New Approach to Protecting Prion from Altering and 'Cowcatcher' Enzyme Fixes Single-Strand DNA
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New Approach to Protecting Prion from Altering and 'Cowcatcher' Enzyme Fixes Single-Strand DNA

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    New Approach to Protecting Prion from Altering and 'Cowcatcher' Enzyme Fixes Single-Strand DNA New Approach to Protecting Prion from Altering and 'Cowcatcher' Enzyme Fixes Single-Strand DNA Presentation Transcript

    • New Approach to Protecting Prion from Altering and 'Cowcatcher' Enzyme Fixes Single-Strand DNA Oscar Andrés Parra Medicine student III semester UPB
    • MEDICAL UTILITY First. This study puts us one step closer to understand how recently discovered prion caused deseased work and what treatment could be useful to prevent or even cure this deseases, incurable to the moment Second. DNA fixing mechanism are of the most importance in the process of aging, neurodegenerative deaseases and cancer, a better understanding of the proteins involved in genetic repairing is important as a way to further investigate why they fail at their function causing DNA mutation BIBLIOGRAPHY • University of Texas Medical Branch at Galveston (2013, July 29). 'Cowcatcher' enzyme fixes single-strand DNA. ScienceDaily. Retrieved August 4, 2013, from http://www.sciencedaily.com-/ releases/2013/07/130729161751. htm • Case Western Reserve University (2013, July 18). New approach to protecting prion protein from altering shape, becoming infectious.ScienceDaily. Retrieved August 4, 2013, from http://www.sciencedaily.com-/ releases/2013/07/130718130454. htm FOLDING New Approach to Protecting Prion from Altering and 'Cowcatcher' Enzyme Fixes Single-Strand DNA MOLECULAR BIOLOGY Oscar Andrés Parra Medicine student III semester UPB Teacher Lina Maria Martínez Sánchez
    • INTRODUCTION Prions are proteins with an altered structure and a self-replicating capacity, and are identified as the cause of incurable and sometimes transmisible diseases such as the mad cow desease, very little it’s known about the mechanism of these prion deseasean recent studies on how the alter normal proteins may give us a clue for a succesful treatment in the future On the other Hand, DNA Repairing Mechanisms are esential in the comprehension of neurodegenerative deseases, aging mechanisms and cancer, finding a new protein that participates in this proces s can give us a better understanding of why they fail and how to avoid it 'Cowcatcher' Enzyme Fixes Single-Strand DNA Science daily July 29, 2013 Every time a cell divides it exposes its DNA to great danger in the form of single strands, this strands are particularly vulnerable to reactive oxigen species that may alter the information they contain. If left unchecked this mutations can lead to disorders linked to DNA damage such as aging, neurodegenerative deseases and cancer UTMB scienists are working with an enzime called NEIL 1 wich was previosuly known to recognized single stranded DNA and was asosiated with the replication complex, through experiments he researchers found that NEIL 1 actually rides in front of the replication complex, scouting for single-strand DNA damage and as soon as it enconters a base damage, the site is marked and replication stops, then the DNA strands are allowed together again so the damage can be repaired Student Observation : as the article stated, DNA damage its linked to a various number of degenerative deseases Adn comprehension of the repairing mechanism its important to prevent them from failing. NEIL 1 protein function wasn’t really clear before this investigation and from now on, knowing its true purpose new investigations will be focused on this protein New Approach to Protecting Prion Protein from Altering Shape, Becoming Infectious Prion deseases include mad cow desease and fatal failiar insomnia, unlike any other transmisible deseases, prion deseases are caused by an abnormal shaped prion protein it is believed that they self-replicate by binding to normal proteins produciong another abnormal prion thus increasing their numbers. A team of researchers from Case Western Reserve University School of Medicine have identified a mechanism that can prevent the normal prion protein from changing its molecular shape into the abnormal form responsible for neurodegenerative diseases. The researchers generated a variant of prion protein designed to stabilize the normal shape of one specific part of the protein. They accomplished this goal by replacing just one out of more than 200 amino acid residues, the building blocks of the protein. In a series of experiments, the researchers found that the modified prion protein was highly resistant to changing its shape. In other words, this approach may be successful in blocking the coercive action of the abnormal prion protein. Student observation: the result of this research shows a promising start for a prion desease prevention treatment or even a cure of the existing desease, its a first step to greater improvements in the little know field of prion deseases
    • INTRODUCTION Prions are proteins with an altered structure and a self-replicating capacity, and are identified as the the cause of incurable and sometimes transmisible diseases such as the mad cow desease, very little it’s known about the mechanism of these prion deseasean recent studies on how the alter normal proteins may give us a clue for a succesful treatment in the future On the other Hand, DNA Repairing Mechanisms are esentian in the comprehension of neurodegenerative deseases, aging mechanisms and cancer, finding a new protein that participates in this proces s can give us a better understanding of why they fail and how to avoid it . researchers from Case Western Reserve University School of Medicine have gone one step closer on the comprehension of prion desease mechanisms by identifying a mechanism that can prevent a normal prion protein from changing to its abnormal infecting form New Approach to Protecting Prion from Altering UTMB scientists found out more about a protein called NEIL 1 that was previously asociated with the replication complex, they found out that NEIL1 scouts for base errors before the the replication gets to that point of the DNA strand, allowing it to be repaired before continuing the replication 'Cowcatcher' Enzyme Fixes Single-Strand DNA
    • 'Cowcatcher' Enzyme Fixes Single-Strand DNA Science daily July 29, 2013 Every time a cell divides it exposes its DNA to great danger in the form of single strands, this strands are particularly vulnerable to reactive oxigen species that may alter the information they contain. If left unchecked this mutations can lead to disorders linked to DNA damage such as aging, neurodegenerative deseases and cancer UTMB scienists are working with an enzime called NEIL 1 wich was previosuly known to recognized single stranded DNA and was asosiated with the replication complex, through experiments he researchers found that NEIL 1 actually rides in front of the replication complex, scouting for single-strand DNA damage and as soon as it enconters a base damage, the site is marked and replication stops, then the DNA strands are allowed together again so the damage can be repaired Student Observation : as the article stated, DNA damage its linked to a various number of degenerative deseases Adn comprehension of the repairing mechanism its important to prevent them from failing. NEIL 1 protein function wasn’t really clear before this investigation and from now on, knowing its true purpose new investigations will be focused on this protein
    • The researchers at UTMB where working on the protein called NEIL 1 (cowcatcher) This protein was previously related to the replication complex NEIL 1 role in the replication was yet unknown, until now
    • Researchers found that NEIL 1 rides in front of the replication complex And scouts for DNA damage Then flags the abnormal base and stops replication NEIL 1
    • • After replication stops the replication machinery stalls and then regresses, and the two strands come back together • which allows repair of the damaged base in duplex DNA • by replacing the damaged base with the appropriate normal base
    • Observation DNA replication and repairing process is a lot more complex than we usually see in the textbooks, the discovery of the NEIL 1 function proves that, because something that plays a mayor role in DNA error checking and correction such as NEIL 1 was unknown to the moment, that makes me think that there may be a lot of other mechanisms that also are esential in DNA replication that may not be yet found.
    • New Approach to Protecting Prion Protein from Altering Shape, Becoming Infectious Prion deseases include mad cow desease and fatal failiar insomnia, unlike any other transmisible deseases, prion deseases are caused by an abnormal shaped prion protein it is believed that they self-replicate by binding to normal proteins produciong another abnormal prion thus increasing their numbers. A team of researchers from Case Western Reserve University School of Medicine have identified a mechanism that can prevent the normal prion protein from changing its molecular shape into the abnormal form responsible for neurodegenerative diseases. The researchers generated a variant of prion protein designed to stabilize the normal shape of one specific part of the protein. They accomplished this goal by replacing just one out of more than 200 amino acid residues, the building blocks of the protein. In a series of experiments, the researchers found that the modified prion protein was highly resistant to changing its shape. In other words, this approach may be successful in blocking the coercive action of the abnormal prion protein. Student observation: the result of this research shows a promising start for a prion desease prevention treatment or even a cure of the existing desease, its a first step to greater improvements in the little know field of prion deseases New #2
    • The mechanism of abnormal prion protein Self replication its not yet clear The actual theory is that prions replicate by altering the structure of a normal protein, producing a second abnormal prion Based on this theory the researchers created a variant of prion protein designed to stabilize the normal shape of one specific part of a normal protein
    • The researchers found out that the modified prion was highly resistant to changing its shape Showing that this approach may be successful in blocking the pathological action of the abnormal prion protein Then, they created transgenic mice that produced the stabilizer protein and infected them with the mad cow desease to see the outcome
    • The transgenic mice took almost twice the time to show the signs og the desease han the normal mice Proving that the modified protein was succesful in slowing down the desease Giving at least a starting place to look for a cure to a decease with no effective treatment to the moment
    • Observation One of the most interesting aspects of this new is that it almost proves that the actual theory of prion protein replication is correct, because the succes of this proyect was based on the fact that prion proteins modified normal proteins, making it useful to have a normal protein resistant to the modification, if the mechanism is different, the experiment would have not shown any difference between the two mouse groups Also it is a sustantialy important advance in the treatmente of prion deceases, wich are incurable to the moment in humans
    • Medical Utility As stated before, DNA repairing mechanisms are esential to the study of neurodegenerative deceases such as alzheimer or parkinson, in the understanding of natural aging and the causes of cancer. It is necesary to know the reason of a pathology in order to investigate for a better treatment
    • Medical Utility There is a chance that some deceases related to DNA damage are related to the abnormal function of the NEIL 1 enzyme specificaly, so, understanding its role in the replication process may be of key value in future investigation against DNA mutation derived illness
    • Medical Utility This investigation makes the mechanism of prion deceases spreading a lot clearer, since it has been a mistery for medicine from the moment it was discovered that abnormal proteins could serve as a transmissible decease, this can give an starting point for treatment investigations in the future
    • Medical Utility The study proved effective against a prion that normaly infects humans, causing the Creuzfeldt-Jakob disease , and with no effective treatment to the moment it could be the start of a brand new pharmacological strategy consisting of creating molecules that can stabilize prion proteins in order to prevent the propagation of the symptoms
    • Bibliography • University of Texas Medical Branch at Galveston (2013, July 29). 'Cowcatcher' enzyme fixes single-strand DNA. ScienceDaily. Retrieved August 4, 2013, from http://www.sciencedaily.com-/releases/2013/07/13072 9161751.htm • Case Western Reserve University (2013, July 18). New approach to protecting prion protein from altering shape, becoming infectious.ScienceDaily. Retrieved August 4, 2013, from http://www.sciencedaily.com-/releases/2013/07/13071 8130454.htm
    • tThanks!