Important association of estrogen receptor binding site variation women with bipolar disorder.

Depression is two times of women compared with men. In bipolar disorder, depressive episodes in female patients reported more common. In addition, depression often and hormonal fluctuations period. Hormone signal connection between these emotional obstacles, therefore, is considered in many studies. Estrogen, a major female hormone, and its effect mainly by binding to estrogen receptors (ERs). Nuclear ers function as a transcription factor and regulating gene transcription is bound to a specific DNA sequence. A nucleotide changes may change the binding of binding sequence efficiency, this may affect the adjacent gene transcription level. To investigate if the variable ER DNA binding sequence may be involved in emotional obstacles, we performed a genome-wide research the patient's ER DNA binding diagnosed with depression or bipolar disorder. Association study in each gender separately, the result is more than the correct Bonferroni test method. In the women's bipolar affective disorder material significant results are found rs6023059 association (correction p-value = 0.023; odds ratio (or 0.681, 95% confidence interval (CI) 0.570-0.814), a single nucleotide polymorphisms (SNPS) placed tream genes encoding transglutaminase 2 (TGM2). Therefore, women with a specific genotype in the SNP may be more prone to fluctuation of estrogen level, which can act as a trigger factors on bipolar affective disorder.

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Function characteristics of naturally occurring transglutaminase 2 mutant and early onset of type 2 diabetes.

Transglutaminase 2 (TG2) is a kind o enzyme and different biological function. Transamidation TG2 catalytic reaction, has intrinsic kinase activity, and ACTS as a g protein within the cell signal. TG2 (Tgm2) null mice blood glucose intolerance, damaged biology insulin secretion (GSIS). In addition, three naturally occurring missense mutation, gene in human TGM2 corresponding Met330Arg amino acid substitutions, Ile331Asn, Asn333Ser TG2 in protein, report and found to be related to the type 2 diabetes and early onset. However, their influence is still not fully understand TG2 function. In order to prove this point, we have again naturally occurring mutation site-directed mutagenesis TG2 use. In the INS - 1 e express Myc - TG2 mutant cells leads to reduce GSIS and cell excessive expression compared with wild type Myc - TG2 (WT - TG2). The biggest decrease was found in cell excessive express Ile331Asn - TG2 (32%), the second is Met330Arg - TG2 (20%), at least in the Asn333Ser - TG2 (7%). Enzyme analysis suggests that transamidation TG2 mutant damaged and kinase activity and WT - TG2 compared. Tests show the GTP binding TG2 mutant also changed the GTP binding ability, it is found that modulation response glucose stimulation. In general, these data show that naturally occurring mutations affecting the transamidation TG2, kinase, GTP binding TG2 function. Although reduce insulin secretion, because naturally occurring mutations, is due to TG2 detract from more than one biological function, it is transamidation TG2 function, it seems to be in the first stage is impaired, and GTP binding function will affect the second stage of insulin secretion.

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Transglutaminase 2 and the nf-kappa B: a strange couples, shape breast cancer phenotype.

Because many professional survival target genes, abnormal activation of the nf-kappa B transcription factor is a kind of drug resistance phenotypic correlation and aggressive breast cancer behavior. 

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, a ubiquitously expressed protein crosslinking enzyme, activate the nf-kappa B through the unconventional mechanism, disable I κ B α inhibitors. Our company recently records, TG2 genes (known as TGM2) is a direct nf-kappa B transcription goal. These development uncover a self-enforcing molecular feedback loop, novel nf-kappa B TG2 activation, in turn, the nf-kappa B direct upregulates TGM2 transcription. The manuscript of the literature review, support are TG2 / nf-kappa B signal cycle, nature of the signal transduction, activate the circulation, and phenotypic consequences from abnormal activation of the novel signal mechanism in breast cancer

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Branch geometric induced lung automatic adjustment of growth.

Branch morphogenesis is a widely distributed in natural phenomenon. In organogenesis, which results in uneven growth, leading to the epithelium single branch into the surrounding mesoderm repeat. Lung morphogenesis is a landmark case, tree organogenesis the most common mammals. The core network is very sure, especially Fgf10 / SHH couples, need to start and the maintenance branch. In the previous study, we show that limit Fgf10 expression domain hiss distal interstitial spontaneously entice differential epithelial hyperplasia lead to branch. A simple Laplacian model copy FGF10 qualitative dynamic interstitial and spontaneous self avoid branch morphogenesis. However, the early lung cancer geometry several conspicuous features, remain to be resolved. In this paper, we mainly research, through the simulation and analysis of data, if FGF10 - diffusion in the scene of the following aspects of the lung morphology: size dispersion, asymmetric branch events and distal epithelium mesothelium balance. We report said, they appear in the model of spontaneous, and most of the bottom mechanism can be understood as dynamic gradient and the interaction between the shape. This shows that the specific provisions may not need these emergent compelling geometrical characteristic

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Teeth agenesis association claims to have a family history of cancer.

It has been put forward, the tooth agenesis and cancer development has a common molecular pathways. We conducted a cross-sectional study survey of molecular epidemiology and the correlation between and readme teeth agenesis of the cancer family history. Eighty-two people with tooth agenesis and 328 people do not have the same institution of recruiting birth defects. Teeth dysplasia is evaluation in permanent teeth and definition based on participants' age, when the initial form teeth should radiology visible. We also investigated the action of the genes involved in dental development involved in tumorigenesis and 14 mark, FGF3 AXIN2, FGF10, FGFR2 were genotyped. Teeth agenesis people have greater risks have a family history of cancer (p = 0.00006; or = 2.7; 95% ci, 1.6 to 4.4). A connection between AXIN2, FGF3, FGF10, and teeth agenesis (or FGFR2. Personal carry polymorphism allelic FGFR2 (rs1219648) puts forward higher risk have premolar hypoplasia (p = 0.02; or = 1.8; 95% ci, 1.1-3.0)]. In a word, the tooth dysplasia is and positive self report of cancer family history and variant in AXIN2, FGF3,FGF10, FGFR2. Prospective study is needed to confirm if the teeth agenesis can be used as a risk marker for cancer.

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imulation demonstrates a simple network enough to control branch point selection, vascular smooth muscle and the formation of the system in the lung branch morphogenesis.

Appropriate lung function not only need a proper structure of conductive airway tree, but also the development of the smooth muscles and blood vessels. Lung branch morphogenesis strong rigidity and includes recursive use only three kinds of modes of the branch. We've confirmed that the interaction between the description fibroblast growth factor (FGF) 10, sonic hedgehog (SHH) and repair (Ptc) can produce a Turing machine system, not only breeding experimental observation to the wild type branching pattern, part of the reason is counterintuitive, pattern in the mutant mice. Here we show that although many protein influence the formation of smooth muscle and Vegfa expression, an inducer formation of blood vessels, it is enough to FGF9 added to the FGF10 / boo/Ptc module successfully predicted at the same time appear smooth muscle growth between crystallization, Vegfa lung bud expression in the distal joint epithelial cells stroma. Our model reproduces the phenotype, and related mutant mice wild type, and most of the culture conditions described in the literature

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