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The role of thyroid hormone(T3)in chondrocytes and osteoblasts to control bone development and maintenance,but the signaling pathways that regulate these functions is not clear.Recently,Imperial College London,UK,Graham R.Williams,who found that mutation of the thyroid hormone receptor(TRβPV)can activate Wnt signaling in bone in the body,and to clarify the interaction between T3 and Wnt signaling pathway during bone development.Related papers published in the March 22,"Resident Weekly"(Journal of Biological Chemistry).

The dominant negative mutant T3 receptors(TRβPV)can not be combined with the T3 to interfere with the function of wild-type TR,ThrbPV/the PV mouse pituitary thyroid axis is severely damaged,and elevated levels of thyroid hormones.ThrbPV/PV mice through an unknown mechanism to accelerate bone development.The researchers used microarray from the wild-type mice and ThrbPV/PV mice osteoblasts.Confirmed by in situ hybridization analysis of skeletal Wnt target gene expression ThrbPV/PV mice in the post-natal growth period activation of Wnt signaling.In contrast,T3 treatment can inhibit osteoblasts Wnt signaling,suggesting that T3 by promoting proteasomal degradation ofβ-catenin,preventing its accumulation in the nucleus,thereby inhibiting the Wnt signaling pathway.The in ThrbPV/PV mice,however,the Wnt signaling pathway is activated,stabilizedβ-catenin due to the function TRβPV.

This study illustrates the interaction between T3 and Wnt signaling pathways in regulating bone development and formation.
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- Bone during the development of T3 and Wnt signaling pathway interactions

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 Important factor-mediated TGF-βand AKT signaling pathway crosstalk Alerter l'administrateur Recommander à un ami Lien de l'article 

Transforming growth factor-βtype 1 receptor(transforming growth factor-βof type I receptor TβRI)determine the level of TGF-βsignaling pathway in the cell membrane localization and stability.SMAD7-SMURF2 complex to targeting TβRI,and its degradation through the ubiquitin pathway. In this paper researchers through the genome-wide functional screening,ubiquitin specific protease 4(ubiquitin-specific protease,USP4)can enhance the level of TGF-βsignaling pathway.USP4 be able to directly interact with TβRI and prevent its ubiquitination degradation pathway,so that the cell membrane surface of TβRI maintained at a high level.The removal USP4 can weaken the process of transforming epithelial cells by TGF-βpathway mediated by mesenchymal cells. It is worth noting that the poor prognosis of breast cancer related to AKT protein(ie,directly and USP4 role of protein kinase B)phosphorylation,phosphorylation USP4 to reposition,transfer from the nucleus to the cytoplasm and membrane,stability is very important for the maintenance of USP4.The researchers also found that to remove USP4 and inhibition of the TβRI kinase can inhibit AKT-mediated breast cancer cell migration. This study reveals USP4 is the decisive factor of the TGF-βpathway and the AKT pathway crosstalk and provide a new way to prevent and control the AKT-mediated breast cancer cell metastasis.

  Aucun commentaire | Ecrire un nouveau commentaire Posté le 04-07-2012 à 05h20

 Liver exists an alternate signal path of the regulation of glucose metabolism Alerter l'administrateur Recommander à un ami Lien de l'article 

After a meal,Insulin will interrupt the glucose production in the liver, however, when the body to produce insulin resistance, the body will be a problem when the insulin is no longer effective in lowering blood glucose. The research team has confirmed that the liver in the absence of Akt1 and Akt2 gene in mice will not only generate insulin resistance, and loss of response to high sugar diet. These mice, blood sugar in the diet will still be maintained at a high level. In the body when the lack of Akt, another gene Foxo will continue to play a role, so that the liver that "the body in a fasting state. In response, the liver will continue to generate glucose for the cells continued to supply energy-rich molecules. Now, however, the article's senior author, Professor Morris Birnbaum, deputy director of the IDOM, said: "In further experiments, we had expected that Akt and Foxo gene knock out mice in the supply of food will be due to Akt and Foxo missing in the metabolic to maintain the fed state, however, we were surprised to find that the liver of these mice in the diet to make a normal response, so we are not only questioned the case of Akt and Foxo-deficient Are there any other mechanism for regulation of liver glucose production ? " These results undoubtedly Birnbaum laboratory 10 years ago hepatic metabolism before and after the classic model of contradictions. Birnbaum team confirmed that Akt protein is absolutely necessary for normal insulin signaling pathway. Today, the research team to guess that there must be an alternative signaling pathway to regulate glucose metabolism in the liver. 10 years ago, Birnbaum research group in a study published in the journal Science describes Akt2 protein inactivation will lead to diabetic mice. The researchers pointed out that the insulin can not play a role in fat cells and liver of these mice. This suggests that Akt is a necessary condition for insulin to function properly. Since then, turn off the Foxo1 by Akt, is widely regarded as the signaling pathways of insulin regulation of blood sugar. In particular, when Foxo1 gene is turned on, will promote glucose production. After feeding, machine experience inhibition of Akt Foxo1 activity, which stops glucose production, and ensure that blood glucose is maintained within a safe range. Birnbaum said: "Initially, we carry out the purpose of the current experiment is to see how this signaling pathway applied to other areas of metabolic regulation, which we would expect to see in the literature on the basis of the results." Why do animals need to seemingly redundant signaling pathways? The researchers believe that the situation should be in the fasting and postprandial insulin receptors of other organizations have played a role in communication with the liver. The organ is the brain of this candidate. Other laboratory research results show that the brain insulin receptor, indicating that perhaps the existence of such a signal, however, many scientists have been reluctant to accept the view of this conflicting data. Birnbaum laboratory results explain why scientists are difficult to find a backup signaling pathway: destruction of insulin signaling in the liver, the organ will lose the ability to respond to external signals. The team speculates that the body under normal circumstances, most of the time Foxo are turned off, but in the diabetic state, Foxo was not properly activated. Foxo gene open, non-normal state, the machine experience to stop issued by the liver, the brain glucose synthesis start or stop signal to respond. The research team is working to verify this hypothesis.

  Aucun commentaire | Ecrire un nouveau commentaire Posté le 06-07-2012 à 05h26

 Latest research to reveal the mechanism of CD37-mediated apoptosis Alerter l'administrateur Recommander à un ami Lien de l'article 

Four transmembrane proteins(Tetraspannin)is a cell death trigger factor,is also a potential target for cancer treatment.May 14,the famous magazine of the International Oncology Cancer Cell published a research paper of the Ohio State University research team led by John C.Byrd Tetraspanin CD37 the Directly Mediates Transduction of Survival and Apoptotic Signals". The study showed that the Tetraspanin family members of the CD37 molecule expression in mature or transformed B-cell surface under normal circumstances,activation of the tyrosine phosphorylation can be connected to each other.This phosphorylation event of CD37 with neighboring molecules linked to triggering apoptosis cascade reaction. Even more interesting is that the researchers also found that two of the CD37 molecule on the opposite regulatory function of tyrosine sites:one located in the N-terminal immunoreceptor tyrosine-based inhibitory motif(ITIM)-like motif region,mediated the SHP1 dependent on the death;another in the C-terminal immunoreceptor tyrosine-based activation motif(ITAM)-like motif region mediated through the phosphatidylinositol ring has six alcohol-3-kinase-dependent survival of antagonistic death signal.

  Aucun commentaire | Ecrire un nouveau commentaire Posté le 09-07-2012 à 09h04

 Japanese study found that promote nerve regeneration in C. elegans protein Alerter l'administrateur Recommander à un ami Lien de l'article 

July 4th, Nagoya University, Japan Graduate School of Matsumoto Bang Hung and colleagues in the British journal "neural science" (Nature, Neuroscience,) network version of the report said, they study the nematode body of about 15,000 proteins, found in nerve cells external inductionthis proliferation of secreted proteins and is located within the nerve cell membrane receptor proteins in axonal regeneration plays an important role. The combination of these two proteins can help to axonal regeneration.   Nematode nerve cells raised the matter - the axons after the accident fracture, a small number of axons magically composite recycling. How they do it? Japanese researchers found that this "again later thanks to the special role of the two proteins.   The nerve axon is the output channels of the nerve cells responsible for the cell issued by the transmission of nerve impulses to other nerve cells or muscle, glands. If the axon is completely broken, the nerve can no longer play a role.   In the experiment, the researchers through genetic manipulation, so that the nematodes can be a lot of synthesis of these two proteins, and then cut off their axons. Finally, in 40-60% of the axons can regenerate disconnected axons. Under normal circumstances, the C. elegans axon is cut off, only 5 percent renewable.   States Hiroshi Matsumoto, the function of some human proteins may be similar with the two nematode proteins, such as to promote regeneration of these human proteins in future studies to confirm efficacy and injected into specific parts of the nerve damage, it is possible to make the neural complex regeneration of serious injuries

  Lire les 5 commentaires | Ecrire un nouveau commentaire Posté le 11-07-2012 à 05h32

 With dengue shock syndrome-related mutations Alerter l'administrateur Recommander à un ami Lien de l'article 

Recently,researchers found a genetic variation associated with dengue shock syndrome,and new results are published in the online publication of Nature-Genetics journal.Dengue shock syndrome is a life-threatening serious illness,children suffering from dengue fever often this happens. Martin Hibberd and colleagues,the pan-genome study of 2008 cases of Dengue shock syndrome in children from Vietnam,and 1737 cases of children with repeat these studies.Dengue fever in children in vivo,they identified two dengue shock syndrome susceptibility loci.One is located in the MHC region,which contains many genes related to the regulation of the immune system.The second correlation PLCE1 region containing the mutation,the variability of the region and the nephrotic syndrome.

  Lire le commentaire | Ecrire un nouveau commentaire Posté le 13-07-2012 à 04h46

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  Blog créé le 02-07-2012 à 09h19 | Mis à jour le 14-12-2012 à 10h12 | Note : Pas de note