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Dna Repair Mechanisms
This document discusses DNA repair mechanisms and two related studies. It first provides an introduction to how cells use DNA repair mechanisms to detect and correct damage to prevent mutations. It then summarizes two studies: one identifying the FAN1 gene which may be involved in repairing DNA damage in the Fanconi anemia pathway, and another finding that the drug Olaparib, which inhibits the DNA repair enzyme PARP, caused tumors to shrink in women with BRCA gene mutations and breast or ovarian cancer. It concludes by discussing the potential medical applications of further understanding DNA repair mechanisms and using drugs like Olaparib to treat cancer.
Folding
This document summarizes two scientific articles. The first article discusses how the condensin protein folds chromosome arms during cell division in yeast, helping prevent errors. The second article discusses how scientists identified molecular mechanisms behind DNA breakage, a hallmark of cancer cells, finding some DNA regions are more susceptible to damage and cancer results when repair mechanisms fail. The document discusses potential medical applications, like developing new treatments that target these molecules to help prevent genetic disorders and cancers.
Folding plegable
1. The p53 protein, known as the "guardian of the genome", plays an important role in protecting against cancer by preventing DNA mutations. Scientists have discovered that p53 is activated during meiosis to closely monitor DNA breaks and repairs, helping prevent mutations from being passed onto gametes.
2. Researchers discovered that the Mec1 protein in yeast acts as the "guardian of the genome" by repairing damaged DNA and replication machinery. Mec1 phosphorylates the SLX4 protein, triggering it to anchor to the replication machinery and perform repairs.
3. Understanding how proteins repair DNA damage provides insights that could lead to new approaches for curing diseases caused by genetic mutations, such as cancer
Splicing / Molecular Biology
This presentation is aimed at show some of the benefits of alternative splicing from the analysis of some current researchs.
DNA REPLICATION
The document summarizes two scientific articles from ScienceDaily about recent discoveries related to cell division and DNA replication that could provide new insights into cancer. The first article discusses a discovery of a protein complex called Ska that helps anchor DNA and distribute it correctly as cells divide. Understanding this complex could help develop new anti-cancer drugs. The second article describes an international study that improves ability to predict hereditary cancer risk by better classifying genetic variants associated with Lynch syndrome. This allows more accurate genetic counseling and preventive measures for at-risk families.
Seminario Biologia molecular pdf
This study evaluated the effect of radiation therapy on the expression of EGFR, ERCC1, and p53 in cervical cancer cell lines and tumor tissues from 10 patients with cervical cancer. Two cervical cancer cell lines were exposed to different radiation doses and analyzed for cell mortality and gene expression changes. Tumor samples from 10 cervical cancer patients undergoing radiotherapy were analyzed via immunohistochemistry for protein expression of EGFR, ERCC1, and p53 before and after treatment. The results showed that radiation therapy did not significantly induce changes in expression of p53, ERCC1, or EGFR in the tumor tissues or cell lines, suggesting that radiotherapy may not be the best treatment option for advanced cervical cancer.
“HOW SOME UNUSUAL RNA MOLECULES HOME IN ON TARGETS ” AND “UNIQUE EPIGENOMIC ...
The document summarizes two scientific articles about RNA molecules and epigenomic coding during human development. The first article discusses how long non-coding RNA (lncRNA) molecules like Xist help regulate gene expression by organizing chromatin structure and packaging genetic information. The second article finds that non-CG DNA methylation, rather than typical CG methylation, is predominant in mature human neurons and changes with age and brain development, influencing learning and memory through cell differentiation. Both discoveries have potential medical applications, like using Xist to treat Down syndrome or studying epigenetic changes related to psychiatric disorders.
HOW SOME UNUSUAL RNA MOLECULES HOME IN ON TARGETS ” AND “UNIQUE EPIGENOMIC C...
The document summarizes two scientific articles about RNA molecules and epigenomic coding during human development. The first article discusses how long non-coding RNA (lncRNA) molecules like Xist help regulate gene expression by organizing chromatin structure and packaging genetic information. The second article finds that non-CG DNA methylation, rather than typical CG methylation, is predominant in mature human neurons and changes with age and brain development, influencing learning and memory through cell differentiation. Both studies provide insights with potential medical applications like gene therapy for Down syndrome.
Recommended
Dna Repair Mechanisms
This document discusses DNA repair mechanisms and two related studies. It first provides an introduction to how cells use DNA repair mechanisms to detect and correct damage to prevent mutations. It then summarizes two studies: one identifying the FAN1 gene which may be involved in repairing DNA damage in the Fanconi anemia pathway, and another finding that the drug Olaparib, which inhibits the DNA repair enzyme PARP, caused tumors to shrink in women with BRCA gene mutations and breast or ovarian cancer. It concludes by discussing the potential medical applications of further understanding DNA repair mechanisms and using drugs like Olaparib to treat cancer.
Folding
This document summarizes two scientific articles. The first article discusses how the condensin protein folds chromosome arms during cell division in yeast, helping prevent errors. The second article discusses how scientists identified molecular mechanisms behind DNA breakage, a hallmark of cancer cells, finding some DNA regions are more susceptible to damage and cancer results when repair mechanisms fail. The document discusses potential medical applications, like developing new treatments that target these molecules to help prevent genetic disorders and cancers.
Folding plegable
1. The p53 protein, known as the "guardian of the genome", plays an important role in protecting against cancer by preventing DNA mutations. Scientists have discovered that p53 is activated during meiosis to closely monitor DNA breaks and repairs, helping prevent mutations from being passed onto gametes.
2. Researchers discovered that the Mec1 protein in yeast acts as the "guardian of the genome" by repairing damaged DNA and replication machinery. Mec1 phosphorylates the SLX4 protein, triggering it to anchor to the replication machinery and perform repairs.
3. Understanding how proteins repair DNA damage provides insights that could lead to new approaches for curing diseases caused by genetic mutations, such as cancer
Splicing / Molecular Biology
This presentation is aimed at show some of the benefits of alternative splicing from the analysis of some current researchs.
DNA REPLICATION
The document summarizes two scientific articles from ScienceDaily about recent discoveries related to cell division and DNA replication that could provide new insights into cancer. The first article discusses a discovery of a protein complex called Ska that helps anchor DNA and distribute it correctly as cells divide. Understanding this complex could help develop new anti-cancer drugs. The second article describes an international study that improves ability to predict hereditary cancer risk by better classifying genetic variants associated with Lynch syndrome. This allows more accurate genetic counseling and preventive measures for at-risk families.
Seminario Biologia molecular pdf
This study evaluated the effect of radiation therapy on the expression of EGFR, ERCC1, and p53 in cervical cancer cell lines and tumor tissues from 10 patients with cervical cancer. Two cervical cancer cell lines were exposed to different radiation doses and analyzed for cell mortality and gene expression changes. Tumor samples from 10 cervical cancer patients undergoing radiotherapy were analyzed via immunohistochemistry for protein expression of EGFR, ERCC1, and p53 before and after treatment. The results showed that radiation therapy did not significantly induce changes in expression of p53, ERCC1, or EGFR in the tumor tissues or cell lines, suggesting that radiotherapy may not be the best treatment option for advanced cervical cancer.
“HOW SOME UNUSUAL RNA MOLECULES HOME IN ON TARGETS ” AND “UNIQUE EPIGENOMIC ...
The document summarizes two scientific articles about RNA molecules and epigenomic coding during human development. The first article discusses how long non-coding RNA (lncRNA) molecules like Xist help regulate gene expression by organizing chromatin structure and packaging genetic information. The second article finds that non-CG DNA methylation, rather than typical CG methylation, is predominant in mature human neurons and changes with age and brain development, influencing learning and memory through cell differentiation. Both discoveries have potential medical applications, like using Xist to treat Down syndrome or studying epigenetic changes related to psychiatric disorders.
HOW SOME UNUSUAL RNA MOLECULES HOME IN ON TARGETS ” AND “UNIQUE EPIGENOMIC C...
The document summarizes two scientific articles about RNA molecules and epigenomic coding during human development. The first article discusses how long non-coding RNA (lncRNA) molecules like Xist help regulate gene expression by organizing chromatin structure and packaging genetic information. The second article finds that non-CG DNA methylation, rather than typical CG methylation, is predominant in mature human neurons and changes with age and brain development, influencing learning and memory through cell differentiation. Both studies provide insights with potential medical applications like gene therapy for Down syndrome.
SPLICING
The document discusses RNA splicing and its importance. It covers how splicing removes introns and joins exons to create mature RNA for protein production. Alternative splicing can generate multiple protein isoforms from a single gene with different functions. Myotonic dystrophy type 1 is discussed as an example of a disorder caused by aberrant splicing, changing the form of the PKM2 enzyme critical for muscle cell metabolism. A new complex called the Little Elongation Complex is revealed to play a key role in transcription of small nuclear RNAs required for splicing. Understanding splicing machinery could open doors to novel disease treatment approaches.
Eukaryotic RNA processing: alternative RNA splicing
Alternative splicing is a process by which cells produce multiple protein isoforms from individual genes. Understanding the functions and interactions of alternatively spliced protein isoforms is important for understanding disease. A new study found that two proteins, PRMT1 and RBM15, regulate the differentiation of megakaryocytes, blood cells involved in platelet production, through alternative splicing. Mutations in these proteins have been linked to blood cancers. Further research on alternative splicing may help identify new disease targets and therapies.
Dna replication, repair, recombination
The document summarizes DNA replication, repair, and recombination. It discusses the key components and processes involved in DNA replication, including replication origins, forks, primers, and polymerases. It also examines DNA repair mechanisms for errors, damage like depurination, and double-stranded breaks. Finally, it briefly touches on mobile genetic elements and retrotransposons that can move locations in the genome.
Stopping and Starting Cancer Cell Cycle Weakens and Defeats Multiple Myeloma...
The document discusses the cell cycle and its role in cancer development. It explains that cancers occur when cells divide uncontrollably due to damaged mechanisms that normally control the cell cycle and induce apoptosis. The cell cycle is regulated by cyclins and cyclin-dependent kinases that coordinate processes like DNA replication and cell division. Alterations in these regulatory enzymes at checkpoints in the cell cycle can lead to cancer. Understanding and modifying the cell cycle may help cure cancer by preventing abnormal cell proliferation and repairing damaged organs through accelerated growth of healthy cells.
“HOW SOME UNUSUAL RNA MOLECULES HOME IN ON TARGETS ” AND “UNIQUE EPIGENOMIC ...
This document summarizes two scientific articles. The first article discusses how long non-coding RNA (lncRNA) molecules like Xist help regulate gene expression by organizing chromatin structure and packaging genetic information. The second article finds that non-CpG methylation, rather than CpG methylation, dominates DNA methylation patterns in mature human neurons and is important for brain development and function. Abnormal epigenetic changes may also contribute to psychiatric disorders.
DNA Stretching Mystery and Chaperone Enzyme Provides new Target for Cancer T...
Scientists discovered that DNA's ability to dramatically extend at 65 pN does not require nicks or loose ends in its backbone. They attached one end of a looped DNA strand to a microbead and stapled the other end to a surface, allowing rotation but no loose ends. When they applied force, this DNA extended at the same force as nicked DNA, indicating the extension mechanism is the same with or without nicks. The researchers also found that the Cdc7 protein regulates a "chaperone" enzyme's recruitment of Pol eta to sites of DNA damage, ensuring accurate repair during the cell cycle stage most vulnerable to cancer mutations. Targeting Cdc7's dual roles may offer a potential cancer therapy
New Approach to Protecting Prion from Altering and 'Cowcatcher' Enzyme Fixes ...
Researchers made two discoveries about proteins involved in DNA replication and prion diseases:
1) Scientists at UTMB found that the protein NEIL1 acts as a "cowcatcher" by scanning DNA for errors ahead of the replication machinery and signaling it to stop so repairs can be made. This revealed NEIL1's previously unknown role in replication error correction.
2) Researchers at Case Western modified a prion protein to stabilize its normal shape and prevent conversion to the abnormal form that causes diseases. Mice with this variant were resistant to prion infection, demonstrating this approach could block prion disease progression.
These studies provide new insights into DNA repair mechanisms and potential treatments for prion diseases.
folding molecular biology
This document summarizes two scientific studies on chromosome defects and genetic diseases. The first study discovered a chromosome therapy technique to correct severe chromosome defects by replacing an abnormal ring chromosome with a normal duplicated chromosome in stem cells. This could help repair birth defects. The second study found that analyzing chromatin architecture, the organization of DNA and proteins in chromosomes, could help identify regulatory DNA anomalies and better diagnose genetic diseases, since DNA sequencing alone is insufficient. This discovery paves the way for improved understanding and diagnosis of many genetic conditions.
DNA Methylation
The document discusses two studies related to DNA methylation. The first study found that cancer incidence increases with age due to age-related methylation across the human genome, which can negatively impact gene expression and increase cancer risk. The second study discovered a new type of non-CpG methylation in brain cells that is more dynamic and potentially reversible, challenging the idea that methylation changes are permanent. This has implications for better understanding diseases like Rett syndrome that involve methylation enzymes. Both studies provide insights with potential medical applications like new cancer prevention or treatment strategies.
Trabajo plegable biomol
Researchers have discovered two new mechanisms related to DNA replication and gene expression. First, they found an enzyme called NEIL1 that repairs damaged DNA and could enhance cancer treatments if inhibited in cancer cells. Second, they uncovered a new mechanism where a fragment of the CACNA1A gene causes spinocerebellar ataxia type-6 by producing toxic proteins, offering potential treatment by inhibiting production of the mutant fragment. The discoveries provide insights into cellular processes that could be targeted to develop new disease treatments.
REPARATION AND GENE EXPRESSION
The document discusses recent scientific findings related to DNA repair and gene expression regulation. It describes a study that linked epigenetic mechanisms controlling gene expression to bone and joint damage in ankylosing spondylitis. The study examined 75 patients over several years, finding that genes are not always expressed and require triggers to start expression processes. Maintaining high DNA methylation can also relate to non-expression of genes. Separately, it mentions the discovery of a "DNA ambulance" motor protein complex in yeast cells that repairs damaged DNA, though inaccurately and in a way that could lead to cancer. Researchers are working to better understand these DNA repair mechanisms and how genomic damage relates to disease progression and pathology.
Mutasi gen p53
This document discusses detecting p53 germline mutations in families with Li-Fraumeni syndrome (LFS). LFS is an autosomal dominant familial cancer syndrome where affected individuals often develop sarcomas before age 45 and have relatives with other cancers. Around 70% of LFS cases are caused by mutations in the p53 gene. Sequencing and single strand conformation polymorphism analysis can be used to detect p53 germline mutations in LFS families. These techniques may help understand the increased cancer risk in families caused by inherited defects in tumor suppressor genes like p53.
Plegable biomol
Researchers at the UT Southwestern Medical Center and the University of Geneva studied how certain genes and proteins involved in maintaining genetic stability can sometimes contribute to cancer development. They found:
1) Mutations in the p53 tumor suppressor gene, which normally restrains mobile genetic elements, were prevalent in cancer samples. This leads to genomic instability by allowing increased movement of these elements within chromosomes.
2) The APOBEC protein, intended to fight viruses by modifying single-stranded DNA, can exploit weaknesses during human DNA replication to introduce mutations, as detected in tumor cells. It acts on the single strands present during replication fork separation.
3) Understanding how p53 and APOBEC influence genetic
Genomic instability
Genomic instability plays an important role in cancer development by accelerating the accumulation of genetic changes in cancer cells. Several mechanisms can cause genomic instability, including defects in DNA repair pathways like base excision repair, mismatch repair, and double-strand break repair. Loss of function in DNA repair genes like MLH1 and MSH2 can lead to hypermutation and microsatellite instability in colorectal cancer. Other causes include problems with DNA replication, chromosome segregation, and telomere dysfunction. Genetic disorders involving genomic instability include ataxia-telangiectasia, neurofibromatosis type 1, Bloom syndrome, and ring chromosomes.
Plegable biologia molecular
The document discusses several topics related to DNA replication and repair:
1) A study found that faulty proteins involved in DNA repair may be linked to ovarian cancer recurrence and response to PARP inhibitor drugs.
2) PARP inhibitors are being tested for ovarian cancer patients with BRCA1/BRCA2 mutations or other damaged DNA repair proteins.
3) Research is exploring an earlier genetic molecule called TNA that may have preceded DNA and RNA due to its simpler structure and ability to self-replicate, providing insights into the origins of life.
4) Understanding DNA repair mechanisms and how they relate to disease could help develop new treatments, such as genomic therapies that insert missing genes.
Telomere paper
Dr. Elizabeth Blackburn gives a lecture on telomeres and telomerase, and their implications for aging and age-related diseases. She explains that telomeres are repetitive DNA sequences that cap the ends of chromosomes and protect genetic material. Telomerase is an enzyme that adds telomere sequences to chromosomes to maintain their length during cell division. Studies show genetics play a role in longevity, and stress and caregiving can impact telomere length by reducing telomerase activity and increasing oxidative stress. Shorter telomeres are associated with increased mortality and disease susceptibility.
Sperm dna fragmentation
Sperm DNA fragmentation can negatively impact fertility and pregnancy outcomes. DNA becomes vulnerable during spermatogenesis when protamine replaces histones in chromatin compaction. Tests can evaluate sperm DNA fragmentation levels, which are correlated with lower fertilization and implantation rates. Factors like oxidative stress, temperature, and infections can intrinsically or extrinsically damage sperm DNA. Repair mechanisms attempt to resolve DNA double-strand breaks, but extensive unrepaired damage may be incompatible with embryo development. Treatments aim to address underlying causes of DNA fragmentation or use testicular sperm or ICSI to bypass ejaculated sperm issues.
genetic in stability and its role in cancer
Genomic instability can occur at both the chromosomal and nucleotide levels and plays an important role in cancer development. Chromosomal instability results in gains and losses of whole chromosomes and structural changes, while instability at the nucleotide level is caused by defects in DNA repair pathways like mismatch repair and base excision repair. Many mechanisms help maintain genomic stability during cell division, including DNA repair pathways, epigenetic modifications, telomere protection, and proteins like ATM, ATR, BRCA1 and BRCA2. Cancer arises through a multi-step process as mutations accumulate in single cells, allowing their uncontrolled growth and proliferation into malignant tumor masses.
Festival of Genomics 2016 London: Analyze Genomes: A Federated In-Memory Comp...
This presentation covers the "Analyze Genomes: A Federated In-Memory Computing Platform for Life Sciences" presentation of the 2016 Festival of Genomics workshop "Big Medical Data in Precision Medicine: Challenges or Opportunities?" on Jan 19, 2016 in London.
Festival of Genomics 2016 London: Real-time Exploration of the Cancer Genome,...
This presentation covers the NCT presentation of the 2016 Festival of Genomics workshop "Big Medical Data in Precision Medicine: Challenges or Opportunities?" on Jan 19, 2016 in London.
Bobby (1973) Fashion Analysis
One small and simple ppt I made for the Summer Project where we were asked to choose a movie related to fashion. I chose closer home :) There's not much text because I did most of the talking.
Home
The document summarizes the five generations of computers:
1) First generation used vacuum tubes and were room-sized, expensive to operate, and prone to failure.
2) Second generation used transistors which made computers smaller, faster, cheaper and more reliable.
3) Third generation used integrated circuits which further increased speed and efficiency by placing transistors on silicon chips. This made computers accessible to the mass market.
More Related Content
What's hot
SPLICING
The document discusses RNA splicing and its importance. It covers how splicing removes introns and joins exons to create mature RNA for protein production. Alternative splicing can generate multiple protein isoforms from a single gene with different functions. Myotonic dystrophy type 1 is discussed as an example of a disorder caused by aberrant splicing, changing the form of the PKM2 enzyme critical for muscle cell metabolism. A new complex called the Little Elongation Complex is revealed to play a key role in transcription of small nuclear RNAs required for splicing. Understanding splicing machinery could open doors to novel disease treatment approaches.
Eukaryotic RNA processing: alternative RNA splicing
Alternative splicing is a process by which cells produce multiple protein isoforms from individual genes. Understanding the functions and interactions of alternatively spliced protein isoforms is important for understanding disease. A new study found that two proteins, PRMT1 and RBM15, regulate the differentiation of megakaryocytes, blood cells involved in platelet production, through alternative splicing. Mutations in these proteins have been linked to blood cancers. Further research on alternative splicing may help identify new disease targets and therapies.
Dna replication, repair, recombination
The document summarizes DNA replication, repair, and recombination. It discusses the key components and processes involved in DNA replication, including replication origins, forks, primers, and polymerases. It also examines DNA repair mechanisms for errors, damage like depurination, and double-stranded breaks. Finally, it briefly touches on mobile genetic elements and retrotransposons that can move locations in the genome.
Stopping and Starting Cancer Cell Cycle Weakens and Defeats Multiple Myeloma...
The document discusses the cell cycle and its role in cancer development. It explains that cancers occur when cells divide uncontrollably due to damaged mechanisms that normally control the cell cycle and induce apoptosis. The cell cycle is regulated by cyclins and cyclin-dependent kinases that coordinate processes like DNA replication and cell division. Alterations in these regulatory enzymes at checkpoints in the cell cycle can lead to cancer. Understanding and modifying the cell cycle may help cure cancer by preventing abnormal cell proliferation and repairing damaged organs through accelerated growth of healthy cells.
“HOW SOME UNUSUAL RNA MOLECULES HOME IN ON TARGETS ” AND “UNIQUE EPIGENOMIC ...
This document summarizes two scientific articles. The first article discusses how long non-coding RNA (lncRNA) molecules like Xist help regulate gene expression by organizing chromatin structure and packaging genetic information. The second article finds that non-CpG methylation, rather than CpG methylation, dominates DNA methylation patterns in mature human neurons and is important for brain development and function. Abnormal epigenetic changes may also contribute to psychiatric disorders.
DNA Stretching Mystery and Chaperone Enzyme Provides new Target for Cancer T...
Scientists discovered that DNA's ability to dramatically extend at 65 pN does not require nicks or loose ends in its backbone. They attached one end of a looped DNA strand to a microbead and stapled the other end to a surface, allowing rotation but no loose ends. When they applied force, this DNA extended at the same force as nicked DNA, indicating the extension mechanism is the same with or without nicks. The researchers also found that the Cdc7 protein regulates a "chaperone" enzyme's recruitment of Pol eta to sites of DNA damage, ensuring accurate repair during the cell cycle stage most vulnerable to cancer mutations. Targeting Cdc7's dual roles may offer a potential cancer therapy
New Approach to Protecting Prion from Altering and 'Cowcatcher' Enzyme Fixes ...
Researchers made two discoveries about proteins involved in DNA replication and prion diseases:
1) Scientists at UTMB found that the protein NEIL1 acts as a "cowcatcher" by scanning DNA for errors ahead of the replication machinery and signaling it to stop so repairs can be made. This revealed NEIL1's previously unknown role in replication error correction.
2) Researchers at Case Western modified a prion protein to stabilize its normal shape and prevent conversion to the abnormal form that causes diseases. Mice with this variant were resistant to prion infection, demonstrating this approach could block prion disease progression.
These studies provide new insights into DNA repair mechanisms and potential treatments for prion diseases.
folding molecular biology
This document summarizes two scientific studies on chromosome defects and genetic diseases. The first study discovered a chromosome therapy technique to correct severe chromosome defects by replacing an abnormal ring chromosome with a normal duplicated chromosome in stem cells. This could help repair birth defects. The second study found that analyzing chromatin architecture, the organization of DNA and proteins in chromosomes, could help identify regulatory DNA anomalies and better diagnose genetic diseases, since DNA sequencing alone is insufficient. This discovery paves the way for improved understanding and diagnosis of many genetic conditions.
DNA Methylation
The document discusses two studies related to DNA methylation. The first study found that cancer incidence increases with age due to age-related methylation across the human genome, which can negatively impact gene expression and increase cancer risk. The second study discovered a new type of non-CpG methylation in brain cells that is more dynamic and potentially reversible, challenging the idea that methylation changes are permanent. This has implications for better understanding diseases like Rett syndrome that involve methylation enzymes. Both studies provide insights with potential medical applications like new cancer prevention or treatment strategies.
Trabajo plegable biomol
Researchers have discovered two new mechanisms related to DNA replication and gene expression. First, they found an enzyme called NEIL1 that repairs damaged DNA and could enhance cancer treatments if inhibited in cancer cells. Second, they uncovered a new mechanism where a fragment of the CACNA1A gene causes spinocerebellar ataxia type-6 by producing toxic proteins, offering potential treatment by inhibiting production of the mutant fragment. The discoveries provide insights into cellular processes that could be targeted to develop new disease treatments.
REPARATION AND GENE EXPRESSION
The document discusses recent scientific findings related to DNA repair and gene expression regulation. It describes a study that linked epigenetic mechanisms controlling gene expression to bone and joint damage in ankylosing spondylitis. The study examined 75 patients over several years, finding that genes are not always expressed and require triggers to start expression processes. Maintaining high DNA methylation can also relate to non-expression of genes. Separately, it mentions the discovery of a "DNA ambulance" motor protein complex in yeast cells that repairs damaged DNA, though inaccurately and in a way that could lead to cancer. Researchers are working to better understand these DNA repair mechanisms and how genomic damage relates to disease progression and pathology.
Mutasi gen p53
This document discusses detecting p53 germline mutations in families with Li-Fraumeni syndrome (LFS). LFS is an autosomal dominant familial cancer syndrome where affected individuals often develop sarcomas before age 45 and have relatives with other cancers. Around 70% of LFS cases are caused by mutations in the p53 gene. Sequencing and single strand conformation polymorphism analysis can be used to detect p53 germline mutations in LFS families. These techniques may help understand the increased cancer risk in families caused by inherited defects in tumor suppressor genes like p53.
Plegable biomol
Researchers at the UT Southwestern Medical Center and the University of Geneva studied how certain genes and proteins involved in maintaining genetic stability can sometimes contribute to cancer development. They found:
1) Mutations in the p53 tumor suppressor gene, which normally restrains mobile genetic elements, were prevalent in cancer samples. This leads to genomic instability by allowing increased movement of these elements within chromosomes.
2) The APOBEC protein, intended to fight viruses by modifying single-stranded DNA, can exploit weaknesses during human DNA replication to introduce mutations, as detected in tumor cells. It acts on the single strands present during replication fork separation.
3) Understanding how p53 and APOBEC influence genetic
Genomic instability
Genomic instability plays an important role in cancer development by accelerating the accumulation of genetic changes in cancer cells. Several mechanisms can cause genomic instability, including defects in DNA repair pathways like base excision repair, mismatch repair, and double-strand break repair. Loss of function in DNA repair genes like MLH1 and MSH2 can lead to hypermutation and microsatellite instability in colorectal cancer. Other causes include problems with DNA replication, chromosome segregation, and telomere dysfunction. Genetic disorders involving genomic instability include ataxia-telangiectasia, neurofibromatosis type 1, Bloom syndrome, and ring chromosomes.
Plegable biologia molecular
The document discusses several topics related to DNA replication and repair:
1) A study found that faulty proteins involved in DNA repair may be linked to ovarian cancer recurrence and response to PARP inhibitor drugs.
2) PARP inhibitors are being tested for ovarian cancer patients with BRCA1/BRCA2 mutations or other damaged DNA repair proteins.
3) Research is exploring an earlier genetic molecule called TNA that may have preceded DNA and RNA due to its simpler structure and ability to self-replicate, providing insights into the origins of life.
4) Understanding DNA repair mechanisms and how they relate to disease could help develop new treatments, such as genomic therapies that insert missing genes.
Telomere paper
Dr. Elizabeth Blackburn gives a lecture on telomeres and telomerase, and their implications for aging and age-related diseases. She explains that telomeres are repetitive DNA sequences that cap the ends of chromosomes and protect genetic material. Telomerase is an enzyme that adds telomere sequences to chromosomes to maintain their length during cell division. Studies show genetics play a role in longevity, and stress and caregiving can impact telomere length by reducing telomerase activity and increasing oxidative stress. Shorter telomeres are associated with increased mortality and disease susceptibility.
Sperm dna fragmentation
Sperm DNA fragmentation can negatively impact fertility and pregnancy outcomes. DNA becomes vulnerable during spermatogenesis when protamine replaces histones in chromatin compaction. Tests can evaluate sperm DNA fragmentation levels, which are correlated with lower fertilization and implantation rates. Factors like oxidative stress, temperature, and infections can intrinsically or extrinsically damage sperm DNA. Repair mechanisms attempt to resolve DNA double-strand breaks, but extensive unrepaired damage may be incompatible with embryo development. Treatments aim to address underlying causes of DNA fragmentation or use testicular sperm or ICSI to bypass ejaculated sperm issues.
genetic in stability and its role in cancer
Genomic instability can occur at both the chromosomal and nucleotide levels and plays an important role in cancer development. Chromosomal instability results in gains and losses of whole chromosomes and structural changes, while instability at the nucleotide level is caused by defects in DNA repair pathways like mismatch repair and base excision repair. Many mechanisms help maintain genomic stability during cell division, including DNA repair pathways, epigenetic modifications, telomere protection, and proteins like ATM, ATR, BRCA1 and BRCA2. Cancer arises through a multi-step process as mutations accumulate in single cells, allowing their uncontrolled growth and proliferation into malignant tumor masses.
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Eukaryotic RNA processing: alternative RNA splicing
Eukaryotic RNA processing: alternative RNA splicing
Stopping and Starting Cancer Cell Cycle Weakens and Defeats Multiple Myeloma...
Stopping and Starting Cancer Cell Cycle Weakens and Defeats Multiple Myeloma...
“HOW SOME UNUSUAL RNA MOLECULES HOME IN ON TARGETS ” AND “UNIQUE EPIGENOMIC ...
“HOW SOME UNUSUAL RNA MOLECULES HOME IN ON TARGETS ” AND “UNIQUE EPIGENOMIC ...
DNA Stretching Mystery and Chaperone Enzyme Provides new Target for Cancer T...
DNA Stretching Mystery and Chaperone Enzyme Provides new Target for Cancer T...
New Approach to Protecting Prion from Altering and 'Cowcatcher' Enzyme Fixes ...
New Approach to Protecting Prion from Altering and 'Cowcatcher' Enzyme Fixes ...
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Festival of Genomics 2016 London: Analyze Genomes: A Federated In-Memory Comp...
This presentation covers the "Analyze Genomes: A Federated In-Memory Computing Platform for Life Sciences" presentation of the 2016 Festival of Genomics workshop "Big Medical Data in Precision Medicine: Challenges or Opportunities?" on Jan 19, 2016 in London.
Festival of Genomics 2016 London: Real-time Exploration of the Cancer Genome,...
This presentation covers the NCT presentation of the 2016 Festival of Genomics workshop "Big Medical Data in Precision Medicine: Challenges or Opportunities?" on Jan 19, 2016 in London.
Bobby (1973) Fashion Analysis
One small and simple ppt I made for the Summer Project where we were asked to choose a movie related to fashion. I chose closer home :) There's not much text because I did most of the talking.
Home
The document summarizes the five generations of computers:
1) First generation used vacuum tubes and were room-sized, expensive to operate, and prone to failure.
2) Second generation used transistors which made computers smaller, faster, cheaper and more reliable.
3) Third generation used integrated circuits which further increased speed and efficiency by placing transistors on silicon chips. This made computers accessible to the mass market.
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The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive functioning. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms.
The King: The Rejected King
The document discusses why Jesus was rejected by the people during his time, noting that he was not the type of king they expected and did not follow the traditions of the elders. It also examines how Jesus reacted to rejection, including being unable to perform great miracles in towns that lacked faith. Finally, it considers how people nowadays show they reject Jesus, such as by being unbelievers or failing to keep his commandments despite being believers.
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Scientists have discovered seven new DNA regions that are linked to an increased risk of prostate cancer. A study of prostate cancer patients found variants in these DNA regions that are associated with carcinogenesis. This discovery may help explain the 25% risk of familial prostate cancer. Identifying the specific genes influencing prostate cancer risk can lead to new prevention techniques.
Biology molecular vanessa
Scientists have discovered seven new DNA regions that are linked to an increased risk of prostate cancer. A study of prostate cancer patients found variants in these DNA regions that are associated with carcinogenesis. This discovery may help explain the 25% risk of familial prostate cancer. Identifying the specific genes and DNA regions involved in prostate cancer risk could allow for new prevention techniques.
Dna Repair Mechanisms
DNA repair mechanisms are indispensable for cell maintenance. The most common repair mechanisms are base excision repair (BER) and nucleotide excision repair (NER). Deficiencies in repair can lead to diseases like cancer or myelodysplastic syndrome. Studies have found that some viruses like murine polyomavirus activate DNA damage repair proteins like ATR and MRE11 to promote viral replication. Understanding DNA repair is important for developing new treatments for diseases linked to repair deficiencies and viral infections.
Presentación del plegable
The document discusses the importance of DNA replication for life and medicine. DNA replication is essential for cell division and is targeted by chemotherapy drugs to stop the growth of cancer cells. Understanding DNA replication better through research could help develop preventative treatments for diseases and improve medical knowledge.
DNA structure, chromosomes and reparation
Noticias acerca de cancer colorectal y nuevos enfoques terapeuticos desde biologia molecular y la inactivacion del cromosoma X.
Plegable
Scientists have identified molecular bases for DNA breakage, a hallmark of cancer cells. Studying DNA replication in fragile sites could provide insights into cancer development. Understanding weak areas in the DNA that are prone to breakage may help advise new therapeutic interventions and allow modification of cancer progression. More accurate DNA testing techniques in laboratories could help physicians improve cancer diagnosis and treatment.
DNA REPAIR MECHANISMS - Plegable Biología Molecular
DNA repair mechanisms are developed by cells to repair various types of DNA damage induced by chemicals, radiation, and other factors. These repair mechanisms include base excision repair, nucleotide excision repair, strand break repair, and mismatch repair. Recent studies have found new enzymes and gene switches that may play an important role in DNA repair and preventing cancer by contributing to accurate chromosome segregation and reducing genome instability. Understanding DNA repair pathways could provide opportunities to develop new cancer therapies by preventing initial DNA damage or enhancing the body's natural repair processes.
Diapositivas Pleglable
TrovaGene, Inc. obtained an exclusive license for novel mutations associated with prognosis and chemotherapy response in leukemia. Researchers discovered that a mutation in the U2 RNA splicing factor gene can cause neurodegeneration in mice by preventing proper splicing of pre-mRNA into mRNA. The SF3B1 splicing factor mutation was also found to be important for diagnosing and treating chronic lymphocytic leukemia patients. These discoveries provide new insights into disease diagnosis and treatment.
Plegable pp1
Eukaryotic DNA is organized differently than prokaryotes, containing multiple chromosomes made of linear DNA molecules packaged around histone proteins to form chromatin. The cell cycle regulates cell division, ensuring daughter cells receive a full copy of the genome through DNA replication and cell growth or repair. Researchers found inhibiting signaling pathways in brain cancer cells stopped their reproduction and migration, making them more sensitive to chemotherapy. Studying chromatin remodeling genes in pancreatic cancer showed restoring expression of missing genes slowed cancer cell growth and induced senescence.
Plegable pp1
Eukaryotic DNA is organized differently than prokaryotes, containing multiple chromosomes made of linear DNA molecules packaged around histone proteins to form chromatin. The cell cycle regulates cell division, ensuring daughter cells receive a full copy of the genome through DNA replication and cell growth or repair. Researchers found inhibiting signaling pathways in brain cancer cells stopped their reproduction and migration, making them more sensitive to chemotherapy. Studying chromatin remodeling genes in pancreatic cancer showed restoring expression of missing genes slowed cancer cell growth and induced senescence.
Plegable pp1
Eukaryotic DNA is organized differently than prokaryotic DNA, containing multiple chromosomes made of linear DNA molecules packaged around histone proteins to form chromatin. The cell cycle regulates cell division, ensuring daughter cells receive a complete copy of the genome through DNA replication and cell growth or repair. Researchers found inhibiting signaling pathways in brain cancer cells stopped their reproduction and migration, making them more sensitive to chemotherapy. Studying chromatin remodeling genes in pancreatic cancer showed restoring expression of missing genes slowed cancer cell growth and induced senescence.
The central-dogma-oh-genetic-information
The central dogma of genetics describes the flow of genetic information from DNA to RNA to proteins. Two articles discuss cancer-causing mechanisms related to this dogma. One found that the enzyme APOBEC3G can induce mutations during DNA replication that lead to cancer. The other identified that cancer cells rely on the protein SMARCAL1 to resolve replication stress and maintain telomere length through the ALT pathway. Further research is needed to identify targets of these carcinogenic processes to develop new treatment strategies.
New Insight Into the Human Genome Through the Lens of Evolution and decode M...
New Insight Into the Human Genome Through the Lens of Evolution and decode M...Christian Sanchez Valencia
DNA contains the genetic blueprint for human life. It can be used to diagnose diseases by comparing DNA sequences between past and present humans. DNA is transcribed into RNA, some of which encodes proteins and some that performs regulatory functions by determining gene expression. Scientists have discovered that up to 30% of human DNA is conserved at the RNA structure level through a process called transcription. Understanding how RNA is regulated through interactions with proteins and sequences is important for identifying patterns involved in diseases and their treatment.Biology m(1)
The document discusses two studies on the causes of cancer at the chromosomal and DNA level. The first study found that dramatic structural changes to chromosomes could not be explained by standard models of DNA damage and were a major cause of cancer proliferation. The second study discovered the overexpression of repetitive satellite DNA sequences in common tumor cells that are normally found in heterochromatin and centromeres. Understanding the molecular causes of diseases like cancer will enable early diagnosis, new therapeutic targets, and improved treatment strategies.
Plegable biomol Ana Maria Parada Pérez.
The document discusses two scientific discoveries. The first is that an enzyme called UvrD was found to reverse stalled transcription machinery in E. coli, allowing RNA polymerase to backtrack and expose problems in the DNA strand to facilitate repair without terminating transcription. The second discovery found that a genetic mutation in the DNA repair gene POLB in mice unexpectedly caused lupus-like symptoms, identifying a potential genetic cause of the autoimmune disease lupus in humans. Finding the causes of diseases like lupus could help develop new and less toxic treatments. Both discoveries provide insights that could improve understanding of diseases and lead to better prevention and treatment options.
Mechanisms of genetic material repair.
The mechanisms of DNA repair help us maintain the body in a normal physiological state, despite of the constant inducing damage that we are exposed.
But if these repair mechanisms fail for some reason it could cause mutations, cell death and many diseases.
Therefore, a low mutation rate indicates the efficiency of repair mechanisms, but a failure of these will be the cause of several mutations.
Several studies point to the discovery of new mechanisms of repair, so try to create treatments for diseases.
DNA Repair
DNA Repair is a process that corrects a damage in the cell but not always it is good for her, sometimes this reparation is the real problem.
Seminario biologia molecular- Maria Upegui
This document summarizes a study on the effects of inhibiting Notch1 activation to enhance the DNA damage induced by cisplatin in cervical cancer. The study used techniques like western blotting, immunofluorescence staining, immunohistochemistry, and TUNEL assay on cervical cancer cell lines. The results showed that inhibiting Notch1 increased the sensitivity of tumor cells to cisplatin-induced DNA damage. This suggests that inhibiting Notch1 activation could improve the therapeutic efficacy of cisplatin for cervical cancer treatment.
RNA processing
This document discusses RNA processing and the roles of various proteins involved. It describes how angiogenin regulates hematopoietic stem and progenitor cells by inducing different types of RNA processing - tiRNA to promote quiescence in stem cells and rRNA to promote proliferation in myeloid progenitor cells. This has implications for improving stem cell transplantation outcomes. The document also discusses how PARP proteins regulate gene expression and RNA processing, with PARP inhibitors being used in cancer treatments, and how further understanding their targets could improve cancer therapies.
Folding plegable
1. The p53 protein, known as the "guardian of the genome", plays an important role in protecting against cancer by preventing DNA mutations. Scientists have discovered that p53 is activated during meiosis to closely monitor DNA breaks and repairs, preventing mutations from being passed onto gametes.
2. Researchers discovered that the Mec1 protein in yeast acts as the "guardian of the genome" by repairing damaged DNA and replication machinery. Mec1 phosphorylates the SLX4 protein, triggering it to anchor to the replication machinery and perform repairs.
3. Understanding how proteins repair DNA damage provides insights that could lead to new approaches for curing diseases caused by genetic mutations, such as cancer.
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DNA REPAIR MECHANISMS - Plegable Biología Molecular
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MOLECULAR BIOLOGY
- 1. Sara Berdugo Mesa Medicine Student 3rd Semester Universidad Pontificia Bolivariana
- 4. Although cancer is still being a genetic paradigm, nowadays it is believe that is related with factors that alters the replication enzimatic activity and creates mutations given by the cell stress.
- 5. Understand the machinism of an irregular DNA duplication and the uncontrolled division could be the future for the cancer treatment.
- 6. There are proteins like ORC (origin recognition complex) that may originate conformational changes binding to the molecule that is going to be replicated.
- 7. ORC Multiproteinic complex that is compound by 6 proteins. Interacts with molecules at atomic level.
- 8. ORC Facilitate the helicase binding to DNA. It is similar to other proteint that holds the DNA polymerase. Improves the replication.
- 9. The genetic material is the most important target in the cancer genesis, because the cell ignores the mechanisms of growing, proliferation and death. It would be a good strategy to find drugs that act either in the helicase and DNA polymerase in order to achive a control in the replication process and regulate the cell for the cancer treatment.
- 11. The brakings may happen in normal conditions to resting cells that not replicate and have a fragmented DNA.
- 12. All starts when the replication fork is generated, where each DNA strand separetes. The first one is manipulated by the DNA polymerase and generates a new strand, the second one is copied and generates two chromosomes, this leads to DNA breaking by a crash between DNA and RNA polymerase. .
- 13. The DNA breaking can not happen in the replication, so it makes by R-LOOP, that generates double partitions and makes the traduction a fragile moment.
- 14. It is fundamental to make new studies like this to achive knowing the points where the breaks occur, or the points that are fragile for a possible mutation. In this way we can avoid treatments resistance in diseases like cancer and others where the alteration is given by a genomic destabilization.
- 15. Although the initial cause is unknown, is clear that if a normal cell becomes cancerous and transmitted to their descendants, the change is given at the level of genetic material.
- 16. Is important to do experiments to discover new white dots and know that way you can try and repair the alteration.
- 17. These is important to generate treatments that without any doubt be able of attack the target and stop the replication problem. .
- 18. The purpose of these experiments is to find solutions to problems and to generate drugs that help give a better quality of life to people.
- 19. • Key step in molecular ‘dance’ that duplicates DNA deciphered. Science newsline biology; 2013 [cited 2013 Julio 14]; Available from: http://www.sciencenewsline.com/summary/2012071422-120006.html. • BCM Scientists Unravel Mystery Behind DNA Breaks In Resting Cells. Bionews Texas; 2013 [cited 2013 Julio 17]; Available from: http://bionews- tx.com/news/2013/07/17/bcm-scientists-unravel-mystery-behind-dna-breaks-in- resting-cells/.