Plegable BM Juliana Molina

441 views

Published on

0 Comments
0 Likes
Statistics
Notes
  • Be the first to comment

  • Be the first to like this

No Downloads
Views
Total views
441
On SlideShare
0
From Embeds
0
Number of Embeds
2
Actions
Shares
0
Downloads
5
Comments
0
Likes
0
Embeds 0
No embeds

No notes for slide

Plegable BM Juliana Molina

  1. 1. DNA REPAIR MECHANISM Juliana Molina Valencia Third Semester Medicine UPB Molecular Biology February 2012 http://make-family-tree.com/dnagenealogy.html
  2. 2. FOLDING
  3. 3. FOLDING
  4. 4. INTRODUCTION Given the changes in the internal or external environment the body has the ability to respond to changes. Without these skills, the cells wouldn't have the capacity to live and continue reproducing.
  5. 5. SMALLER SIBLING PROTEIN CALLS THE SHOTS IN CELL DIVISION SCIENCEDAILY (JAN. 3, 2012) <ul><li>Scientists have found a smaller sibling of protein ChK1, they named ChK1-s. </li></ul>
  6. 6. SMALLER SIBLING PROTEIN CALLS THE SHOTS IN CELL DIVISION SCIENCEDAILY (JAN. 3, 2012) Taken from: http://en.wikipedia.org/wiki/DNA_repair The protein Chk1 works as a checkpoint in cell development, this protein avoids cell division until their DNA has been fully replicated or repaired.
  7. 7. SMALLER SIBLING PROTEIN CALLS THE SHOTS IN CELL DIVISION SCIENCEDAILY (JAN. 3, 2012) <ul><li>In cancer cells and in fetal tissue, the levels of shorter form is higher, both require accelerated cell division. </li></ul><ul><li>Studies revealed that Chk1-S actually reduce tumor growth and prompt premature cell division and death in other cells. </li></ul>
  8. 8. SMALLER SIBLING PROTEIN CALLS THE SHOTS IN CELL DIVISION SCIENCEDAILY (JAN. 3, 2012) <ul><li>Chk1 and Chk1-S are made by the same gene they are just spliced differently, Chk1-S is only expressed at a time when DNA is replicated or repaired antagonizing its sibling protein. </li></ul>Taken from: http://biofinity.org/interest.htm
  9. 9. PERSONAL OPINION <ul><li>“ Advances in medicine can improve care protocols with many diseases, leading to a less traumatic treatment in the patient’s life and with better results, the discovery of this protein allows to have a deeper knowledge about the DNA repair mechanisms, the studies of this important regulator has allowed the use of the protein in the treatment of cancer patients, showing improvements in their health.” </li></ul>
  10. 10. INFLAMMATORY MEDIATOR PROMOTES COLORECTAL CANCER BY STIFLING PROTECTIVE GENES SCIENCEDAILY (JAN. 22, 2012) The development of colorectal cancer by shutting down genes that suppress tumors and repair damaged DNA it's increase by the function of a chemical that promotes inflammation, called prostaglandin E2 (PGE2).
  11. 11. INFLAMMATORY MEDIATOR PROMOTES COLORECTAL CANCER BY STIFLING PROTECTIVE GENES SCIENCEDAILY (JAN. 22, 2012) <ul><li>Levels of PGE2 correlate with levels of two methyltransferases, DNMT1 and DNMT3, in human colorectal cancer specimens. </li></ul>
  12. 12. INFLAMMATORY MEDIATOR PROMOTES COLORECTAL CANCER BY STIFLING PROTECTIVE GENES SCIENCEDAILY (JAN. 22, 2012) Taken from: http://www.astronoo.com/articles/regeneracionDeLosTejidos-es.html Mice treated with azacitidine (demethylating agent) experienced a 60% reduction in tumors, and those treated with celecoxib (anti-inflammatory agent), a 77%.
  13. 13. INFLAMMATORY MEDIATOR PROMOTES COLORECTAL CANCER BY STIFLING PROTECTIVE GENES SCIENCEDAILY (JAN. 22, 2012) <ul><li>The most powerful response occurred when both, an anti-inflammatory drug and a demethylating agent were used together, for reduced the size and number of tumors in mice with colorectal cancer: 93%. </li></ul>
  14. 14. PERSONAL OPINION <ul><li>“ Improve the patient's life is one of the most important objectives in medicine, is necessary to do studies like this for his achievement, as the combined use of two drugs in animal experiments has decreased the risk of developing cancer, it is possible to perform clinical trials in patients and use the results favoring society” </li></ul>
  15. 15. MEDICAL UTILITY Adaptation is the mainstay of life and evolution, cells are adapted all the time to stay alive and be healthy.
  16. 16. MEDICAL UTILITY <ul><li>Cells has many repair mechanisms to allow the body to stay healthy, when the mechanism is not working a process of cell apoptosis starts, but when the mutated cells stay in the body, they can grow and alter the balance of the organism. </li></ul>Taken from: http://elconocimientodesi.blogspot.com/2011/11/el-prejuicio-paterno-filial.html
  17. 17. MEDICAL UTILITY <ul><li>Health promotion and prevention: many factors can be controlled to avoid mutations, basic practices such as using sunscreen, not smoking and look after the mental and physical health, can help a lot. </li></ul>Taken from: http://coloreardibujo.com/dibujos-sobre-la-salud-para-colorear
  18. 18. MEDICAL UTILITY <ul><li>Also some elements of DNA repair process may help to diagnose and treat cancer and other diseases related with abnormal repair mechanisms. </li></ul>Taken from: http://en.wikipedia.org/wiki/File:Proteinviews-1tim.png
  19. 19. BIBLIOGRAPHY <ul><li>Navjotsingh P,  Zheng D. Smaller Sibling Protein Calls the Shots in Cell Division. ScienceDaily (Jan. 3, 2012). Accessed: February 23, 2012. </li></ul><ul><li>DuBois R, Dianren X, Dingzhi W, Sun-Hee K, et al. Inflammatory Mediator Promotes Colorectal Cancer by Stifling Protective Genes. ScienceDaily (Jan. 22, 2012). Accessed: February 23, 2012 </li></ul><ul><li>Martínez Sánchez LM, Vargas Grisales N, Toro Montoya AE, et al. Biología Molecular. Libro de clase. 6.ed. Medellín: UPB. Fac. de Medicina, 2011. 81-84 pág. </li></ul>
  20. 20. STAND UP TO CANCER Taken from: http://tujhaml.blogspot.com/2011/11/lazos-solidarios.html

×