PFK-1 or decrease F2,6BP and PFK-1 activity resulting in increased shunting of glucose 6-phosphate for NADPH and ribose production. PFKFB4 was observed to be over-expressed in human tumors indicating a potential role in cancer development and/or progression. This protein is highly expressed in cancer cells and is induced by hypoxia and is essential to the survival of cancer cells under conditions of hypoxia. This suggests that PFKFB4 may be a useful molecular target for the development of anti-neoplastic agents. 

Wuhan EIAab Science Co., Ltd has developed PFKFB4 protein, PFKFB4 antibody, PFKFB4 ELISA KIT. Welcome scientific research workers to choose and purchase.

 

 

 



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