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kill zombie cells can help stay young

Posted by star on 2018-01-14 22:59:49
Hits:149

         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 improv......

ELISA kit for Interleukin-2 and IL-2 receptors

Posted by star on 2018-01-08 21:56:14
Hits:278

          IL-2 (interleuin-2) is a kind of Interleukin, mainly produced by T cells or T cell lines. It is a type of cell growth factor in the immune system. It can regulate the activity of white blood cells in the immune system, promote the proliferation of Th0 and CTL. It participates in antibody response and the moderation of haematogenesis function. It also plays an important role in oncological surveillance. 

          IL-2 is part of the body's natural response to microbial infection, IL-2 mediates its effects by binding to IL-2 receptors, which is a heterotrimeric protein expressed on the surface of certain immune cells, such as lymphocytes. IL-2R consist of three chains : α(also called IL-2Rα, CD25, or Tac antigen), β  (also called IL-2Rβ, or CD122), and γ (also called IL-2Rγ, γc, common gamma chain, or CD132).

 

           Welcome to choose and purchase the related products from Wuhan Eiaab Science Co.,Ltd , we have ELISA kit for Interleukin-2 and IL-2 receptors , which origin from different species, such as human, bovine, dog, pig, mouse, rat and rabbit.



High salt intake changes the gut flora in mice

Posted by star on 2018-01-07 17:27:50
Hits:126

         November 16, "Nature" online published a report that high salt intake will change the intestinal flora of mice. The above findings highlight the potential of gut microbiomes as potential therapeutic targets for salt-resistant diseases, given the growing acceptance of gut flora in the disease.

         High salt intake, which is linked to modern lifestyles, may lead to hypertension and cardiovascular disease. TH17 cells may also be linked to hypertension by inducing autoimmunity by proinflammatory TH17 cells.

        To determine the effect of high salt intake on gut flora, Dominik Müller and colleagues at the Max Breck Molecular Institute in Berlin, Germany, analyzed fecal samples from mice fed normal-salt and salt-fed diets. As a result, it was found that on the 14th day, there was a significant reduction in various microorganisms in mice fed high salt diet. Later, they used 16S ribosomal DNA sequencing and computational methods to identify the most important reduced flora and found that one Lactobacillus murinus was most associated with high-salt foods.

        Further studies showed that injection of Lactobacillus murinus into mice decreased TH17 cells and prevented salt-induced exacerbation of actively-induced experimental autoimmune encephalomyelitis (encephalitis mouse model) and salt-sensitive hypertension. Another small pilot study in healthy humans found that increasing salt intake reduced the survival of a wide range of Lactobacilli bacteria with an increase in TH17 cells and an increase in blood pressure, consistent with the above findings. However, further research is needed in humans.

 




 

           Tumor metabolic reprogramming and abnormal cell cycle regulation are two important characteristics of tumors. However, it is unclear how the two are coordinated to promote tumor cell proliferation and tumor development. This team found for the first time that in tumor cells, Plk1, an important cyclic regulatory protein, regulates the activity of G6PD, a key metabolic enzyme in the pentose phosphate pathway, and thus promotes the synthesis of biological macromolecules and the proliferation of tumor cells both in vitro and in vivo. Further mechanistic studies revealed that Plk1 modifies G6PD by binding and phosphorylation, resulting in an increase of G6PD-forming dimers, thereby promoting enzyme activity and the entire pentose phosphate pathway. Enhanced pentose phosphate pathway for tumor cell cycle progression and the occurrence and development of tumors have an important role in promoting. This study, for the first time, uncovered the new function of Plk1 in the regulation of biological macromolecule synthesis, revealed a new mechanism of coordination between metabolic reprogramming and cycle regulation and promotion of rapid proliferation of tumor cells, and potential therapeutic targets for clinical tumor Guiding significance.

          Wuhan EIAab Science Co., Ltd is advantage in technology, product, dedicated to provide quality and reliable for all users of products. There are some related products sold in our company related to this paper, such as Plk1(E1662h)、G6PD(E0716h) etc.

         doi:10.1038/s41467-017-01647-5

 

 

 



iNKT cells induces weight loss and restores glycemic control in obesity

Posted by star on 2017-12-27 17:24:05
Hits:116

         Obesity threatens to shorten the human lifespan by 5–20 years and refers to many aspects of biology ,rather than that was previously appreciated, What’s worse is the obesity-induced diseases. Currently, therapy for curing obesity is limited by fully understanding of the mechanism for controlling obesity.

         A promising potential approach for treating obesity is activation of brown adipose tissue (BAT). In contrast to energy-storing white adipose tissue (WAT), BAT contains many thermogenic mitochondria which secretes uncoupling protein 1 (UCP-1) that converted chemical energy into heat, Recent studies have defined the role of the adipose innate immune system in the regulation of metabolism and control of body weight, Invariant natural killer T ( iNKT ) cells are one such innate immune cell type with an important role in weight and glycemic control.

         iNKT cells are key player in metabolic regulation, iNKT cells are innate lipid sensors , using their prototypic ligand  a-galactosylceramide  (aGalCer) to being activtion can lead to weight loss and glycemic control. Here, iNKT activation induced fibroblast growth factor 21 (FGF21) production and thermo-genic browning of white fat. Complete metabolic analysis revealed that iNKT cell activation induced increased body temperature and fatty acid oxidation, without affecting food intake or activity. FGF21 induction played a major role in iNKT cell-induced weight loss, as FGF21 null mice lost significantly less weight after aGalCer treatment. The glucagon-like peptide 1 (GLP-1) receptor agonist-liraglutide also activated iNKT cells in humans and mice. In iNKT-deficient mice, liraglutide    promoted satiety but failed to induce FGF21, which resulting in less weight loss. These findings indicates an iNKT cell-FGF21 axis may defines a new immune-mediated pathway that could ......

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