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Irisin, a novel muscle factor and a hydrolysate of FNDC5

Posted by star on 2018-06-05 18:47:47
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    Irisin is a novel muscle factor which was discovered in 2012 and is a hydrolyzed product of FNDC5. The result of the mass spectrometry analysis reveals that Irisin is a soluble N-glycosylated protein hormone with a molecular weight of approximately 12 kDa consisting of 112 amino acids. Irisin is highly conserved in evolution and the mouse and human irisin share 100% identity in the sequences. Irisin is synthesized and secreted by skeletal muscle, white adipose tissue, etc. And the skeletal muscle is the main source.

    Irisin was identified at the beginning of discovery as having the biological effects of promoting browning of white adipose tissue, accelerating body energy expenditure, regulating energy metabolism, and improving insulin resistance. Subsequent investigations show that irisin also plays an important role in neurological diseases, cardiovascular diseases, non-alcoholic fatty liver, and tumors.

    Irisin can promote the expression of UCP1 which can promote browning of white adipose tissue, accelerate body energy expenditure, regulate energy metabolism and can reduce insulin resistance by promoting beta-trophin and β-cell regeneration; irisin can reduce atherosclerotic plaque, lipid deposition, and macrophage accumulation by up-regulating the expression of ERK-dependent microRNA126-5p; irisin can activate AMPK-Akt-eNOS pathway which promotes the release of nitric oxide from endothelial cells thus lowers blood pressure; irisin also improves the skill of learning and memory by regulating the expression of BDNF which promotes dopamine release and increases neuronal survival. The molecular mechanism has yet to be further studied.



The protein histidine phosphatase LHPP is a tumour suppressor

Posted by star on 2018-06-03 19:11:39
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    Phospholysine phosphohistidine inorganic pyrophosphate phosphatase (LHPP) belongs to the HAD-like hydrolase superfamily. LHPP is an exceptional enzyme which hydrolyzes not only oxygen-phosphorus bonds in inorganic pyrophosphate but also nitrogen-phosphorus bonds in phospholysine, phosphohistidine and imidodiphosphate in vitro. LHPP is expressed in the liver, kidney and moderately in the brain.

    On March 21, 2018, Nature published an article called The protein histidine phosphatase LHPP is a tumour suppressor. The article points out that LHPP is a protein histidine phosphatase and tumour suppressor, suggesting that deregulated histidine phosphorylation is oncogenic.

    Histidine phosphorylation, the so-called hidden phosphoproteome, is a poorly characterized post-translational modification of proteins. In this article, the authors demonstrate that LHPP is indeed a protein histidine phosphatase. Consistent with observations, global histidine phosphorylation was significantly upregulated in the liver tumours. Sustained, hepatic expression of LHPP in the hepatocellular carcinoma mouse model reduced tumour burden and prevented the loss of liver function. Finally, in patients with hepatocellular carcinoma, low expression of LHPP correlated with increased tumour severity and reduced overall survival. Thus, LHPP is a protein histidine phosphatase and tumour suppressor, suggesting that deregulated histidine phosphorylation is oncogenic.

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




   

    Squalene monooxygenase (also called squalene epoxidase) is an enzyme that uses NADPH and molecular oxygen to oxidize squalene to 2,3-oxidosqualene (squalene epoxide). Squalene epoxidase catalyzes the first oxygenation step in sterol biosynthesis and is thought to be one of the rate-limiting enzymes in this pathway. In humans, squalene epoxidase is encoded by the SQLE gene. Squalene monooxygenase (SqMO) was formerly referred to as squalene epoxidase (SqE) in the literature.

    On May 16, 2018, Nature published an article called The cancer-associated microprotein CASIMO1 controls cell proliferation and interacts with squalene epoxidase modulating lipid droplet formation. The article points out that squalene epoxidase (SQLE) as a key enzyme in cholesterol synthesis and a known oncogene in breast cancer knockdown mimicked the Cancer-Associated Small Integral Membrane Open reading frame 1 (CASIMO1, a novel microprotein of 10 kDa), knockdown phenotype and in turn SQLE overexpression fully rescued the effect of CASIMO1 knockdown.

    Breast cancer is a leading cause of cancer-related death in women. CASIMO1 RNA is overexpressed predominantly in hormone receptor-positive breast tumors. Its knockdown leads to decreased proliferation in multiple breast cancer cell lines. Its loss disturbs the organization of the actin cytoskeleton, leads to inhibition of cell motility, and causes a G0/G1 cell cycle arrest. The proliferation phenotype upon overexpression is observed only with CASIMO1 protein expression, but not with a non-translatable mutant attributing the effects to the sORF-derived protein rather than a lncRNA function. CASIMO1 microprotein interacts with squalene epoxidase (SQLE). Overexpression of CASIMO1 leads to SQLE protein accumulation ......


    SE (also called squalene epoxidase or squalene monooxygenase, SM EC 1.14.99.7) is a 64 kDa enzyme codified by Human SQLE gene. It was first detected in rat liver microsomes, in 1969. SE is located in the endoplasmic reticulum of cells, and although ubiquitous, it is present at very low levels in most non-cholesterolemic mammalian tissues, while it is highly expressed in liver, neural tissue, in the gut, and in the skin.

    Oncogenic alteration of the cholesterol synthesis pathway is a recognized mechanism of metabolic adaptation. SE is a rate-limiting enzyme leading to effective inhibition of cholesterol synthesis when blocked: if the step of squalene oxygenation catalyzed by SE is influenced, the synthesis of sterols and cell membrane or even cell growth will be subsequently affected. In addition to this transcriptional regulation, the rapid shutdown of cholesterol synthesis requires post-transcriptional control: SE is directly regulated by cholesterol itself which results in its degradation via the ubiquitin-proteasome system.

    High expression of SQLE has been implicated in lethal prostate cancer pathogenesis, in colorectal cancer, and in squamous lung cancer occurrence and development. In that context, SQLE has been suggested as a new molecular marker predicting poor prognosis. Finally, a recent study suggests the involvement of SE in leukemia. In particular, approximately threefold-higher SQLE transcript levels were observed in the daunorubicin-resistant leukemia CEM/R2 cell line.

    Wuhan EIAab Science Co., Ltd has developed squalene epoxidase protein, antibody. Welcome scientific research workers to choose and purchase.



Novel compounds inhibit cervical cancer

Posted by star on 2018-05-31 18:54:23
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    Japanese researchers recently reported that they had invented a compound that inhibits cervical cancer and that they have confirmed efficacy in animal experiments. The next plan is to conduct clinical trials during the year.

    Human papillomavirus (HPV) is the main cause of cervical cancer. Researchers at Kyoto University and other institutions in Japan recently published a paper in the American academic journal Clinical Cancer Research. They said that they invented a compound called FIT-039. In experiments using cervical epithelial cells in patients with cervical cancer, Compounds can inhibit viral proliferation.

    The team conducted an animal experiment, transplanted human cervical cancer cells into experimental mice, and fed with this compound. It was found that it also inhibited cancer cell proliferation in mice. After 3 weeks, compared with the control group, the proliferation rate of the experimental mice fed with the drug was reduced by 30%, and no side effects occurred.

    Researchers believe that this compound may be a new option for preventing cervical cancer. In the future, they will also confirm their impact on reproductive function. They plan to conduct clinical trials on early cervical cancer patients in 2018.



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