Molecular biology
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The document discusses two recent discoveries in molecular biology that could have applications for preventing and treating cancer. It describes the identification of TZAP, a protein that controls telomere trimming and cellular aging without causing cancer like other similar proteins. It also outlines the finding of a motor protein called KlpA that can move in both directions, unlike other directional motor proteins, and how motor proteins in general influence processes involved in cancer development.
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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.
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.Diploma Thesis - Abstract
Cancer is one of the leading causes of death in developed countries. The glioblastoma is the most aggressive type of brain tumor. Serglycin (SG) is an intracellular proteoglycan that regulates the storage and activity of inflammatory mediators and bioactive molecules in secretory vesicles. Studies have shown SG is overexpressed in several cancer cell lines and promotes an aggressive phenotype. The thesis studied the effect of suppressing the SG gene in highly metastatic brain cancer cells LN-18. The results revealed that suppressing SG reduced cell proliferation, mobility, and expression of bioactive molecules in the extracellular matrix.
DNA TRANSCRIPTION
This document summarizes two studies on genetic transcription factors and their role in disease. The first study finds that the transcription factor RUNX1 exacerbates acute myeloid leukemia by amplifying the mutant form of FLT3, and inhibiting RUNX1 reduced tumor formation in mice. The second study discovers that ovarian hormones influence transcription of genes in breast stem cells linked to cancer, providing insight into cancer progression. Both studies provide new understanding of transcription factors and disease evolution that could improve current treatment approaches.
Plegable biología molecular
The document discusses two recent studies that focused on the "control code" of DNA replication and RNA transcription in order to better understand causes of diseases like cancer and autism. The studies revealed new insights into how small signaling molecules regulate genome expression by controlling protein complexes that switch genes on and off. Understanding the interactions between proteins that control replication and transcription could allow developing new treatments for many misunderstood diseases.
Arpin downregulation is associated with poor prognosis in pancreatic ductal a...
This document discusses pancreatic ductal adenocarcinoma (PDAC) and the protein Arpin. PDAC is a form of pancreatic cancer with a low 5-year survival rate. Arpin inhibits the Arp2/3 complex, which generates branched actin networks involved in cell motility and migration. The study examined Arpin expression in PDAC tissues using immunohistochemistry and western blot. Results showed Arpin was diminished in PDAC tissues. Low Arpin expression correlated with higher tumor stage and poorer prognosis. As Arpin inhibits Arp2/3, lower Arpin allows increased Arp2/3 activation and cell migration, supporting rapid PDAC metastasis.
Molecular Biology Seminary by Nicolas calle
This is a molecular biology article review seminary showing some relevant characteristics of the micro RNA and its influences in prostate cancer
Protein array, protein chip by kk sahu sir
troduction
History
Types of array
Protein arrays in situ
Protein in-situ arrays
PISA
NAPPA
DAPA
Application
Conclusion
References
Recommended
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.
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.Diploma Thesis - Abstract
Cancer is one of the leading causes of death in developed countries. The glioblastoma is the most aggressive type of brain tumor. Serglycin (SG) is an intracellular proteoglycan that regulates the storage and activity of inflammatory mediators and bioactive molecules in secretory vesicles. Studies have shown SG is overexpressed in several cancer cell lines and promotes an aggressive phenotype. The thesis studied the effect of suppressing the SG gene in highly metastatic brain cancer cells LN-18. The results revealed that suppressing SG reduced cell proliferation, mobility, and expression of bioactive molecules in the extracellular matrix.
DNA TRANSCRIPTION
This document summarizes two studies on genetic transcription factors and their role in disease. The first study finds that the transcription factor RUNX1 exacerbates acute myeloid leukemia by amplifying the mutant form of FLT3, and inhibiting RUNX1 reduced tumor formation in mice. The second study discovers that ovarian hormones influence transcription of genes in breast stem cells linked to cancer, providing insight into cancer progression. Both studies provide new understanding of transcription factors and disease evolution that could improve current treatment approaches.
Plegable biología molecular
The document discusses two recent studies that focused on the "control code" of DNA replication and RNA transcription in order to better understand causes of diseases like cancer and autism. The studies revealed new insights into how small signaling molecules regulate genome expression by controlling protein complexes that switch genes on and off. Understanding the interactions between proteins that control replication and transcription could allow developing new treatments for many misunderstood diseases.
Arpin downregulation is associated with poor prognosis in pancreatic ductal a...
This document discusses pancreatic ductal adenocarcinoma (PDAC) and the protein Arpin. PDAC is a form of pancreatic cancer with a low 5-year survival rate. Arpin inhibits the Arp2/3 complex, which generates branched actin networks involved in cell motility and migration. The study examined Arpin expression in PDAC tissues using immunohistochemistry and western blot. Results showed Arpin was diminished in PDAC tissues. Low Arpin expression correlated with higher tumor stage and poorer prognosis. As Arpin inhibits Arp2/3, lower Arpin allows increased Arp2/3 activation and cell migration, supporting rapid PDAC metastasis.
Molecular Biology Seminary by Nicolas calle
This is a molecular biology article review seminary showing some relevant characteristics of the micro RNA and its influences in prostate cancer
Protein array, protein chip by kk sahu sir
troduction
History
Types of array
Protein arrays in situ
Protein in-situ arrays
PISA
NAPPA
DAPA
Application
Conclusion
References
Potential cancer cells and therapy to treat melanoma
This document discusses potential therapies for treating cancer cells and melanoma. It describes how certain genes like P53 and Cyclin-F help regulate the cell cycle and suppress cancer-causing genes. Researchers found Cyclin-F inhibits the oncogene B-Myb to control cell division. The document also discusses a study combining an AURKA inhibitor and MDM2 antagonist to stop melanoma cell growth in mouse models. Understanding more gene mechanisms could lead to more effective long-lasting cancer treatments.
Plegable biología molecular
Two scientific studies focused on understanding the "control code" of DNA replication and RNA transcription in order to learn more about human diseases like cancer and autism. The studies revealed that RNA transcription, like DNA replication, is regulated by proteins. One study identified the RBFOX1 protein, which ensures activity of important brain genes, is turned off in autism patients. The other study found that inositol phosphates regulate histone deacetylases, enzymes that control DNA replication by packaging DNA tightly and switching genes off. Understanding these protein interactions that control genetic expression could enable new treatments for misunderstood diseases.
Magnetic Resonance Spectroscopy and Metabolomics
Magnetic Resonance Spectroscopy, MRI, Human Connectome, 2-HG, 2-hydroxyglutarate, zoom, zoom MRSI, reduced field of View, rFOV, Cerebellum, High-resolution, IDH, Isocitrate, IDH1, IDH2, Cancer, Glioma, Parcellation, Macro Anatomical
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MR Spectroscopy Study Group
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Bradley Christopher Kruithoff conducted undergraduate research on RNA and its role in gene expression through the Department of Chemistry and Biochemistry at The Ohio State University. The goal of the research was to understand how microRNAs (miRNAs) and small interfering RNAs (siRNAs) regulate gene expression by targeting specific messenger RNA strands for degradation. This research aimed to gain a deeper understanding of the molecular mechanisms by which non-coding RNAs and the Argonaute protein regulate basic cellular processes and how this knowledge could be applied to manipulate gene expression and potentially treat human diseases.
Plegable biología molecular
Two studies investigated the "control code" of DNA replication and RNA transcription to better understand diseases like cancer and autism. One study found that RNA transcription is regulated by proteins similar to how DNA replication is regulated. The other study discovered that inositol phosphates regulate genome expression by controlling enzymes that switch genes on and off. Understanding how proteins control replication and transcription could help develop new treatments for diseases caused by defects in the genetic control code.
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The document discusses recent discoveries about cell division and chromosomes that could help understand disorders like cancer. Researchers discovered the Ska complex of proteins that stabilize cell division by anchoring DNA to cell strands during division. Mistakes in this process can cause cancer. Scientists also used normal chromosomes to replace defective ring chromosomes in skin cells, correcting genetic disorders. Understanding these processes may enable new treatments for cancer and genetic disorders by controlling cell division and repairing chromosome defects.
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 replication
The document discusses DNA replication and how it can go awry. It normally faithfully copies DNA but the APOBEC protein, which normally protects against viruses, can instead cause mutations by interfering with replication. This can lead to cancer. Researchers identified that the protein SMARCAL1 is key to alternative lengthening of telomeres (ALT), a pathway cancer cells use to maintain telomere length and bypass growth arrest. Understanding these replication and repair pathways could lead to new targeted cancer therapies.
Dna replication 2
The document discusses DNA replication and the role of the APOBEC protein. It summarizes that DNA replication is the process where one DNA molecule makes two identical copies of itself. It then explains that the APOBEC protein normally protects against viruses but can also cause mutations during DNA replication, potentially leading to cancer. The student notes it is important to understand these mechanisms to research ways to prevent cancer. A second section discusses how cancer cells can maintain telomere length to continue replicating, and researchers have identified the protein SMARCAL1 as playing a key role in this alternative lengthening of telomeres pathway used by some cancer cells. Understanding this pathway could lead to new targeted cancer therapies.
Protein function
The document discusses two studies: 1) A study showing that the RNF20 protein is required for amplification of MLL-rearranged leukemia. 2) A study describing how multiple RNA binding proteins cooperatively control genetic splicing codes.
Dieter Egli, "Towards Clinical Use of Mitochondrial Replacement"
Dieter Egli, "Towards Clinical Use of Mitochondrial Replacement"The Petrie-Flom Center for Health Law Policy, Biotechnology, and Bioethics
A 2015 Congressional amendment precludes Mitochondrial Replacement Therapy (MRT), a life-saving IVF-based procedure that could prevent a plethora of mitochondrial DNA diseases in the U.S. Individuals do not, at present, have access to this technology to prevent the devastating consequences of mitochondrial DNA disease. At the same time, MRT continues to move forward in other countries, such as the UK.
Has the time come to revisit the federal prohibition of this preventive therapy and research?
Expert panelists discussed the future of MRT policy in the U.S., reviewing the latest technological developments, the regulatory barriers, and the ethical challenges affecting the clinical application of MRT.
This event was free and open to the public.IncellDx Oncobreast 3Dx CSUPERB Poster
This document describes a new multi-parametric assay being developed by IncellDx to simultaneously analyze genomic, proteomic, and cell cycle markers in breast cancer samples. The assay aims to measure 9 markers including ER, PR, HER2, E-cadherin, DNA content and proliferation. Initial studies mixing breast cancer cell lines expressing different markers demonstrated the ability to differentiate markers. Further studies on clinical breast cancer samples found the assay could simultaneously detect HER2 mRNA and protein levels that matched immunohistochemistry results. Future studies will evaluate the assay's clinical performance on 50 breast tumors and 10 normal samples compared to standard pathology.
PROTEINS (Molecular Biology)
The document discusses two studies related to protein synthesis and cancer. The first study developed a new method to selectively silence genes encoding proteins to determine their function in tumor cells. The second study identified the protein components responsible for inserting membrane proteins, resolving a mechanism that was previously unknown. Understanding protein functions and interactions is important for gaining insights into the origins of cancer and developing prevention and treatment strategies.
Leiddy reflection
This study examines using metabolite profiling to detect recurrent breast cancer through nuclear magnetic resonance (NMR) and mass spectrometry (MS). These techniques are used to analyze serum samples and identify putative biomarkers, which are then validated through supervised and unsupervised methods. The supervised method determines if cancer is present, while the unsupervised method detects clusters. This metabolite profiling approach provides a more sensitive detection method than mammography and blood tests and could significantly help increase breast cancer survival rates if applied in clinical practice.
Molecular switch that regulates DNA replication and tracking DNA
Scientists have identified a molecular switch called TEFM that regulates DNA replication and transcription in mitochondria. TEFM acts as a switch to turn transcription and replication processes on and off, and also has an anti-termination activity. This discovery could help prevent collisions between transcription and replication processes in mitochondrial DNA. Additionally, scientists have found that tracking leftover scaffolding from DNA replication can help trace the origins of genetic errors, as these regions tend to accumulate mutations in important regulatory switches. These findings may help scientists better understand diseases and develop new drug therapies.
Shoukrhat Mitalipov, "Mitochondrial Replacement Therapy"
Shoukrhat Mitalipov, "Mitochondrial Replacement Therapy"The Petrie-Flom Center for Health Law Policy, Biotechnology, and Bioethics
Mitochondrial replacement therapy aims to prevent genetic disorders by transferring mitochondria from a donor egg to one with mutations in the mitochondrial DNA. This technique allows for the inheritance of healthy mitochondrial DNA instead of disease-causing mutations. Preclinical animal studies have shown this therapy to be safe and effective, with donor mitochondrial DNA being passed down to subsequent generations. It represents the first form of germline gene therapy for inherited mitochondrial diseases.Mar Gonzales Porta, One gene One transcript, fged_seattle_2013
This document analyzes RNA-seq data from 16 human tissues and 5 cell lines to investigate whether genes typically express multiple isoforms at similar levels or have a single dominant transcript. The analysis found that:
1) For around 79% of genes, one isoform is expressed at least twice as strongly as the next highest isoform.
2) The major transcript of a gene tends to be consistently highly expressed across different tissues, though some switches between dominant transcripts were observed.
3) Around 85% of all mRNA comes from these dominant transcripts. This suggests that despite transcriptome complexity, the traditional view of one gene producing one protein may be closer to the truth than previously believed.
Seminario de bilogia molecular copia
This presentation contain information about molecular biology and laboratory technics, specially alternative splicing.
all of them to try to explain cancer etiology, give on the molecular bases.
TRIM 47 accelerates aerobic glycolysis and tumor progression through regulati...
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This document summarizes key aspects of pancreatic cancer. It begins by defining the pancreas and describing the two main types of pancreatic cancer - adenocarcinoma and neuroendocrine tumors. Adenocarcinoma accounts for about 95% of pancreatic cancers. Current treatment options for pancreatic cancer are then outlined, including surgery, radiation therapy, chemotherapy, targeted therapy, and immunotherapy. The document also provides brief descriptions of two genes - FBP1 and TRIM47 - that are relevant to pancreatic cancer. It concludes by stating that ubiquitination plays a vital role in pancreatic cancer pathogenesis and targeting ubiquitination regulation could be a potential treatment approach.Could we be the solution?
This document discusses how cells can combat chromosome imbalance and discusses potential medical applications. It describes how researchers discovered that when cells detect genetic problems in their chromosomes, they signal nearby natural killer cells to destroy them, preventing conditions like cancer. The document also discusses how new technologies may help treat diseases like Parkinson's by using synthetic materials or coded DNA to signal stem cells to proliferate or differentiate into targeted cell types like neurons. This could help develop regenerative treatments for neurodegenerative diseases and other conditions.
Endothelial dysfunction in indian scenario
www,heartsense.in. Endothelial dysfunction is the root pathology in the pathogenesis of hypertension, diabetes and IHD. This technical article is aimed towards health care professionals. For patient information on health and heart disease, visit www.heartsense.in.
Chromosomes and Chromatin
The document discusses two recent discoveries related to genetics and disease. Researchers discovered a mechanism of gene silencing in hormone-dependent breast cancer cells involving a protein that interacts with the progesterone receptor and compacts chromatin. Scientists also discovered an X-chromosome inherited form of brittle bone disease osteogenesis imperfecta caused by two mutations in the MBTPS2 gene on the X chromosome, making men more vulnerable. These findings provide insights that can help improve diagnosis and treatment of these diseases.
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Potential cancer cells and therapy to treat melanoma
This document discusses potential therapies for treating cancer cells and melanoma. It describes how certain genes like P53 and Cyclin-F help regulate the cell cycle and suppress cancer-causing genes. Researchers found Cyclin-F inhibits the oncogene B-Myb to control cell division. The document also discusses a study combining an AURKA inhibitor and MDM2 antagonist to stop melanoma cell growth in mouse models. Understanding more gene mechanisms could lead to more effective long-lasting cancer treatments.
Plegable biología molecular
Two scientific studies focused on understanding the "control code" of DNA replication and RNA transcription in order to learn more about human diseases like cancer and autism. The studies revealed that RNA transcription, like DNA replication, is regulated by proteins. One study identified the RBFOX1 protein, which ensures activity of important brain genes, is turned off in autism patients. The other study found that inositol phosphates regulate histone deacetylases, enzymes that control DNA replication by packaging DNA tightly and switching genes off. Understanding these protein interactions that control genetic expression could enable new treatments for misunderstood diseases.
Magnetic Resonance Spectroscopy and Metabolomics
Magnetic Resonance Spectroscopy, MRI, Human Connectome, 2-HG, 2-hydroxyglutarate, zoom, zoom MRSI, reduced field of View, rFOV, Cerebellum, High-resolution, IDH, Isocitrate, IDH1, IDH2, Cancer, Glioma, Parcellation, Macro Anatomical
Functional
Myeloarchitectonic
CYTO- AND RECEPTOR ARCHITECTONIC MAPPING OF THE HUMAN BRAIN
MR Spectroscopy Study Group
RSA Grant
Bradley Christopher Kruithoff conducted undergraduate research on RNA and its role in gene expression through the Department of Chemistry and Biochemistry at The Ohio State University. The goal of the research was to understand how microRNAs (miRNAs) and small interfering RNAs (siRNAs) regulate gene expression by targeting specific messenger RNA strands for degradation. This research aimed to gain a deeper understanding of the molecular mechanisms by which non-coding RNAs and the Argonaute protein regulate basic cellular processes and how this knowledge could be applied to manipulate gene expression and potentially treat human diseases.
Plegable biología molecular
Two studies investigated the "control code" of DNA replication and RNA transcription to better understand diseases like cancer and autism. One study found that RNA transcription is regulated by proteins similar to how DNA replication is regulated. The other study discovered that inositol phosphates regulate genome expression by controlling enzymes that switch genes on and off. Understanding how proteins control replication and transcription could help develop new treatments for diseases caused by defects in the genetic control code.
Plegable
The document discusses recent discoveries about cell division and chromosomes that could help understand disorders like cancer. Researchers discovered the Ska complex of proteins that stabilize cell division by anchoring DNA to cell strands during division. Mistakes in this process can cause cancer. Scientists also used normal chromosomes to replace defective ring chromosomes in skin cells, correcting genetic disorders. Understanding these processes may enable new treatments for cancer and genetic disorders by controlling cell division and repairing chromosome defects.
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 replication
The document discusses DNA replication and how it can go awry. It normally faithfully copies DNA but the APOBEC protein, which normally protects against viruses, can instead cause mutations by interfering with replication. This can lead to cancer. Researchers identified that the protein SMARCAL1 is key to alternative lengthening of telomeres (ALT), a pathway cancer cells use to maintain telomere length and bypass growth arrest. Understanding these replication and repair pathways could lead to new targeted cancer therapies.
Dna replication 2
The document discusses DNA replication and the role of the APOBEC protein. It summarizes that DNA replication is the process where one DNA molecule makes two identical copies of itself. It then explains that the APOBEC protein normally protects against viruses but can also cause mutations during DNA replication, potentially leading to cancer. The student notes it is important to understand these mechanisms to research ways to prevent cancer. A second section discusses how cancer cells can maintain telomere length to continue replicating, and researchers have identified the protein SMARCAL1 as playing a key role in this alternative lengthening of telomeres pathway used by some cancer cells. Understanding this pathway could lead to new targeted cancer therapies.
Protein function
The document discusses two studies: 1) A study showing that the RNF20 protein is required for amplification of MLL-rearranged leukemia. 2) A study describing how multiple RNA binding proteins cooperatively control genetic splicing codes.
Dieter Egli, "Towards Clinical Use of Mitochondrial Replacement"
Dieter Egli, "Towards Clinical Use of Mitochondrial Replacement"The Petrie-Flom Center for Health Law Policy, Biotechnology, and Bioethics
A 2015 Congressional amendment precludes Mitochondrial Replacement Therapy (MRT), a life-saving IVF-based procedure that could prevent a plethora of mitochondrial DNA diseases in the U.S. Individuals do not, at present, have access to this technology to prevent the devastating consequences of mitochondrial DNA disease. At the same time, MRT continues to move forward in other countries, such as the UK.
Has the time come to revisit the federal prohibition of this preventive therapy and research?
Expert panelists discussed the future of MRT policy in the U.S., reviewing the latest technological developments, the regulatory barriers, and the ethical challenges affecting the clinical application of MRT.
This event was free and open to the public.IncellDx Oncobreast 3Dx CSUPERB Poster
This document describes a new multi-parametric assay being developed by IncellDx to simultaneously analyze genomic, proteomic, and cell cycle markers in breast cancer samples. The assay aims to measure 9 markers including ER, PR, HER2, E-cadherin, DNA content and proliferation. Initial studies mixing breast cancer cell lines expressing different markers demonstrated the ability to differentiate markers. Further studies on clinical breast cancer samples found the assay could simultaneously detect HER2 mRNA and protein levels that matched immunohistochemistry results. Future studies will evaluate the assay's clinical performance on 50 breast tumors and 10 normal samples compared to standard pathology.
PROTEINS (Molecular Biology)
The document discusses two studies related to protein synthesis and cancer. The first study developed a new method to selectively silence genes encoding proteins to determine their function in tumor cells. The second study identified the protein components responsible for inserting membrane proteins, resolving a mechanism that was previously unknown. Understanding protein functions and interactions is important for gaining insights into the origins of cancer and developing prevention and treatment strategies.
Leiddy reflection
This study examines using metabolite profiling to detect recurrent breast cancer through nuclear magnetic resonance (NMR) and mass spectrometry (MS). These techniques are used to analyze serum samples and identify putative biomarkers, which are then validated through supervised and unsupervised methods. The supervised method determines if cancer is present, while the unsupervised method detects clusters. This metabolite profiling approach provides a more sensitive detection method than mammography and blood tests and could significantly help increase breast cancer survival rates if applied in clinical practice.
Molecular switch that regulates DNA replication and tracking DNA
Scientists have identified a molecular switch called TEFM that regulates DNA replication and transcription in mitochondria. TEFM acts as a switch to turn transcription and replication processes on and off, and also has an anti-termination activity. This discovery could help prevent collisions between transcription and replication processes in mitochondrial DNA. Additionally, scientists have found that tracking leftover scaffolding from DNA replication can help trace the origins of genetic errors, as these regions tend to accumulate mutations in important regulatory switches. These findings may help scientists better understand diseases and develop new drug therapies.
Shoukrhat Mitalipov, "Mitochondrial Replacement Therapy"
Shoukrhat Mitalipov, "Mitochondrial Replacement Therapy"The Petrie-Flom Center for Health Law Policy, Biotechnology, and Bioethics
Mitochondrial replacement therapy aims to prevent genetic disorders by transferring mitochondria from a donor egg to one with mutations in the mitochondrial DNA. This technique allows for the inheritance of healthy mitochondrial DNA instead of disease-causing mutations. Preclinical animal studies have shown this therapy to be safe and effective, with donor mitochondrial DNA being passed down to subsequent generations. It represents the first form of germline gene therapy for inherited mitochondrial diseases.Mar Gonzales Porta, One gene One transcript, fged_seattle_2013
This document analyzes RNA-seq data from 16 human tissues and 5 cell lines to investigate whether genes typically express multiple isoforms at similar levels or have a single dominant transcript. The analysis found that:
1) For around 79% of genes, one isoform is expressed at least twice as strongly as the next highest isoform.
2) The major transcript of a gene tends to be consistently highly expressed across different tissues, though some switches between dominant transcripts were observed.
3) Around 85% of all mRNA comes from these dominant transcripts. This suggests that despite transcriptome complexity, the traditional view of one gene producing one protein may be closer to the truth than previously believed.
Seminario de bilogia molecular copia
This presentation contain information about molecular biology and laboratory technics, specially alternative splicing.
all of them to try to explain cancer etiology, give on the molecular bases.
TRIM 47 accelerates aerobic glycolysis and tumor progression through regulati...
TRIM 47 accelerates aerobic glycolysis and tumor progression through regulati...MariaFernandaMazoPar
This document summarizes key aspects of pancreatic cancer. It begins by defining the pancreas and describing the two main types of pancreatic cancer - adenocarcinoma and neuroendocrine tumors. Adenocarcinoma accounts for about 95% of pancreatic cancers. Current treatment options for pancreatic cancer are then outlined, including surgery, radiation therapy, chemotherapy, targeted therapy, and immunotherapy. The document also provides brief descriptions of two genes - FBP1 and TRIM47 - that are relevant to pancreatic cancer. It concludes by stating that ubiquitination plays a vital role in pancreatic cancer pathogenesis and targeting ubiquitination regulation could be a potential treatment approach.Could we be the solution?
This document discusses how cells can combat chromosome imbalance and discusses potential medical applications. It describes how researchers discovered that when cells detect genetic problems in their chromosomes, they signal nearby natural killer cells to destroy them, preventing conditions like cancer. The document also discusses how new technologies may help treat diseases like Parkinson's by using synthetic materials or coded DNA to signal stem cells to proliferate or differentiate into targeted cell types like neurons. This could help develop regenerative treatments for neurodegenerative diseases and other conditions.
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Potential cancer cells and therapy to treat melanoma
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Dieter Egli, "Towards Clinical Use of Mitochondrial Replacement"
Dieter Egli, "Towards Clinical Use of Mitochondrial Replacement"
Molecular switch that regulates DNA replication and tracking DNA
Molecular switch that regulates DNA replication and tracking DNA
Shoukrhat Mitalipov, "Mitochondrial Replacement Therapy"
Shoukrhat Mitalipov, "Mitochondrial Replacement Therapy"
Mar Gonzales Porta, One gene One transcript, fged_seattle_2013
Mar Gonzales Porta, One gene One transcript, fged_seattle_2013
TRIM 47 accelerates aerobic glycolysis and tumor progression through regulati...
TRIM 47 accelerates aerobic glycolysis and tumor progression through regulati...
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Chromosomes and Chromatin
The document discusses two recent discoveries related to genetics and disease. Researchers discovered a mechanism of gene silencing in hormone-dependent breast cancer cells involving a protein that interacts with the progesterone receptor and compacts chromatin. Scientists also discovered an X-chromosome inherited form of brittle bone disease osteogenesis imperfecta caused by two mutations in the MBTPS2 gene on the X chromosome, making men more vulnerable. These findings provide insights that can help improve diagnosis and treatment of these diseases.
All about genes oncogenes mutations-cloning-gene therapy
1) DNA contains the genetic code and is located in chromosomes within the nucleus. DNA is transcribed into RNA and translated into proteins, which allows genes to be expressed.
2) Mutations in genes can be caused by errors in DNA replication or exposure to mutagens and can have neutral, harmful, or beneficial effects depending on where they occur. Mutations in proto-oncogenes can transform them into oncogenes and promote cancer development.
3) Cloning techniques allow for the duplication of DNA, whole organisms, or embryonic stem cells for research and potential therapies. Gene cloning is used to study and modify genes, while reproductive and therapeutic cloning are more controversial due to ethical concerns.
Genetic Testing (Eastern Biotech & Life Sciences)
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Oncogenes
Cancer is characterized by uncontrolled cell growth and spread. At the cellular level, cancer cells proliferate excessively, grow in an uncoordinated manner, and infiltrate surrounding tissues. This uncontrolled growth is caused by genetic disorders that affect genes regulating cell growth. Cancer cells lose control over growth and multiplication and do not self-destruct like normal cells. They crowd out healthy cells. Genetic changes can activate oncogenes or inactivate tumor suppressor genes, disrupting the normal balance between cell proliferation and cell death. A variety of genetic, environmental, and viral factors can cause these genetic changes and contribute to cancer development.
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The document discusses how normal cells are transformed into cancer cells through multiple genetic changes over many years. It describes several key changes that occur during this process, including immortalization where cells can divide indefinitely, transformation where cells grow independently of external signals, and metastasis where cancer cells invade other tissues. Several types of genetic alterations are also discussed that can activate oncogenes or inactivate tumor suppressor genes, such as mutations, amplification, insertion, or translocation events. This leads to deregulated cell growth and proliferation by disrupting normal cell signaling pathways.
Cell & Molecular Biology
This course involves the study of 4 units: Cell and Molecular Biology, Environmental Biology, Physiology, Health & Exercise, and Investigation. The Cell and Molecular Biology unit covers the structure and function of prokaryotic and eukaryotic cells and their components. It also examines molecular interactions in cells and applications of DNA technology. Practical work is included in the first three units, while the fourth unit involves a student-designed research experiment and report.
Oncogenes
Cancer is caused by mutations in genes that regulate cell growth and proliferation. These mutations can activate proto-oncogenes into oncogenes or inactivate tumor suppressor genes. Oncogenes promote cell growth while tumor suppressor genes normally inhibit cell proliferation. Common mechanisms of proto-oncogene activation include chromosomal translocations, gene amplifications, and point mutations. Disruptions to cell cycle checkpoints, apoptosis, telomere maintenance and DNA repair pathways can also contribute to cancer development by allowing abnormal cell growth and survival.
Cancer and the immune system
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Cancer mm
Cancer is characterized by uncontrolled cell growth and the ability of cells to invade other tissues. Normal cells grow and divide in an orderly way, while cancer cells continue growing and dividing instead of dying. Cancer develops due to damaged DNA that is not repaired. Lifestyle factors like tobacco use, pollution, diet, obesity, and ultraviolet radiation exposure can damage DNA and increase cancer risk. Antioxidants from fruits and vegetables help neutralize free radicals that damage cells. Exercise, nutrition, and staying at a healthy weight can help prevent cancer development. Cancer treatments include chemotherapy, radiation, and surgery, but prevention through lifestyle is most effective.
Oncogenes
An oncogene is a gene that has the potential to cause cancer. In tumor cells, they are mutated or expressed at high levels. Most normal cells undergo a programmed form of rapid cell death (apoptosis) when critical functions are altered.
Introduction to next generation sequencing
This document provides an introduction to next generation sequencing (NGS) technologies. It begins with an outline of topics to be covered, including the evolution of NGS technologies, their descriptions and comparisons, bioinformatics challenges of NGS data analysis, and some aspects of NGS data analysis workflows and tools. The document then delves into explanations of specific NGS platforms, their performance characteristics, and the sequencing processes. It discusses the large computational infrastructure and data management needs of NGS, as well as quality control, preprocessing of NGS data, and popular analysis tools and workflows.
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Presentation on the basic principles of Next Generation Sequencing, delivered at the Belgian Scientific Institute of Public Health on Oct 10, 2014.
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Molecular biology
- 1. Molecular biology in progress against cancer Gabriela Coronado Magalhães MEDICINE STUDENT
- 4. IMPORTANT RESEARCHERS HELP IN SO MANY ADVANCES FOR PREVENTS AND TREATS CANCER
- 5. MASTER REGULATOR OF CELLULAR AGING DISCOVERED TZAP IT’S A PROTEIN, THAT BINDS THE ENDS OF CHROMOSOMES ;DETERMINES HOW LONG TELOMERES CAN BE.
- 6. MASTER REGULATOR OF CELLULAR AGING DISCOVERED The researcher found that TZAP controls a process called telomere trimming, ensuring that telomeres do not become too long.
- 7. Others proteins like telomerase has the same function as TZAP , but this last protein does not develop cancer. MASTER REGULATOR OF CELLULAR AGING DISCOVERED
- 8. This discovery was a surprise for many scientists in the field believed there were no additional proteins binding to telomeres. MASTER REGULATOR OF CELLULAR AGING DISCOVERED
- 9. STUDENT OBSERVATION This protein can be clinically useful, because besides of replicating the sequenes of telomeric DNA it does not produce cancer
- 10. Scientists discover a molecular motor has a 'gear' for directional switching Oregon State University January 4, 2017
- 11. SCIENTISTS DISCOVER A MOLECULAR MOTOR HAS A 'GEAR' FOR DIRECTIONAL SWITCHING Motor proteins are molecular machines that has an important function becouse this protein converts chemical energy into mechanical work,They are considered"vehicles" of a cell
- 12. SCIENTISTS DISCOVER A MOLECULAR MOTOR HAS A 'GEAR' FOR DIRECTIONAL SWITCHING The function of many motor proteins are still unclear, but they know that motor proteins shuttle cellular cargos between locations and generate forces to position chromosomes
- 13. SCIENTISTS DISCOVER A MOLECULAR MOTOR HAS A 'GEAR' FOR DIRECTIONAL SWITCHING For the discovery of a new motor protein called KlpA, the Researchers used a high-sensitivity light microscopy method to directly follow the movement of individual KlpA molecules on the cytoskeleton track. They discovered that KlpA is able to move in opposite directions.Making the difference between other motor proteins that are undirectional.
- 14. STUDENT OBSERVATION • This protein can be clinically useful, because besides of replicating the sequences of telomeric DNA it does not produce cancer
- 15. MEDICAL UTILITY • The discovery of the proteins klpa and tzap, even though their principal functions differ, they still have great clinical importance.
- 16. MEDICAL UTILITY TZAP by their enzymatic activities they can help prevent and treat cancer.
- 17. MEDICAL UTILITY • TZAP Allow how long telomeres can be, which is very important because telomeres set the lifespan of cells in the body, dictating critical processes such as aging and the incidence of cancer.
- 18. MEDICAL UTILITY • KlpA-like motors proteins in humans are a influation of cancer cell and eventually can helps to lead to novel approaches to cancer treatment.
- 19. Bibliografía • Master regulator of cellular aging discovered. (2017). ScienceDaily. Retrieved 9 February 2017, from https://www.sciencedaily.com/releases/2017/01/ 170112141350.htm • Scientists discover a molecular motor has a 'gear' for directional switching. (2017). ScienceDaily. Retrieved 9 February 2017, from https://www.sciencedaily.com/releases/2017/01/ 170104103552.htm