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<channel>
	<title>Molecular Staging</title>
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	<link>http://molecularstaging.aussieblogs.com.au</link>
	<description>Molecular Staging is addressing this demand with a portfolio of products and services based on technologies that are transforming the detection and measurement of both proteins and nucleic acids.</description>
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		<title>Parallel evolution of the venom of snakes and integrin</title>
		<link>http://molecularstaging.aussieblogs.com.au/2012/12/26/parallel-evolution-of-the-venom-of-snakes-and-integrin/</link>
		<comments>http://molecularstaging.aussieblogs.com.au/2012/12/26/parallel-evolution-of-the-venom-of-snakes-and-integrin/#comments</comments>
		<pubDate>Thu, 08 Apr 2010 06:55:33 +0000</pubDate>
		<dc:creator>Aussie Blogs</dc:creator>
				<category><![CDATA[Bioscience]]></category>
		<category><![CDATA[Biomedicine]]></category>
		<category><![CDATA[Institute]]></category>
		<category><![CDATA[integrin]]></category>
		<category><![CDATA[snakes]]></category>
		<category><![CDATA[Structural Proteomics Group]]></category>
		<category><![CDATA[venom]]></category>

		<guid isPermaLink="false">http://molecularstaging.com/?p=855</guid>
		<description><![CDATA[Structural Proteomics Group, Institute of Biomedicine of Valencia (CSIC) develops several years studies on the evolution and functional characteristics of different proteins from the venom of snakes, from the Mediterranean region. These proteins selectively block the function of cell surface receptors of the integrin family. Becoming available and genomic libraries of tissues and many different [...]]]></description>
				<content:encoded><![CDATA[<p><img src="http://molecularstaging.aussieblogs.com.au/files/2010/04/images24.jpeg" alt="images24" title="images24" width="146" height="136" class="alignleft size-full wp-image-856" align="left" />Structural Proteomics Group, Institute of Biomedicine of Valencia (CSIC) develops several years studies on the evolution and functional characteristics of different proteins from the venom of snakes, from the Mediterranean region. These proteins selectively block the function of cell surface receptors of the integrin family.</p>
<p>Becoming available and genomic libraries of tissues and many different agencies. In this case, researchers in Valencia have been cloned and sequenced cDNA fragments of the venom-producing gland in Cerastes Viper and short disintegrins encoding and subunits of dimeric disintegrins.<span id="more-855"></span> From the analysis of messenger RNA conclude that these molecules could be distributed over a larger number of tissue than initially believed. Furthermore, sequence comparison suggests a common ancestor for short disintegrins for dimeric disintegrins precursor chains. </p>
<p>The most interesting part of the study is that for the first time, shows the parallel evolution of the blocking sequence of the disintegrins from the venom of snakes and integrin alpha chains, which are cellular receptors. Also presented are specific patterns of evolutionary adaptation of the antagonists of snake venom ligand regions of the integrin receptor. </p>
<p>These studies are also directly related to the laboratory can produce potent inhibitors of angiogenesis, which could be used in the design of new ant tumor drugs directed against surface receptors of cancer cells.</p>
<h4>This page was tagged:</h4><ul><li><a href="http://molecularstaging.aussieblogs.com.au/2012/12/26/parallel-evolution-of-the-venom-of-snakes-and-integrin/" title="parallel evolution of snakes">parallel evolution of snakes</a></li></ul>]]></content:encoded>
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		<item>
		<title>Complex networks of stress and tumors</title>
		<link>http://molecularstaging.aussieblogs.com.au/2012/12/25/complex-networks-of-stress-and-tumors/</link>
		<comments>http://molecularstaging.aussieblogs.com.au/2012/12/25/complex-networks-of-stress-and-tumors/#comments</comments>
		<pubDate>Thu, 08 Apr 2010 06:50:19 +0000</pubDate>
		<dc:creator>Aussie Blogs</dc:creator>
				<category><![CDATA[Bioscience]]></category>
		<category><![CDATA[DNA]]></category>
		<category><![CDATA[biological process]]></category>
		<category><![CDATA[Cancer]]></category>
		<category><![CDATA[Complex networks]]></category>
		<category><![CDATA[stress]]></category>
		<category><![CDATA[tumors]]></category>

		<guid isPermaLink="false">http://molecularstaging.com/?p=851</guid>
		<description><![CDATA[Cancer, such as biological process that goes beyond the laws of development and cellular growth, requires relocation process and investigate molecular mechanisms that lead to uncontrolled cell division, genomic instability and tumor development. The identification of these new patterns of growth and development can be very important to understand and combat processes tumorogénesis.1 It appears [...]]]></description>
				<content:encoded><![CDATA[<p><img src="http://molecularstaging.aussieblogs.com.au/files/2010/04/images23.jpeg" alt="images23" title="images23" width="143" height="153" class="alignleft size-full wp-image-852" align="left" />Cancer, such as biological process that goes beyond the laws of development and cellular growth, requires relocation process and investigate molecular mechanisms that lead to uncontrolled cell division, genomic instability and tumor development. The identification of these new patterns of growth and development can be very important to understand and combat processes tumorogénesis.1 It appears from research such as referenced here, the Cdc6 and other cellular components are joined, forming complexes prerreplicativos before initiated DNA duplication. <span id="more-851"></span></p>
<p>The coupling of these protein structures determined at what point is the origin of initiation of DNA replication. Described the mechanism directly involved in the regulation of a locus, under conditions of cellular stress, which seems essential to avoid the initiation of tumor growth: Ink4/Arc locus, coding for three tumor suppressor. Previously had been proposed that certain alterations in this gene could cause the appearance of tumores.2 The description of this genomic region as a regulator opens new avenues in drug research and avoid blocking the inactivation of tumor suppressor involved . </p>
<p>These new lines, followed by young researchers (increasingly more often, in our own country), to suggest alternatives to regulate senescence and apoptosis processes as yet unidentified, may represent the key to investigations not too remote in time pointing in a more accurate and effective in preventing tumors right there where its true origin or desencadenamiento.3 A tool and an approach to take into account.</p>
<h4>This page was tagged:</h4><ul><li><a href="http://molecularstaging.aussieblogs.com.au/2012/12/25/complex-networks-of-stress-and-tumors/" title="dna sequencing">dna sequencing</a></li><li><a href="http://molecularstaging.aussieblogs.com.au/2012/12/25/complex-networks-of-stress-and-tumors/" title="molecular relationship between cell division and development of cancer">molecular relationship between cell division and development of cancer</a></li><li><a href="http://molecularstaging.aussieblogs.com.au/2012/12/25/complex-networks-of-stress-and-tumors/" title="séquençage principe Sanger ADN">séquençage principe Sanger ADN</a></li><li><a href="http://molecularstaging.aussieblogs.com.au/2012/12/25/complex-networks-of-stress-and-tumors/" title="sanger-coulson method of dna sequencing">sanger-coulson method of dna sequencing</a></li><li><a href="http://molecularstaging.aussieblogs.com.au/2012/12/25/complex-networks-of-stress-and-tumors/" title="sanger sequencing">sanger sequencing</a></li><li><a href="http://molecularstaging.aussieblogs.com.au/2012/12/25/complex-networks-of-stress-and-tumors/" title="proteína SCC1">proteína SCC1</a></li><li><a href="http://molecularstaging.aussieblogs.com.au/2012/12/25/complex-networks-of-stress-and-tumors/" title="molecular relationships between cancer and cell division">molecular relationships between cancer and cell division</a></li><li><a href="http://molecularstaging.aussieblogs.com.au/2012/12/25/complex-networks-of-stress-and-tumors/" title="maxam gilbert sequencing">maxam gilbert sequencing</a></li><li><a href="http://molecularstaging.aussieblogs.com.au/2012/12/25/complex-networks-of-stress-and-tumors/" title="DNA sequencing 35S 32p">DNA sequencing 35S 32p</a></li><li><a href="http://molecularstaging.aussieblogs.com.au/2012/12/25/complex-networks-of-stress-and-tumors/" title="sequenciation sanger method">sequenciation sanger method</a></li></ul>]]></content:encoded>
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		<title>New mechanism of regulation of tumor suppressor</title>
		<link>http://molecularstaging.aussieblogs.com.au/2012/12/25/new-mechanism-of-regulation-of-tumor-suppressor/</link>
		<comments>http://molecularstaging.aussieblogs.com.au/2012/12/25/new-mechanism-of-regulation-of-tumor-suppressor/#comments</comments>
		<pubDate>Thu, 08 Apr 2010 06:38:54 +0000</pubDate>
		<dc:creator>Aussie Blogs</dc:creator>
				<category><![CDATA[Bioscience]]></category>
		<category><![CDATA[News]]></category>
		<category><![CDATA[CNIO]]></category>
		<category><![CDATA[congratulabamos]]></category>
		<category><![CDATA[mechanism]]></category>
		<category><![CDATA[Molecular Biology]]></category>
		<category><![CDATA[the laboratories]]></category>
		<category><![CDATA[tumor suppressor]]></category>

		<guid isPermaLink="false">http://molecularstaging.com/?p=847</guid>
		<description><![CDATA[In our earlier &#8220;A Fund&#8221; section opened with the analysis of a Spanish paper published in Nature (Ferris Marco et al., 2006). And we congratulabamos therefore it is still uncommon to see in that publication a study conducted entirely by Spanish investigators. It seems that our discussion had taken effect in the minds of so [...]]]></description>
				<content:encoded><![CDATA[<p><img src="http://molecularstaging.aussieblogs.com.au/files/2010/04/images22.jpeg" alt="images22" title="images22" width="154" height="143" class="alignleft size-full wp-image-848" align="left" />In our earlier &#8220;A Fund&#8221; section opened with the analysis of a Spanish paper published in Nature (Ferris Marco et al., 2006). And we congratulabamos therefore it is still uncommon to see in that publication a study conducted entirely by Spanish investigators. It seems that our discussion had taken effect in the minds of so renowned editorial publication, and this month we have an equivalent opportunity to rejoice at the appearance of another article malignancy in Spanish on the British magazine par excellence. This time it&#8217;s a research on the regulation of a tumor suppressor locus.<span id="more-847"></span></p>
<p>The research was led by Manuel Serrano, one of the young scientists with their own research group at the CNIO, and the development of work have helped other groups in the center of cancer research, as well as Salamanca and Hospital October 12 . It appears that the work that led to the consolidation of the CNIO in 2003 is bearing fruit, with a handful of scientists are particularly active in leading-edge research on cancer, and their roots in the valuable work of training young researchers carried out especially by Margarita Salas and Gins Morata, among others, during the past two decades from the laboratories of the Center for Molecular Biology Severo Ochoa.</p>
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		<item>
		<title>Biosynthesis of essential amino acids</title>
		<link>http://molecularstaging.aussieblogs.com.au/2012/12/24/biosynthesis-of-essential-amino-acids/</link>
		<comments>http://molecularstaging.aussieblogs.com.au/2012/12/24/biosynthesis-of-essential-amino-acids/#comments</comments>
		<pubDate>Thu, 08 Apr 2010 06:31:31 +0000</pubDate>
		<dc:creator>Aussie Blogs</dc:creator>
				<category><![CDATA[Bioscience]]></category>
		<category><![CDATA[News]]></category>
		<category><![CDATA[amino acids]]></category>
		<category><![CDATA[Biosynthesis]]></category>
		<category><![CDATA[isoleucine]]></category>
		<category><![CDATA[Lysine]]></category>
		<category><![CDATA[methionine]]></category>
		<category><![CDATA[Molecular Biology]]></category>
		<category><![CDATA[threonine]]></category>

		<guid isPermaLink="false">http://molecularstaging.com/?p=843</guid>
		<description><![CDATA[Mammals are unable to synthesize metabolically various amino acids necessary for protein synthesis and should incorporate foods from the diet. These amino acids are called essential. Photosynthetic organisms can synthesize it. Has long been accepted that the metabolic pathways involved in the biosynthesis of amino acids in plants are identical to those in microorganisms. However, [...]]]></description>
				<content:encoded><![CDATA[<p><img src="http://molecularstaging.aussieblogs.com.au/files/2010/04/images21.jpeg" alt="images21" title="images21" width="142" height="141" class="alignleft size-full wp-image-844" align="left" />Mammals are unable to synthesize metabolically various amino acids necessary for protein synthesis and should incorporate foods from the diet. These amino acids are called essential. Photosynthetic organisms can synthesize it. Has long been accepted that the metabolic pathways involved in the biosynthesis of amino acids in plants are identical to those in microorganisms. However, recent results indicate significant differences and a higher level of complexity due to the existence of multiple enzymes that are distributed in different subcellular compartments. <span id="more-843"></span></p>
<p>Lysine, threonine, methionine and isoleucine are essential amino acids that share the common precursor aspartate and which are synthesized in the chloroplasts of plant leaves or in the plastids of non-photosynthetic organs, such as seeds and roots. Until now it was believed that the aspartate was synthesized by the action of aspartate aminotransferase similar to that in mammals, although gene knockout mutants did not show any phenotype. </p>
<p>A study carried out in the Department of Biochemistry and Molecular Biology, University of Malaga has demonstrated the existence in plastids of plants of another form of aspartate aminotransferase enzyme very similar to cyanobacteria and has greater affinity for the enzyme glutamate previously characterized. In an article published in Plant Journal, the authors propose that the physiological role of this new enzyme is the conversion of glutamate to aspartate for the biosynthesis of lysine, threonine, methionine and isoleucine. It is estimated that about 18% of plant genes derived from cyanobacteria. This gene transfer to plants by endosymbiotic event would explain the absence of this enzyme in animals and the essential nature of these amino acids in the diet.</p>
<h4>This page was tagged:</h4><ul><li><a href="http://molecularstaging.aussieblogs.com.au/2012/12/24/biosynthesis-of-essential-amino-acids/" title="biosynthesis of essential amino acids">biosynthesis of essential amino acids</a></li><li><a href="http://molecularstaging.aussieblogs.com.au/2012/12/24/biosynthesis-of-essential-amino-acids/" title="compartment and biosynthesis and isoleucine">compartment and biosynthesis and isoleucine</a></li></ul>]]></content:encoded>
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		<item>
		<title>Topoisomerase-II rolls better</title>
		<link>http://molecularstaging.aussieblogs.com.au/2012/12/24/topoisomerase-ii-rolls-better/</link>
		<comments>http://molecularstaging.aussieblogs.com.au/2012/12/24/topoisomerase-ii-rolls-better/#comments</comments>
		<pubDate>Tue, 06 Apr 2010 06:47:52 +0000</pubDate>
		<dc:creator>Aussie Blogs</dc:creator>
				<category><![CDATA[Bioscience]]></category>
		<category><![CDATA[chromosomes]]></category>
		<category><![CDATA[DNA]]></category>
		<category><![CDATA[molecules]]></category>
		<category><![CDATA[the coil voltage]]></category>
		<category><![CDATA[Topoisomerase-II]]></category>

		<guid isPermaLink="false">http://molecularstaging.com/?p=840</guid>
		<description><![CDATA[All processes of gene activity are accompanied by alterations in DNA helical tension. Consequently, the double helix twists on itself, or supercoiled to remain stable throughout its length. This tension may be very high during the processes of transcription and DNA replication, since the two strands, always linked in the double helix, are forced to [...]]]></description>
				<content:encoded><![CDATA[<p><img src="http://molecularstaging.aussieblogs.com.au/files/2010/04/7.jpeg" alt="7" title="7" width="144" height="135" class="alignleft size-full wp-image-841" align="left" />All processes of gene activity are accompanied by alterations in DNA helical tension. Consequently, the double helix twists on itself, or supercoiled to remain stable throughout its length. This tension may be very high during the processes of transcription and DNA replication, since the two strands, always linked in the double helix, are forced to separate, in part or total. Due to the enormous length and the large condensation of DNA molecules in chromosomes, the coil voltage can not dissipate spontaneously.<span id="more-840"></span> </p>
<p>The natural solution to the problem is offered by the so-called topoisomerases, resulting in transient cuts the strands of DNA to relax the tension coil. A team from the Institute of Molecular Biology of Barcelona, CSIC has described the mechanism by which stress relaxes when helical DNA is condensed into chromosomes. The results of work directed by Joaquim Roca and published in EMBO Journal contradict the general view of the role of topoisomerases. So far, it was believed that the topoisomerase-I was the main relaxing the DNA, while topoisomerase-II was the only function and trigger untangle DNA before dividing. This study demonstrates that topoisomerase-II is also the main relaxing of tension when the DNA is folded into chromosomes. </p>
<p>The key finding has been to discover the precise type of cut made by each enzyme DNA: features of the two strands of double helix-II topoisomerase cuts both, allowing another DNA chain nearby temporary pass through this gate that just opened. Thus, it relieves tension and knots are removed. By contrast, the topoisomerase-I just cut one strand, and therefore is not effective in reducing tension in the whole molecule.</p>
<h4>This page was tagged:</h4><ul><li><a href="http://molecularstaging.aussieblogs.com.au/2012/12/24/topoisomerase-ii-rolls-better/" title="joaquim roca csic">joaquim roca csic</a></li></ul>]]></content:encoded>
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		<title>Deficient and cell survival kinases</title>
		<link>http://molecularstaging.aussieblogs.com.au/2012/12/23/deficient-and-cell-survival-kinases/</link>
		<comments>http://molecularstaging.aussieblogs.com.au/2012/12/23/deficient-and-cell-survival-kinases/#comments</comments>
		<pubDate>Tue, 06 Apr 2010 06:40:22 +0000</pubDate>
		<dc:creator>Aussie Blogs</dc:creator>
				<category><![CDATA[Bioscience]]></category>
		<category><![CDATA[cell survival kinases]]></category>
		<category><![CDATA[Deficient]]></category>
		<category><![CDATA[interactions]]></category>
		<category><![CDATA[mechanisms]]></category>
		<category><![CDATA[various]]></category>

		<guid isPermaLink="false">http://molecularstaging.com/?p=835</guid>
		<description><![CDATA[Efforts to characterize the process of apoptosis, or programmed cell death, are probably one of the clearest examples to represent the inherent complexity of regulatory mechanisms and interactions between enzymes, signals and various growth factors in a cell. Among these mechanisms, the role played by the kinase p38aMAP object of interest is the group of [...]]]></description>
				<content:encoded><![CDATA[<p><img class="alignleft size-full wp-image-836" title="6" alt="6" src="http://molecularstaging.aussieblogs.com.au/files/2010/04/6.jpeg" width="138" height="92" align="left" />Efforts to characterize the process of apoptosis, or programmed cell death, are probably one of the clearest examples to represent the inherent complexity of regulatory mechanisms and interactions between enzymes, signals and various growth factors in a cell. Among these mechanisms, the role played by the kinase p38aMAP object of interest is the group of the Faculty of Pharmacy of the Universidad Complutense de Madrid, coordinated by Almudena Porras. In a paper published in the online edition of Cell Signal, this team has characterized cell lines derived from cardiomyocytes and mouse embryonic fibroblasts deficient in p38aMAP normal, with the aim to detect different responses to the process of apoptosis. <span id="more-835"></span></p>
<p>It is clear from the comments, p38aMAP deficient cells are more resistant to enter apoptosis, by reducing the expression of proapoptotic proteins Bax and Fas, and enhancing the expression of a specific pattern of survival. The results also show an increased Akt activity in these cells leads to increased survival time of p38aMAP deficient cardiomyocytes. Akt is a key protein complex in the path of cell survival by inhibiting apoptotic signals, with a clear implication in cancer and other diseases. The conclusions of the study postulated a possible modulator of Akt activity mediated by the kinase negatively p38αMAP through regulating the interaction between caveolin-1 and protein phosphatase PP2A that requires a binding mechanism in the cell membrane. One more example of the different and complex levels of interaction that control cell signaling patterns determination and fate of animal cells.</p>
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		<title>Who controls centrosome duplication?</title>
		<link>http://molecularstaging.aussieblogs.com.au/2012/12/23/who-controls-centrosome-duplication/</link>
		<comments>http://molecularstaging.aussieblogs.com.au/2012/12/23/who-controls-centrosome-duplication/#comments</comments>
		<pubDate>Tue, 06 Apr 2010 06:31:39 +0000</pubDate>
		<dc:creator>Aussie Blogs</dc:creator>
				<category><![CDATA[Bioscience]]></category>
		<category><![CDATA[CDK2]]></category>
		<category><![CDATA[Cdk2 deficiency]]></category>
		<category><![CDATA[centrosome]]></category>
		<category><![CDATA[contrast]]></category>
		<category><![CDATA[DNA]]></category>
		<category><![CDATA[duplication]]></category>
		<category><![CDATA[general scheme]]></category>

		<guid isPermaLink="false">http://molecularstaging.com/?p=831</guid>
		<description><![CDATA[The transition between each of the phases of the cell cycle is controlled by phosphorylation processes carried out by enzymes known as cyclin dependent kinase (CDK). In mammalian cells, the enzyme bound to CDK2 cyclin A acts as the main promoter of the transition from G1 to S phase cell cycle progression and S phase, [...]]]></description>
				<content:encoded><![CDATA[<p><img src="http://molecularstaging.aussieblogs.com.au/files/2010/04/5.jpeg" alt="5" title="5" width="150" height="147" class="alignleft size-full wp-image-832" align="left" />The transition between each of the phases of the cell cycle is controlled by phosphorylation processes carried out by enzymes known as cyclin dependent kinase (CDK). In mammalian cells, the enzyme bound to CDK2 cyclin A acts as the main promoter of the transition from G1 to S phase cell cycle progression and S phase, when DNA replication. Thus, the cyclin A-CDK2 complex binds to a large number of regulatory proteins at different times during cell cycle progression. <span id="more-831"></span></p>
<p>Within this general scheme, CDK2 has been proposed as a key regulator of centrosome duplication. Research published in Oncogene, with Spanish participation Mariano Barbacid group, the National Cancer Centre (CNIO), has used mouse embryonic fibroblasts with the Cdk2 gene deletions, to show the effect of this protein in the process of doubling DNA during the S phase The authors have observed that CDK2 is not required for normal duplication of centrosomes or for mitotic spindle formation.</p>
<p>By contrast, Cdk2 deficiency appears to suspend the aberrant centrosome duplication induced by the activity of a viral oncogene, used as a tool for determining mechanisms of progression and tumor development. The results indicate a differential requirement for CDK2 activity in normal and impaired duplication of centrosomes, suggesting a role of CDK2 in licensing requirements for aberrant duplication of centrosomes. The conclusions of the work affect the chances of CDK2 as a potential therapeutic target for inhibition of chromosomal instability associated with the development of tumor cells.</p>
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		<title>Tigar or how p53 controls glycolysis</title>
		<link>http://molecularstaging.aussieblogs.com.au/2012/12/22/tigar-or-how-p53-controls-glycolysis/</link>
		<comments>http://molecularstaging.aussieblogs.com.au/2012/12/22/tigar-or-how-p53-controls-glycolysis/#comments</comments>
		<pubDate>Tue, 06 Apr 2010 06:26:56 +0000</pubDate>
		<dc:creator>Aussie Blogs</dc:creator>
				<category><![CDATA[Bioscience]]></category>
		<category><![CDATA[glycolysis]]></category>
		<category><![CDATA[irreparable]]></category>
		<category><![CDATA[Oxidative Stress]]></category>
		<category><![CDATA[p53 protein]]></category>
		<category><![CDATA[Tigar]]></category>

		<guid isPermaLink="false">http://molecularstaging.com/?p=828</guid>
		<description><![CDATA[Catalan researchers of the Institute for Biomedical Research of Bellvitge in Barcelona and the Beatson Institute for Cancer Research in Glasgow, published in Cell the discovery of Tigar, the first gene involved in the antioxidant cellular mechanism associated with the prevention of tumor formation. This paper shows that low concentrations of p53 protein are sufficient [...]]]></description>
				<content:encoded><![CDATA[<p><img src="http://molecularstaging.aussieblogs.com.au/files/2010/04/4.jpeg" alt="4" title="4" width="143" height="144" />Catalan researchers of the Institute for Biomedical Research of Bellvitge in Barcelona and the Beatson Institute for Cancer Research in Glasgow, published in Cell the discovery of Tigar, the first gene involved in the antioxidant cellular mechanism associated with the prevention of tumor formation. This paper shows that low concentrations of p53 protein are sufficient to activate the gene Tigar. <span id="more-828"></span></p>
<p>Researchers have found that this gene acts as a reducer of glycolysis. p53 is operated against cellular stress. When the damage caused by cell stress is relatively mild, the p53 protein activates the mechanism of cell cycle arrest, resulting in the repair of DNA damage. If the damage is substantial or irreparable, p53 initiates the process of apoptosis. </p>
<p>One of the main agents that cause mutations in the DNA of cells are molecules called reactive oxygen species (ROS), which include the known free radicals. In case of mild cellular stress, p53 activates the gene Tigar, which decreases the rate of glycolysis and hence the presence of ROS in the cell. However, if cell stress is irreparable, it produces the opposite strategy and p53 induces a greater presence of ROS molecules to trigger apoptosis or cell death, preventing the proliferation of cells with altered DNA. </p>
<p>The authors have shown how, in the event of loss of Tigar, cells rapidly entered apoptosis with minimal stress. And propose a model of p53 function, whereby at first, after oxidative stress, this protein activated the antioxidant gene Tigar to gain control of ROS molecules and facilitate DNA repair before they increase the stress and will trigger a possible tumor proliferation.</p>
<h4>This page was tagged:</h4><ul><li><a href="http://molecularstaging.aussieblogs.com.au/2012/12/22/tigar-or-how-p53-controls-glycolysis/" title="tigar p53">tigar p53</a></li><li><a href="http://molecularstaging.aussieblogs.com.au/2012/12/22/tigar-or-how-p53-controls-glycolysis/" title="p53 activates tigar">p53 activates tigar</a></li><li><a href="http://molecularstaging.aussieblogs.com.au/2012/12/22/tigar-or-how-p53-controls-glycolysis/" title="tigar or">tigar or</a></li></ul>]]></content:encoded>
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		<title>Molecular link between aging and cancer</title>
		<link>http://molecularstaging.aussieblogs.com.au/2012/12/22/molecular-link-between-aging-and-cancer/</link>
		<comments>http://molecularstaging.aussieblogs.com.au/2012/12/22/molecular-link-between-aging-and-cancer/#comments</comments>
		<pubDate>Tue, 06 Apr 2010 06:21:06 +0000</pubDate>
		<dc:creator>Aussie Blogs</dc:creator>
				<category><![CDATA[Bioscience]]></category>
		<category><![CDATA[Cancer]]></category>
		<category><![CDATA[DNA]]></category>
		<category><![CDATA[genes]]></category>
		<category><![CDATA[Molecular]]></category>
		<category><![CDATA[reintroduction]]></category>

		<guid isPermaLink="false">http://molecularstaging.com/?p=825</guid>
		<description><![CDATA[A rare disease characterized by premature aging is modeled after a group of Spanish scientists to better understand the relationship between cancer, genes and aging. This is Werner syndrome, an inherited disorder characterized by premature aging of the individual, genomic instability and an increased incidence of tumors. The study was conducted jointly by researchers at [...]]]></description>
				<content:encoded><![CDATA[<p><img src="http://molecularstaging.aussieblogs.com.au/files/2010/04/3.jpeg" alt="3" title="3" width="148" height="134" class="alignleft size-full wp-image-826" align="left" />A rare disease characterized by premature aging is modeled after a group of Spanish scientists to better understand the relationship between cancer, genes and aging. This is Werner syndrome, an inherited disorder characterized by premature aging of the individual, genomic instability and an increased incidence of tumors. The study was conducted jointly by researchers at the Hospital Clinic of Barcelona, Biomedical Research Center of Navarre, the National Institute on Aging U.S., and the group of Manel Esteller of the CNIO. <span id="more-825"></span></p>
<p>Aging is the major risk factor for tumor development and yet, until recently not well known the molecular reasons for this relationship, it was logical to assume that inactivation of a gene that prevents aging (such as causing Werner&#8217;s syndrome) could have a role in the development of cancer. According to the study, the loss of activity of this gene by methylation of their regulatory region, has been detected in various tumor types, including soft and solid, and being the first tumor suppressor gene with such wide distribution. </p>
<p>The function of this gene is to protect cells from injury, through its helicase and exonuclease activity that promotes DNA repair. However, its inactivation by methylation causes the onset of chromosome fragmentation and development of genomic instability prior to tumor development. The reintroduction of the defective gene in a cell-tumor properties in laboratory cell cultures and in mouse models, opening the door to improved treatment of certain tumors, based on the understanding of these interactions.</p>
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		<title>Development and morphogenesis: potentialities from common patterns</title>
		<link>http://molecularstaging.aussieblogs.com.au/2012/12/21/development-and-morphogenesis-potentialities-from-common-patterns/</link>
		<comments>http://molecularstaging.aussieblogs.com.au/2012/12/21/development-and-morphogenesis-potentialities-from-common-patterns/#comments</comments>
		<pubDate>Tue, 06 Apr 2010 06:15:18 +0000</pubDate>
		<dc:creator>Aussie Blogs</dc:creator>
				<category><![CDATA[Bioscience]]></category>
		<category><![CDATA[coordinated morphological change]]></category>
		<category><![CDATA[differentiation]]></category>
		<category><![CDATA[migration]]></category>
		<category><![CDATA[morphogenesis]]></category>
		<category><![CDATA[patterns]]></category>
		<category><![CDATA[potentialities]]></category>
		<category><![CDATA[subsequent proliferation]]></category>

		<guid isPermaLink="false">http://molecularstaging.com/?p=822</guid>
		<description><![CDATA[Embryonic development and morphogenesis of individual organs are common schemes based processes. In them, groups of undifferentiated cells, they initiate a series of complex interactions with internal and external signals, in order to establish patterns that direct cells to their subsequent proliferation, differentiation, coordinated morphological change and migration. This seemingly elementary, requires the integration of [...]]]></description>
				<content:encoded><![CDATA[<p><img src="http://molecularstaging.aussieblogs.com.au/files/2010/04/2.jpeg" alt="2" title="2" width="142" height="145" class="alignleft size-full wp-image-823" align="left" />Embryonic development and morphogenesis of individual organs are common schemes based processes. In them, groups of undifferentiated cells, they initiate a series of complex interactions with internal and external signals, in order to establish patterns that direct cells to their subsequent proliferation, differentiation, coordinated morphological change and migration. This seemingly elementary, requires the integration of a series of activations and changes in the expression levels of a few basic genes. Two mechanisms are paramount in this general scheme: the proper control of temporal and spatial activation patterns of cell signaling, and the union of these patterns with cellular effectors that activate cellular responses in terms of gene activity or cell morphology. <span id="more-822"></span></p>
<p>Since capital works on the establishment of patterns during embryonic development of insectos1 until the discovery of cell adhesion proteins central to the development of the Drosophila tracheal system, 2 Casanova and his group have developed a dynamic activity in this world that seeks to better understand how an organism develops and how it gains the inherent complexity of its various organs. But it is also important to highlight the importance of this work for a global evolutionary vision. Studying the details of character development limiter decipher what is possible in evolution. </p>
<p>Not everything is possible, since development and morphogenesis are limiting factors of the variation available to natural selection. It is something that is evident in works the same group, where different organs or systems with similar functions, but apparently different structure may be homologous in different groups of organisms. This is the case of the tracheal gills of insects and crustaceans, both respiratory function, but some internal and others external to organismo.3</p>
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