Ataxia Telangiectasia Mutated Proteins
Cell Cycle Proteins
Checkpoint Kinase 2
Tumor Suppressor Protein p53
DNA Breaks, Double-Stranded
Tumor Suppressor Proteins
DNA Repair Enzymes
Dose-Response Relationship, Radiation
Reactive Oxygen Species
Cell Cycle Checkpoints
DNA Breaks, Single-Stranded
Saccharomyces cerevisiae Proteins
DNA-Activated Protein Kinase
G2 Phase Cell Cycle Checkpoints
Intracellular Signaling Peptides and Proteins
Replication Protein A
Recombinational DNA Repair
Poly Adenosine Diphosphate Ribose
RNA, Small Interfering
Molecular Sequence Data
SOS Response (Genetics)
Proto-Oncogene Proteins c-mdm2
Cyclin-Dependent Kinase Inhibitor p21
DNA End-Joining Repair
Dose-Response Relationship, Drug
Xeroderma Pigmentosum Group A Protein
Proliferating Cell Nuclear Antigen
Schizosaccharomyces pombe Proteins
Brain Damage, Chronic
Gene Expression Regulation
Linear Energy Transfer
Tumor Cells, Cultured
Chromosomal Proteins, Non-Histone
In Situ Nick-End Labeling
Sister Chromatid Exchange
Amino Acid Sequence
Telomeric Repeat Binding Protein 2
DNA-(Apurinic or Apyrimidinic Site) Lyase
Protein Structure, Tertiary
Chromatin Assembly and Disassembly
S Phase Cell Cycle Checkpoints
DNA-Directed DNA Polymerase
Disease Models, Animal
Free Radical Scavengers
Fanconi Anemia Complementation Group D2 Protein
CDC2 Protein Kinase
DNA Topoisomerases, Type I
Gene Knockdown Techniques
Rad52 DNA Repair and Recombination Protein
Protein Processing, Post-Translational
Rec A Recombinases
E2F1 Transcription Factor
Long-range oxidative damage to DNA: effects of distance and sequence. (1/17364)INTRODUCTION: Oxidative damage to DNA in vivo can lead to mutations and cancer. DNA damage and repair studies have not yet revealed whether permanent oxidative lesions are generated by charges migrating over long distances. Both photoexcited *Rh(III) and ground-state Ru(III) intercalators were previously shown to oxidize guanine bases from a remote site in oligonucleotide duplexes by DNA-mediated electron transfer. Here we examine much longer charge-transport distances and explore the sensitivity of the reaction to intervening sequences. RESULTS: Oxidative damage was examined in a series of DNA duplexes containing a pendant intercalating photooxidant. These studies revealed a shallow dependence on distance and no dependence on the phasing orientation of the oxidant relative to the site of damage, 5'-GG-3'. The intervening DNA sequence has a significant effect on the yield of guanine oxidation, however. Oxidation through multiple 5'-TA-3' steps is substantially diminished compared to through other base steps. We observed intraduplex guanine oxidation by tethered *Rh(III) and Ru(III) over a distance of 200 A. The distribution of oxidized guanine varied as a function of temperature between 5 and 35 degrees C, with an increase in the proportion of long-range damage (> 100 A) occurring at higher temperatures. CONCLUSIONS: Guanines are oxidized as a result of DNA-mediated charge transport over significant distances (e.g. 200 A). Although long-range charge transfer is dependent on distance, it appears to be modulated by intervening sequence and sequence-dependent dynamics. These discoveries hold important implications with respect to DNA damage in vivo. (+info)
Gadd45, a p53-responsive stress protein, modifies DNA accessibility on damaged chromatin. (2/17364)This report demonstrates that Gadd45, a p53-responsive stress protein, can facilitate topoisomerase relaxing and cleavage activity in the presence of core histones. A correlation between reduced expression of Gadd45 and increased resistance to topoisomerase I and topoisomerase II inhibitors in a variety of human cell lines was also found. Gadd45 could potentially mediate this effect by destabilizing histone-DNA interactions since it was found to interact directly with the four core histones. To evaluate this possibility, we investigated the effect of Gadd45 on preassembled mononucleosomes. Our data indicate that Gadd45 directly associates with mononucleosomes that have been altered by histone acetylation or UV radiation. This interaction resulted in increased DNase I accessibility on hyperacetylated mononucleosomes and substantial reduction of T4 endonuclease V accessibility to cyclobutane pyrimidine dimers on UV-irradiated mononucleosomes but not on naked DNA. Both histone acetylation and UV radiation are thought to destabilize the nucleosomal structure. Hence, these results imply that Gadd45 can recognize an altered chromatin state and modulate DNA accessibility to cellular proteins. (+info)
The Saccharomyces cerevisiae ETH1 gene, an inducible homolog of exonuclease III that provides resistance to DNA-damaging agents and limits spontaneous mutagenesis. (3/17364)The recently sequenced Saccharomyces cerevisiae genome was searched for a gene with homology to the gene encoding the major human AP endonuclease, a component of the highly conserved DNA base excision repair pathway. An open reading frame was found to encode a putative protein (34% identical to the Schizosaccharomyces pombe eth1(+) [open reading frame SPBC3D6.10] gene product) with a 347-residue segment homologous to the exonuclease III family of AP endonucleases. Synthesis of mRNA from ETH1 in wild-type cells was induced sixfold relative to that in untreated cells after exposure to the alkylating agent methyl methanesulfonate (MMS). To investigate the function of ETH1, deletions of the open reading frame were made in a wild-type strain and a strain deficient in the known yeast AP endonuclease encoded by APN1. eth1 strains were not more sensitive to killing by MMS, hydrogen peroxide, or phleomycin D1, whereas apn1 strains were approximately 3-fold more sensitive to MMS and approximately 10-fold more sensitive to hydrogen peroxide than was the wild type. Double-mutant strains (apn1 eth1) were approximately 15-fold more sensitive to MMS and approximately 2- to 3-fold more sensitive to hydrogen peroxide and phleomycin D1 than were apn1 strains. Elimination of ETH1 in apn1 strains also increased spontaneous mutation rates 9- or 31-fold compared to the wild type as determined by reversion to adenine or lysine prototrophy, respectively. Transformation of apn1 eth1 cells with an expression vector containing ETH1 reversed the hypersensitivity to MMS and limited the rate of spontaneous mutagenesis. Expression of ETH1 in a dut-1 xthA3 Escherichia coli strain demonstrated that the gene product functionally complements the missing AP endonuclease activity. Thus, in apn1 cells where the major AP endonuclease activity is missing, ETH1 offers an alternate capacity for repair of spontaneous or induced damage to DNA that is normally repaired by Apn1 protein. (+info)
Impaired translesion synthesis in xeroderma pigmentosum variant extracts. (4/17364)Xeroderma pigmentosum variant (XPV) cells are characterized by a cellular defect in the ability to synthesize intact daughter DNA strands on damaged templates. Molecular mechanisms that facilitate replication fork progression on damaged DNA in normal cells are not well defined. In this study, we used single-stranded plasmid molecules containing a single N-2-acetylaminofluorene (AAF) adduct to analyze translesion synthesis (TLS) catalyzed by extracts of either normal or XPV primary skin fibroblasts. In one of the substrates, the single AAF adduct was located at the 3' end of a run of three guanines that was previously shown to induce deletion of one G by a slippage mechanism. Primer extension reactions performed by normal cellular extracts from four different individuals produced the same distinct pattern of TLS, with over 80% of the products resulting from the elongation of a slipped intermediate and the remaining 20% resulting from a nonslipped intermediate. In contrast, with cellular extracts from five different XPV patients, the TLS reaction was strongly reduced, yielding only low amounts of TLS via the nonslipped intermediate. With our second substrate, in which the AAF adduct was located at the first G in the run, thus preventing slippage from occurring, we confirmed that normal extracts were able to perform TLS 10-fold more efficiently than XPV extracts. These data demonstrate unequivocally that the defect in XPV cells resides in translesion synthesis independently of the slippage process. (+info)
Postnatal growth failure, short life span, and early onset of cellular senescence and subsequent immortalization in mice lacking the xeroderma pigmentosum group G gene. (5/17364)The xeroderma pigmentosum group G (XP-G) gene (XPG) encodes a structure-specific DNA endonuclease that functions in nucleotide excision repair (NER). XP-G patients show various symptoms, ranging from mild cutaneous abnormalities to severe dermatological impairments. In some cases, patients exhibit growth failure and life-shortening and neurological dysfunctions, which are characteristics of Cockayne syndrome (CS). The known XPG protein function as the 3' nuclease in NER, however, cannot explain the development of CS in certain XP-G patients. To gain an insight into the functions of the XPG protein, we have generated and examined mice lacking xpg (the mouse counterpart of the human XPG gene) alleles. The xpg-deficient mice exhibited postnatal growth failure and underwent premature death. Since XPA-deficient mice, which are totally defective in NER, do not show such symptoms, our data indicate that XPG performs an additional function(s) besides its role in NER. Our in vitro studies showed that primary embryonic fibroblasts isolated from the xpg-deficient mice underwent premature senescence and exhibited the early onset of immortalization and accumulation of p53. (+info)
Analysis of genomic integrity and p53-dependent G1 checkpoint in telomerase-induced extended-life-span human fibroblasts. (6/17364)Life span determination in normal human cells may be regulated by nucleoprotein structures called telomeres, the physical ends of eukaryotic chromosomes. Telomeres have been shown to be essential for chromosome stability and function and to shorten with each cell division in normal human cells in culture and with age in vivo. Reversal of telomere shortening by the forced expression of telomerase in normal cells has been shown to elongate telomeres and extend the replicative life span (H. Vaziri and S. Benchimol, Curr. Biol. 8:279-282, 1998; A. G. Bodnar et al., Science 279:349-352, 1998). Extension of the life span as a consequence of the functional inactivation of p53 is frequently associated with loss of genomic stability. Analysis of telomerase-induced extended-life-span fibroblast (TIELF) cells by G banding and spectral karyotyping indicated that forced extension of the life span by telomerase led to the transient formation of aberrant structures, which were subsequently resolved in higher passages. However, the p53-dependent G1 checkpoint was intact as assessed by functional activation of p53 protein in response to ionizing radiation and subsequent p53-mediated induction of p21(Waf1/Cip1/Sdi1). TIELF cells were not tumorigenic and had a normal DNA strand break rejoining activity and normal radiosensitivity in response to ionizing radiation. (+info)
Phosphorylation of the DNA repair protein APE/REF-1 by CKII affects redox regulation of AP-1. (7/17364)The DNA repair protein apurinic endonuclease (APE/Ref-1) exerts several physiological functions such as cleavage of apurinic/apyrimidinic sites and redox regulation of the transcription factor AP-1, whose activation is part of the cellular response to DNA damaging treatments. Here we demonstrate that APE/Ref-1 is phosphorylated by casein kinase II (CKII). This was shown for both the recombinant APE/Ref-1 protein (Km=0.55 mM) and for APE/Ref-1 expressed in COS cells. Phosphorylation of APE/Ref-1 did not alter the repair activity of the enzyme, whereas it stimulated its redox capability towards AP-1, thus promoting DNA binding activity of AP-1. Inhibition of CKII mediated phosphorylation of APE/Ref-1 blocked mutagen-stimulated increase in AP-1 binding. It also abrogated the induction of c-Jun protein and rendered cells more sensitive to induced DNA damage. Thus, phosphorylation of APE/Ref-1 appears to be involved in regulating the different physiological activities of the enzyme. CKII mediated phosphorylation of APE/Ref-1 and concomitant increase in AP-1 binding activity appears to be a novel mechanism of cellular stress response, forcing transcription of AP-1 target gene(s) the product(s) of which may exert protective function. (+info)
Differential regulation of p21waf-1/cip-1 and Mdm2 by etoposide: etoposide inhibits the p53-Mdm2 autoregulatory feedback loop. (8/17364)The Mdm2 protein is frequently overexpressed in human non-seminomatous germ cell tumours and transitional carcinoma of the bladder where it may contribute to tolerance of wtp53. Mdm2 forms an autoregulatory feedback loop with p53; the Mdm2 gene is responsive to transactivation by p53 and once synthesized the Mdm2 protein terminates the p53 response. We show here that the topoisomerase poison etoposide, like ultra violet irradiation, inhibits Mdm2 synthesis. Cytotoxic concentrations of etoposide (IC90 for > 3 h) result in inhibition of Mdm2 induction at both the RNA and protein level. Rapid apoptosis ensues. Global transcription is not inhibited: p21waf-1/cip1 and GADD45 expression increase in a dose dependent manner. Inhibition of Mdm2 synthesis depends on the continuous presence of etoposide, suggesting the DNA damage may prevent transcription. Downregulation of Mdm2 transcript occurs in cells expressing HPV16-E6 suggesting that inhibition of Mdm2 transcription is p53-independent. When cells are -treated with a pulse (1 h) of etoposide and reincubated in drug free medium, Mdm2 synthesis commences immediately after damage is repaired (3 h) and the p53 response is attenuated. Induction of apoptosis and loss of clonogenicity are 3-5-fold lower under pulse treatment conditions. This is the first observation of inhibition of Mdm2 transcription following treatment with topoisomerase (topo II) poisons, a feature that may be useful in tumour types where p53 is tolerated by overexpression of Mdm2. (+info)
Ataxia Telangiectasia Mutated (ATM) proteins are a group of enzymes that play a critical role in the maintenance of genomic stability and the response to DNA damage. They are involved in the regulation of cell cycle checkpoints, DNA repair, and the activation of DNA damage response pathways. Mutations in the ATM gene can lead to a genetic disorder called Ataxia Telangiectasia (AT), which is characterized by progressive loss of coordination, telangiectases (abnormal blood vessels), and an increased risk of cancer. ATM proteins are also involved in the regulation of other cellular processes, such as inflammation and cell death.
Cell cycle proteins are a group of proteins that play a crucial role in regulating the progression of the cell cycle. The cell cycle is a series of events that a cell goes through in order to divide and produce two daughter cells. It consists of four main phases: G1 (Gap 1), S (Synthesis), G2 (Gap 2), and M (Mitosis). Cell cycle proteins are involved in regulating the progression of each phase of the cell cycle, ensuring that the cell divides correctly and that the daughter cells have the correct number of chromosomes. Some of the key cell cycle proteins include cyclins, cyclin-dependent kinases (CDKs), and checkpoint proteins. Cyclins are proteins that are synthesized and degraded in a cyclic manner throughout the cell cycle. They bind to CDKs, which are enzymes that regulate cell cycle progression by phosphorylating target proteins. The activity of CDKs is tightly regulated by cyclins, ensuring that the cell cycle progresses in a controlled manner. Checkpoint proteins are proteins that monitor the cell cycle and ensure that the cell does not proceed to the next phase until all the necessary conditions are met. If any errors are detected, checkpoint proteins can halt the cell cycle and activate repair mechanisms to correct the problem. Overall, cell cycle proteins play a critical role in maintaining the integrity of the cell cycle and ensuring that cells divide correctly. Disruptions in the regulation of cell cycle proteins can lead to a variety of diseases, including cancer.
Deoxyguanosine is a nucleoside, which is a building block of DNA and RNA. It is composed of a deoxyribose sugar molecule, a nitrogenous base (guanine), and a phosphate group. In DNA, deoxyguanosine is paired with cytosine through hydrogen bonding, forming the base pair G-C. Deoxyguanosine is an important component of DNA and plays a crucial role in the storage and transmission of genetic information. In the medical field, deoxyguanosine is used as a component of antiviral drugs, such as zidovudine (AZT), which are used to treat HIV infection. It is also used in the treatment of certain types of cancer, such as acute myeloid leukemia and Hodgkin's lymphoma.
Checkpoint kinase 2 (CHK2) is a protein kinase that plays a critical role in regulating cell cycle progression and DNA repair. It is activated in response to DNA damage and is involved in the activation of the DNA damage response pathway, which helps to prevent the accumulation of DNA damage and the development of cancer. CHK2 is also involved in the regulation of cell cycle checkpoints, which ensure that cells do not divide until they have completed the necessary DNA replication and repair processes. In addition, CHK2 has been implicated in the regulation of apoptosis, or programmed cell death, and in the maintenance of genomic stability.
Tumor suppressor protein p53 is a protein that plays a crucial role in regulating cell growth and preventing the development of cancer. It is encoded by the TP53 gene and is one of the most commonly mutated genes in human cancer. The p53 protein acts as a "guardian of the genome" by detecting DNA damage and initiating a series of cellular responses to repair the damage or trigger programmed cell death (apoptosis) if the damage is too severe. This helps to prevent the accumulation of mutations in the DNA that can lead to the development of cancer. In addition to its role in preventing cancer, p53 also plays a role in regulating cell cycle progression, DNA repair, and the response to cellular stress. Mutations in the TP53 gene can lead to the production of a non-functional or mutated p53 protein, which can result in the loss of these important functions and contribute to the development of cancer. Overall, the p53 protein is a critical regulator of cell growth and survival, and its dysfunction is a common feature of many types of cancer.
DNA-binding proteins are a class of proteins that interact with DNA molecules to regulate gene expression. These proteins recognize specific DNA sequences and bind to them, thereby affecting the transcription of genes into messenger RNA (mRNA) and ultimately the production of proteins. DNA-binding proteins play a crucial role in many biological processes, including cell division, differentiation, and development. They can act as activators or repressors of gene expression, depending on the specific DNA sequence they bind to and the cellular context in which they are expressed. Examples of DNA-binding proteins include transcription factors, histones, and non-histone chromosomal proteins. Transcription factors are proteins that bind to specific DNA sequences and regulate the transcription of genes by recruiting RNA polymerase and other factors to the promoter region of a gene. Histones are proteins that package DNA into chromatin, and non-histone chromosomal proteins help to organize and regulate chromatin structure. DNA-binding proteins are important targets for drug discovery and development, as they play a central role in many diseases, including cancer, genetic disorders, and infectious diseases.
Protein-Serine-Threonine Kinases (PSTKs) are a family of enzymes that play a crucial role in regulating various cellular processes, including cell growth, differentiation, metabolism, and apoptosis. These enzymes phosphorylate specific amino acids, such as serine and threonine, on target proteins, thereby altering their activity, stability, or localization within the cell. PSTKs are involved in a wide range of diseases, including cancer, diabetes, cardiovascular disease, and neurodegenerative disorders. Therefore, understanding the function and regulation of PSTKs is important for developing new therapeutic strategies for these diseases.
Tumor suppressor proteins are a group of proteins that play a crucial role in regulating cell growth and preventing the development of cancer. These proteins act as brakes on the cell cycle, preventing cells from dividing and multiplying uncontrollably. They also help to repair damaged DNA and prevent the formation of tumors. Tumor suppressor proteins are encoded by genes that are located on specific chromosomes. When these genes are functioning properly, they produce proteins that help to regulate cell growth and prevent the development of cancer. However, when these genes are mutated or damaged, the proteins they produce may not function properly, leading to uncontrolled cell growth and the development of cancer. There are many different tumor suppressor proteins, each with its own specific function. Some of the most well-known tumor suppressor proteins include p53, BRCA1, and BRCA2. These proteins are involved in regulating cell cycle checkpoints, repairing damaged DNA, and preventing the formation of tumors. In summary, tumor suppressor proteins are a group of proteins that play a critical role in regulating cell growth and preventing the development of cancer. When these proteins are functioning properly, they help to maintain the normal balance of cell growth and division, but when they are mutated or damaged, they can contribute to the development of cancer.
DNA, or deoxyribonucleic acid, is a molecule that carries genetic information in living organisms. It is composed of four types of nitrogen-containing molecules called nucleotides, which are arranged in a specific sequence to form the genetic code. In the medical field, DNA is often studied as a tool for understanding and diagnosing genetic disorders. Genetic disorders are caused by changes in the DNA sequence that can affect the function of genes, leading to a variety of health problems. By analyzing DNA, doctors and researchers can identify specific genetic mutations that may be responsible for a particular disorder, and develop targeted treatments or therapies to address the underlying cause of the condition. DNA is also used in forensic science to identify individuals based on their unique genetic fingerprint. This is because each person's DNA sequence is unique, and can be used to distinguish one individual from another. DNA analysis is also used in criminal investigations to help solve crimes by linking DNA evidence to suspects or victims.
Methyl Methanesulfonate (MMS) is a chemical compound that is used in various industries, including the medical field. In medicine, MMS is primarily used as a chemotherapy agent to treat certain types of cancer. It works by interfering with the growth and division of cancer cells, ultimately leading to their death. MMS is typically administered intravenously or orally, and its effectiveness depends on the type and stage of cancer being treated. However, it is important to note that MMS is a potent and toxic substance, and its use is closely monitored by medical professionals to minimize the risk of side effects and complications. In addition to its use as a chemotherapy agent, MMS has also been studied for its potential use in other medical applications, such as the treatment of viral infections and the prevention of certain types of cancer. However, more research is needed to fully understand the potential benefits and risks of MMS in these contexts.
Histones are proteins that play a crucial role in the structure and function of DNA in cells. They are small, positively charged proteins that help to package and organize DNA into a compact structure called chromatin. Histones are found in the nucleus of eukaryotic cells and are essential for the proper functioning of genes. There are five main types of histones: H1, H2A, H2B, H3, and H4. Each type of histone has a specific role in the packaging and organization of DNA. For example, H3 and H4 are the most abundant histones and are responsible for the formation of nucleosomes, which are the basic unit of chromatin. H1 is a linker histone that helps to compact chromatin into a more condensed structure. In the medical field, histones have been studied in relation to various diseases, including cancer, autoimmune disorders, and neurodegenerative diseases. For example, changes in the levels or modifications of histones have been linked to the development of certain types of cancer, such as breast cancer and prostate cancer. Additionally, histones have been shown to play a role in the regulation of gene expression, which is important for the proper functioning of cells.
Nuclear proteins are proteins that are found within the nucleus of a cell. The nucleus is the control center of the cell, where genetic material is stored and regulated. Nuclear proteins play a crucial role in many cellular processes, including DNA replication, transcription, and gene regulation. There are many different types of nuclear proteins, each with its own specific function. Some nuclear proteins are involved in the structure and organization of the nucleus itself, while others are involved in the regulation of gene expression. Nuclear proteins can also interact with other proteins, DNA, and RNA molecules to carry out their functions. In the medical field, nuclear proteins are often studied in the context of diseases such as cancer, where changes in the expression or function of nuclear proteins can contribute to the development and progression of the disease. Additionally, nuclear proteins are important targets for drug development, as they can be targeted to treat a variety of diseases.
Genomic instability refers to an increased tendency for errors to occur during DNA replication and repair, leading to the accumulation of mutations in the genome. This can result in a variety of genetic disorders, including cancer, and can be caused by a variety of factors, including exposure to mutagenic agents, such as radiation or certain chemicals, and inherited genetic mutations. In the medical field, genomic instability is often studied as a potential mechanism underlying the development of cancer, as well as other genetic disorders.
DNA repair enzymes are a group of proteins that play a crucial role in maintaining the integrity of an organism's DNA. These enzymes are responsible for recognizing and repairing damage to DNA that can occur due to various factors, such as exposure to radiation, chemicals, or errors during DNA replication. There are several types of DNA repair enzymes, each with a specific function in repairing different types of DNA damage. Some examples of DNA repair enzymes include: 1. Base excision repair enzymes: These enzymes remove damaged or incorrect bases from DNA and replace them with the correct base. 2. Nucleotide excision repair enzymes: These enzymes remove larger sections of damaged DNA and replace them with the correct sequence. 3. Mismatch repair enzymes: These enzymes recognize and correct errors that occur during DNA replication. 4. Double-strand break repair enzymes: These enzymes repair double-strand breaks in DNA, which can be caused by radiation or other types of DNA damage. DNA repair enzymes are essential for maintaining the stability and integrity of an organism's DNA, and defects in these enzymes can lead to various diseases, including cancer.
DNA adducts are chemical modifications of DNA that occur when a foreign chemical molecule binds covalently to a DNA base. These modifications can be caused by exposure to environmental toxins, such as tobacco smoke or air pollution, as well as by certain medications or chemotherapy drugs. DNA adducts can lead to mutations in the DNA sequence, which can increase the risk of cancer and other diseases. In the medical field, DNA adducts are often studied as a way to assess a person's exposure to environmental toxins and to monitor the effectiveness of cancer treatments.
Reactive Oxygen Species (ROS) are highly reactive molecules that are produced as a byproduct of normal cellular metabolism. They include oxygen radicals such as superoxide, hydrogen peroxide, and hydroxyl radicals, as well as non-radical species such as singlet oxygen and peroxynitrite. In small amounts, ROS play important roles in various physiological processes, such as immune responses, cell signaling, and the regulation of gene expression. However, when produced in excess, ROS can cause oxidative stress, which can damage cellular components such as lipids, proteins, and DNA. This damage can lead to various diseases, including cancer, cardiovascular disease, and neurodegenerative disorders. Therefore, ROS are often studied in the medical field as potential therapeutic targets for the prevention and treatment of diseases associated with oxidative stress.
Hydrogen peroxide (H2O2) is a colorless, odorless liquid that is commonly used in the medical field as a disinfectant, antiseptic, and oxidizing agent. It is a strong oxidizing agent that can break down organic matter, including bacteria, viruses, and fungi, making it useful for disinfecting wounds, surfaces, and medical equipment. In addition to its disinfectant properties, hydrogen peroxide is also used in wound care to remove dead tissue and promote healing. It is often used in combination with other wound care products, such as saline solution or antibiotic ointment, to help prevent infection and promote healing. Hydrogen peroxide is also used in some medical procedures, such as endoscopy and bronchoscopy, to help clean and disinfect the equipment before use. It is also used in some dental procedures to help remove stains and whiten teeth. However, it is important to note that hydrogen peroxide can be harmful if not used properly. It should not be ingested or applied directly to the skin or mucous membranes without first diluting it with water. It should also be stored in a cool, dry place away from children and pets.
Protein kinases are enzymes that catalyze the transfer of a phosphate group from ATP (adenosine triphosphate) to specific amino acid residues on proteins. This process, known as phosphorylation, can alter the activity, localization, or stability of the target protein, and is a key mechanism for regulating many cellular processes, including cell growth, differentiation, metabolism, and signaling pathways. Protein kinases are classified into different families based on their sequence, structure, and substrate specificity. Some of the major families of protein kinases include serine/threonine kinases, tyrosine kinases, and dual-specificity kinases. Each family has its own unique functions and roles in cellular signaling. In the medical field, protein kinases are important targets for the development of drugs for the treatment of various diseases, including cancer, diabetes, and cardiovascular disease. Many cancer drugs target specific protein kinases that are overactive in cancer cells, while drugs for diabetes and cardiovascular disease often target kinases involved in glucose metabolism and blood vessel function, respectively.
Rad51 recombinase is a protein that plays a crucial role in DNA repair and maintenance. It is involved in the process of homologous recombination, which is a mechanism for repairing DNA damage, such as double-strand breaks. Rad51 recombinase helps to align the two broken ends of the DNA molecule and facilitate the exchange of genetic material between the two strands. This process is essential for maintaining the integrity of the genome and preventing mutations that can lead to cancer and other diseases. In the medical field, Rad51 recombinase is often studied as a potential target for cancer therapy, as its activity is often upregulated in cancer cells.
DNA glycosylases are a class of enzymes that play a crucial role in the repair of damaged DNA. These enzymes recognize and remove damaged or inappropriate nucleotides from the DNA strand, creating an abasic site (also known as an AP site) that can be further processed by other DNA repair enzymes. There are several types of DNA glycosylases, each with a specific substrate specificity. For example, some DNA glycosylases recognize and remove damaged bases such as thymine glycol, 8-oxoguanine, and uracil, while others recognize and remove bulky adducts such as benzo[a]pyrene diol epoxide. DNA glycosylases are important for maintaining the integrity of the genome and preventing mutations that can lead to cancer and other diseases. Mutations in DNA glycosylase genes have been linked to an increased risk of certain types of cancer, such as colon cancer and lung cancer.
Saccharomyces cerevisiae proteins are proteins that are produced by the yeast species Saccharomyces cerevisiae. This yeast is commonly used in the production of bread, beer, and wine, as well as in scientific research. In the medical field, S. cerevisiae proteins have been studied for their potential use in the treatment of various diseases, including cancer, diabetes, and neurodegenerative disorders. Some S. cerevisiae proteins have also been shown to have anti-inflammatory and immunomodulatory effects, making them of interest for the development of new therapies.
BRCA1 Protein is a tumor suppressor gene that plays a crucial role in maintaining genomic stability and preventing the development of cancer. The BRCA1 gene is located on chromosome 17 and produces a protein that functions as a part of a complex that repairs DNA damage. When the BRCA1 gene is mutated or not functioning properly, the body is less able to repair DNA damage, which can lead to the development of cancer, particularly breast and ovarian cancer. Women with a BRCA1 mutation have a significantly increased risk of developing breast and ovarian cancer, and may choose to undergo genetic counseling and testing to determine their risk and make informed decisions about their healthcare.
Hydroxyurea is a medication that is used to treat certain types of blood disorders, including sickle cell anemia and myelofibrosis. It works by slowing down the production of new blood cells in the bone marrow, which can help to reduce the number of abnormal red blood cells in the body and prevent them from getting stuck in small blood vessels. Hydroxyurea is usually taken by mouth in the form of tablets or capsules, and the dosage and frequency of administration will depend on the specific condition being treated and the individual patient's response to the medication. It is important to follow the instructions provided by your healthcare provider and to report any side effects or concerns to them right away.
DNA-activated protein kinase (DNA-PK) is a protein kinase enzyme that plays a critical role in the repair of DNA damage, particularly double-strand breaks (DSBs). It is activated by the binding of DNA ends to the Ku protein complex, which recruits DNA-PK to the site of damage. Once activated, DNA-PK phosphorylates a number of downstream targets, including the histone H2AX protein, which helps to recruit other repair factors to the site of damage. DNA-PK is also involved in the regulation of cell cycle checkpoints and the maintenance of genomic stability. In the medical field, DNA-PK is of interest because its dysfunction has been linked to a number of diseases, including cancer and genetic disorders such as ataxia telangiectasia.
Intracellular signaling peptides and proteins are molecules that are involved in transmitting signals within cells. These molecules can be either proteins or peptides, and they play a crucial role in regulating various cellular processes, such as cell growth, differentiation, and apoptosis. Intracellular signaling peptides and proteins can be activated by a variety of stimuli, including hormones, growth factors, and neurotransmitters. Once activated, they initiate a cascade of intracellular events that ultimately lead to a specific cellular response. There are many different types of intracellular signaling peptides and proteins, and they can be classified based on their structure, function, and the signaling pathway they are involved in. Some examples of intracellular signaling peptides and proteins include growth factors, cytokines, kinases, phosphatases, and G-proteins. In the medical field, understanding the role of intracellular signaling peptides and proteins is important for developing new treatments for a wide range of diseases, including cancer, diabetes, and neurological disorders.
Chromatin is a complex of DNA, RNA, and proteins that makes up the chromosomes in the nucleus of a cell. It plays a crucial role in regulating gene expression and maintaining the structure of the genome. In the medical field, chromatin is studied in relation to various diseases, including cancer, genetic disorders, and neurological conditions. For example, chromatin remodeling is a process that can alter the structure of chromatin and affect gene expression, and it has been implicated in the development of certain types of cancer. Additionally, chromatin-based therapies are being explored as potential treatments for diseases such as Alzheimer's and Parkinson's.
Replication Protein A (RPA) is a complex of three subunits (RPA1, RPA2, and RPA3) that plays a critical role in DNA replication and repair in cells. It is a highly conserved protein found in all eukaryotic organisms, and its function is essential for the maintenance of genomic stability. RPA binds to single-stranded DNA (ssDNA) and protects it from degradation and recombination. It also serves as a platform for the recruitment of other proteins involved in DNA replication and repair, such as DNA polymerases and helicases. In addition, RPA plays a role in the initiation of DNA replication by binding to replication origins and facilitating the assembly of the replication machinery. Disruptions in RPA function can lead to various genetic disorders, including Fanconi anemia, Bloom syndrome, and xeroderma pigmentosum. These disorders are characterized by an increased risk of cancer, developmental abnormalities, and sensitivity to DNA-damaging agents.
DNA helicases are a class of enzymes that unwind or separate the two strands of DNA double helix, allowing access to the genetic information encoded within. They play a crucial role in various cellular processes, including DNA replication, DNA repair, and transcription. During DNA replication, helicases unwind the double-stranded DNA helix, creating a replication fork where new strands of DNA can be synthesized. In DNA repair, helicases are involved in unwinding damaged DNA to allow for the repair machinery to access and fix the damage. During transcription, helicases unwind the DNA double helix ahead of the RNA polymerase enzyme, allowing it to transcribe the genetic information into RNA. DNA helicases are a diverse group of enzymes, with different families and subfamilies having distinct functions and mechanisms of action. Some helicases are ATP-dependent, meaning they use the energy from ATP hydrolysis to unwind the DNA helix, while others are ATP-independent. Some helicases are also processive, meaning they can unwind the entire length of a DNA helix without dissociating from it, while others are non-processive and require the assistance of other proteins to unwind the DNA. In the medical field, DNA helicases are of interest for their potential as therapeutic targets in various diseases, including cancer, viral infections, and neurodegenerative disorders. For example, some viruses, such as HIV and herpes simplex virus, encode their own DNA helicases that are essential for their replication. Targeting these viral helicases with small molecules or antibodies could potentially be used to treat viral infections. Additionally, some DNA helicases have been implicated in the development of certain types of cancer, and targeting these enzymes may be a promising strategy for cancer therapy.
Polyadenosine diphosphate ribose (PAR) is a complex molecule that is involved in various cellular processes, including energy metabolism, gene expression, and cell signaling. It is composed of multiple units of adenosine diphosphate (ADP) linked together by ribose sugars, with the number of ADP units ranging from two to several hundred. In the medical field, PAR is known to play a role in a number of diseases and conditions, including cancer, neurodegenerative disorders, and cardiovascular disease. For example, PAR has been shown to regulate the activity of certain enzymes involved in energy metabolism, and changes in PAR levels have been associated with altered metabolism in cancer cells. PAR has also been implicated in the regulation of gene expression and the development of neurodegenerative diseases such as Alzheimer's and Parkinson's disease. Additionally, PAR has been shown to play a role in the regulation of blood vessel function and the development of cardiovascular disease.
RNA, Small Interfering (siRNA) is a type of non-coding RNA molecule that plays a role in gene regulation. siRNA is approximately 21-25 nucleotides in length and is derived from double-stranded RNA (dsRNA) molecules. In the medical field, siRNA is used as a tool for gene silencing, which involves inhibiting the expression of specific genes. This is achieved by introducing siRNA molecules that are complementary to the target mRNA sequence, leading to the degradation of the mRNA and subsequent inhibition of protein synthesis. siRNA has potential applications in the treatment of various diseases, including cancer, viral infections, and genetic disorders. It is also used in research to study gene function and regulation. However, the use of siRNA in medicine is still in its early stages, and there are several challenges that need to be addressed before it can be widely used in clinical practice.
Proto-oncogene proteins c-mdm2 are a family of proteins that play a role in regulating the activity of the tumor suppressor protein p53. p53 is a transcription factor that is activated in response to cellular stress, such as DNA damage or oncogene activation, and helps to prevent the development of cancer by promoting cell cycle arrest, apoptosis (programmed cell death), and DNA repair. Proto-oncogene proteins c-mdm2 can bind to and inhibit the activity of p53, thereby preventing it from carrying out its tumor suppressor functions. This can contribute to the development of cancer by allowing cells with damaged DNA to continue to divide and proliferate. Proto-oncogene proteins c-mdm2 are therefore considered to be oncogenes, which are genes that have the potential to cause cancer.
Pyrimidine dimers are DNA lesions that occur when two adjacent pyrimidine bases (thymine or cytosine) in the DNA double helix are covalently linked by a cyclobutane ring. This type of DNA damage is primarily caused by exposure to ultraviolet (UV) radiation, particularly UV-B radiation, which has a wavelength of 280-320 nm. Pyrimidine dimers can interfere with normal DNA replication and transcription, leading to mutations and potentially causing cancer or other diseases. The body has mechanisms to repair pyrimidine dimers, including nucleotide excision repair (NER), which involves the removal of the damaged DNA segment and replacement with new nucleotides. However, if the damage is not repaired, it can persist and lead to long-term health effects.
DNA-formamidopyrimidine glycosylase (FPG) is an enzyme that plays a role in the repair of DNA damage. It is a member of the base excision repair pathway, which is a mechanism that removes damaged or incorrect bases from DNA. FPG recognizes and removes damaged bases that have been modified by certain types of chemical agents, such as formamidopyrimidines, which are formed when DNA is exposed to certain types of radiation or chemicals. The removal of these damaged bases by FPG is an important step in maintaining the integrity of the DNA molecule and preventing mutations that can lead to cancer and other diseases.
Mitomycin is a chemotherapy drug that is used to treat various types of cancer, including bladder cancer, head and neck cancer, and sarcoma. It works by interfering with the DNA replication process in cancer cells, which prevents them from dividing and growing. Mitomycin is usually given as an intravenous injection or as a solution that is applied directly to the tumor. It can cause side effects such as nausea, vomiting, diarrhea, and mouth sores.
Micronuclei, chromosome-defective are small nuclear bodies that contain chromosomal material that has not been incorporated into the main nucleus of a cell. They are often formed as a result of DNA damage or errors in cell division, and can be used as a biomarker of genomic instability and cancer risk. In the medical field, the presence of micronuclei, chromosome-defective can be used to assess the genotoxicity of environmental or occupational exposures, as well as to monitor the effectiveness of cancer treatments.
Cyclin-dependent kinase inhibitor p21 (p21) is a protein that plays a role in regulating the cell cycle, which is the process by which cells divide and grow. It is encoded by the CDKN1A gene and is a member of the Cip/Kip family of cyclin-dependent kinase inhibitors. In the cell cycle, the progression from one phase to the next is controlled by a series of checkpoints that ensure that the cell is ready to proceed. One of the key regulators of these checkpoints is the cyclin-dependent kinase (CDK) family of enzymes. CDKs are activated by binding to cyclins, which are proteins that are synthesized and degraded in a cyclic manner throughout the cell cycle. p21 acts as a CDK inhibitor by binding to and inhibiting the activity of cyclin-CDK complexes. This prevents the complexes from phosphorylating target proteins that are required for the progression of the cell cycle. As a result, p21 helps to prevent the cell from dividing when it is not ready, and it plays a role in preventing the development of cancer. In addition to its role in regulating the cell cycle, p21 has been implicated in a number of other cellular processes, including DNA repair, senescence, and apoptosis (programmed cell death). It is also involved in the response of cells to various stressors, such as DNA damage, oxidative stress, and hypoxia.
Guanine is a nitrogenous base that is found in DNA and RNA. It is one of the four nitrogenous bases that make up the genetic code, along with adenine, cytosine, and thymine (in DNA) or uracil (in RNA). Guanine is a purine base, which means it has a double ring structure consisting of a six-membered pyrimidine ring fused to a five-membered imidazole ring. It is one of the two purine bases found in DNA and RNA, the other being adenine. Guanine plays a critical role in the structure and function of DNA and RNA, as it forms hydrogen bonds with cytosine in DNA and with uracil in RNA, which helps to stabilize the double helix structure of these molecules.
Xeroderma Pigmentosum Group A Protein (XPA) is a protein that plays a crucial role in the repair of DNA damage caused by ultraviolet (UV) radiation. It is one of the seven proteins that make up the nucleotide excision repair (NER) pathway, which is responsible for repairing DNA damage caused by a variety of factors, including UV radiation, chemical mutagens, and certain viruses. XPA is involved in the recognition and binding of damaged DNA, which is the first step in the NER pathway. It helps to recruit other proteins to the site of damage, which then work together to remove the damaged DNA segment and replace it with a new, undamaged segment. Mutations in the XPA gene can lead to a rare genetic disorder called xeroderma pigmentosum (XP), which is characterized by extreme sensitivity to UV radiation and an increased risk of skin cancer. People with XP have a defect in their NER pathway, which makes it difficult for their cells to repair DNA damage caused by UV radiation. As a result, they are at a much higher risk of developing skin cancer, particularly in areas of the skin that are exposed to sunlight.
DNA, Fungal refers to the genetic material of fungi, which is a type of eukaryotic microorganism that includes yeasts, molds, and mushrooms. Fungal DNA is composed of four types of nucleotides: adenine (A), thymine (T), cytosine (C), and guanine (G), which are arranged in a specific sequence to form the genetic code that determines the characteristics and functions of the fungus. In the medical field, fungal DNA is often studied in the context of infections caused by fungi, such as candidiasis, aspergillosis, and cryptococcosis. Fungal DNA can be detected in clinical samples, such as blood, sputum, or tissue, using molecular diagnostic techniques such as polymerase chain reaction (PCR) or DNA sequencing. These tests can help diagnose fungal infections and guide treatment decisions. Additionally, fungal DNA can be used in research to study the evolution and diversity of fungi, as well as their interactions with other organisms and the environment.
Ataxia Telangiectasia (AT) is a rare genetic disorder that affects the nervous system and the immune system. It is caused by a mutation in the ATM gene, which is responsible for producing a protein that helps repair DNA damage. People with AT have problems with coordination and balance (ataxia), as well as telangiectasias (small, red or purple blood vessels on the skin and mucous membranes), and an increased risk of developing cancer, particularly leukemia and lymphoma. Other symptoms may include sensitivity to radiation, infertility, and an increased risk of infections. There is currently no cure for AT, but treatments can help manage symptoms and reduce the risk of complications.
Endodeoxyribonucleases are a class of enzymes that cleave DNA strands by hydrolyzing the phosphodiester bonds between the nucleotides. These enzymes are capable of cutting DNA at specific recognition sites, and are often used in molecular biology techniques such as restriction digestion, ligation, and cloning. In the medical field, endodeoxyribonucleases have potential applications in gene therapy, where they can be used to target and cleave specific DNA sequences, or in the treatment of genetic disorders, where they can be used to correct mutations in the genome.
CDC25 phosphatases are a family of enzymes that play a critical role in regulating cell cycle progression in eukaryotic cells. These enzymes are named after the cell division cycle 25 (CDC25) gene family, which encodes for the phosphatases. CDC25 phosphatases are responsible for dephosphorylating tyrosine residues on cyclin-dependent kinases (CDKs), which are key regulators of cell cycle progression. By removing phosphate groups from CDKs, CDC25 phosphatases activate these enzymes, allowing them to phosphorylate and activate other proteins involved in cell cycle progression. In addition to their role in cell cycle regulation, CDC25 phosphatases have also been implicated in a variety of other cellular processes, including DNA repair, apoptosis, and cancer development. Dysregulation of CDC25 phosphatase activity has been linked to several types of cancer, including breast, ovarian, and colorectal cancer. Overall, CDC25 phosphatases are important regulators of cell cycle progression and have important implications for human health and disease.
Proliferating Cell Nuclear Antigen (PCNA) is a protein that plays a crucial role in DNA replication and repair in cells. It is also known as Replication Factor C (RFC) subunit 4 or proliferating cell nuclear antigen-like 1 (PCNA-like 1). PCNA is a highly conserved protein that is found in all eukaryotic cells. It is a homotrimeric protein, meaning that it is composed of three identical subunits. Each subunit has a central channel that can bind to DNA, and it is this channel that is responsible for the interaction of PCNA with other proteins involved in DNA replication and repair. During DNA replication, PCNA forms a complex with other proteins, including DNA polymerase δ and the replication factor C (RFC) complex. This complex is responsible for unwinding the DNA double helix, synthesizing new DNA strands, and ensuring that the newly synthesized strands are correctly paired with the template strands. PCNA is also involved in DNA repair processes, particularly in the repair of DNA damage caused by ultraviolet (UV) radiation. In this context, PCNA interacts with other proteins, such as the X-ray repair cross-complementing protein 1 (XRCC1), to facilitate the repair of DNA damage. Overall, PCNA is a critical protein in the maintenance of genomic stability and the prevention of DNA damage-induced diseases, such as cancer.
In the medical field, antigens are substances that can trigger an immune response in the body. Antigens can be found on the surface of cells or in the body's fluids, and they can be foreign substances like bacteria or viruses, or they can be part of the body's own cells, such as antigens found in the nucleus of cells. Nuclear antigens are antigens that are found within the nucleus of cells. These antigens are typically not exposed on the surface of cells, and they are not usually recognized by the immune system unless there is damage to the cell or the nucleus. In some cases, the immune system may mistakenly recognize nuclear antigens as foreign and mount an immune response against them, which can lead to autoimmune diseases.
Endonucleases are a class of enzymes that cleave DNA or RNA at specific sites within the molecule. They are important in various biological processes, including DNA replication, repair, and gene expression. In the medical field, endonucleases are used in a variety of applications, such as gene therapy, where they are used to target and modify specific genes, and in the treatment of genetic disorders, where they are used to correct mutations in DNA. They are also used in molecular biology research to manipulate and analyze DNA and RNA molecules.
Schizosaccharomyces pombe is a type of yeast that is commonly used in research to study basic cellular processes and genetics. Proteins produced by this yeast can be important tools in the medical field, as they can be used to study the function of specific genes and to develop new treatments for diseases. One example of a Schizosaccharomyces pombe protein that is of interest in the medical field is the protein called CDC48. This protein is involved in a variety of cellular processes, including the assembly and disassembly of cellular structures, and it has been implicated in the development of several diseases, including cancer. Researchers are studying CDC48 in order to better understand its role in these diseases and to develop new treatments based on this knowledge. Other Schizosaccharomyces pombe proteins that are of interest in the medical field include those involved in DNA repair, cell division, and signal transduction. These proteins can be used as tools to study the function of specific genes and to develop new treatments for diseases that are caused by defects in these genes.
Chronic brain damage refers to a type of damage that occurs over a prolonged period of time, typically months or years, and can result from a variety of causes such as stroke, traumatic brain injury, neurodegenerative diseases, infections, or substance abuse. Chronic brain damage can lead to a range of cognitive, emotional, and physical impairments, including memory loss, difficulty with language and communication, mood disorders, motor dysfunction, and changes in personality. The severity and extent of the damage can vary depending on the location and extent of the injury, as well as the individual's age, overall health, and other factors. Treatment for chronic brain damage typically involves a combination of medications, therapy, and lifestyle changes to manage symptoms and improve quality of life. In some cases, rehabilitation may also be necessary to help individuals regain lost skills and function.
Etoposide is a chemotherapy drug that is used to treat various types of cancer, including small cell lung cancer, ovarian cancer, testicular cancer, and some types of leukemia. It works by interfering with the process of cell division, which is necessary for cancer cells to grow and multiply. Etoposide is usually given intravenously or orally, and its side effects can include nausea, vomiting, hair loss, and an increased risk of infection.
Exodeoxyribonucleases (EDNs) are a group of enzymes that degrade DNA by cleaving the phosphodiester bonds between the sugar-phosphate backbone of the DNA molecule. These enzymes are involved in various biological processes, including DNA repair, replication, and transcription. In the medical field, EDNs are often used as tools for studying DNA structure and function, as well as for developing new diagnostic and therapeutic strategies. For example, some EDNs have been used to selectively degrade specific regions of DNA, allowing researchers to study the function of specific genes or regulatory elements. Additionally, some EDNs have been developed as potential cancer therapies, as they can selectively target and degrade cancer cells' DNA, leading to cell death. Overall, EDNs play a critical role in many biological processes and have important applications in the medical field.
Ubiquitin is a small, highly conserved protein that is found in all eukaryotic cells. It plays a crucial role in the regulation of various cellular processes, including protein degradation, cell cycle progression, and signal transduction. In the medical field, ubiquitin is often studied in the context of various diseases, including cancer, neurodegenerative disorders, and autoimmune diseases. For example, mutations in genes encoding ubiquitin or its regulatory enzymes have been linked to several forms of cancer, including breast, ovarian, and prostate cancer. Additionally, the accumulation of ubiquitinated proteins has been observed in several neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease. Overall, understanding the role of ubiquitin in cellular processes and its involvement in various diseases is an active area of research in the medical field.
Ubiquitin-protein ligases, also known as E3 ligases, are a class of enzymes that play a crucial role in the process of protein degradation in cells. These enzymes are responsible for recognizing specific target proteins and tagging them with ubiquitin, a small protein that serves as a signal for degradation by the proteasome, a large protein complex that breaks down proteins in the cell. In the medical field, ubiquitin-protein ligases are of great interest because they are involved in a wide range of cellular processes, including cell cycle regulation, DNA repair, and the regulation of immune responses. Dysregulation of these enzymes has been implicated in a number of diseases, including cancer, neurodegenerative disorders, and autoimmune diseases. For example, some E3 ligases have been shown to play a role in the development of certain types of cancer by promoting the degradation of tumor suppressor proteins or by stabilizing oncogenic proteins. In addition, mutations in certain E3 ligases have been linked to neurodegenerative diseases such as Huntington's disease and Parkinson's disease. Overall, understanding the function and regulation of ubiquitin-protein ligases is an important area of research in the medical field, as it may lead to the development of new therapeutic strategies for a variety of diseases.
Chromosomal proteins, non-histone, are proteins that are not directly involved in the structure of chromatin but play important roles in various cellular processes related to chromosomes. These proteins are typically associated with specific regions of the chromosome and are involved in regulating gene expression, DNA replication, and DNA repair. Examples of non-histone chromosomal proteins include transcription factors, coactivators, and chromatin remodeling factors. Abnormalities in the expression or function of non-histone chromosomal proteins have been implicated in various diseases, including cancer and genetic disorders.
4-Nitroquinoline-1-oxide (4-NQO) is a chemical compound that is commonly used as a mutagen and carcinogen in laboratory studies. It is a yellowish solid that is soluble in water and organic solvents. In the medical field, 4-NQO is often used to study the effects of mutagens and carcinogens on cells and organisms, and to develop new treatments for cancer and other diseases. It is also used as a tool to study the mechanisms of DNA damage and repair, and to identify new biomarkers for cancer. However, it is important to note that 4-NQO is a highly toxic compound and should only be handled by trained professionals in a laboratory setting.
Zinostatin is a synthetic peptide that has been shown to have anti-inflammatory and immunomodulatory effects. It is derived from the venom of the funnel-web spider (Atrax robustus) and has been studied for its potential therapeutic applications in various medical conditions, including inflammatory bowel disease, multiple sclerosis, and cancer. In the medical field, zinostatin is being investigated as a potential treatment for a range of diseases, including inflammatory bowel disease (IBD), multiple sclerosis (MS), and cancer. It is believed to work by inhibiting the activity of certain enzymes involved in the inflammatory response, as well as by modulating the activity of immune cells. Zinostatin has been shown to be safe and well-tolerated in preclinical studies, and clinical trials are currently underway to evaluate its efficacy and safety in humans. While more research is needed to fully understand the potential therapeutic applications of zinostatin, it holds promise as a potential new treatment for a range of inflammatory and immune-mediated diseases.
DNA, single-stranded refers to a molecule of DNA that is not paired with its complementary strand. In contrast, double-stranded DNA is composed of two complementary strands that are held together by hydrogen bonds between base pairs. Single-stranded DNA can exist in cells under certain conditions, such as during DNA replication or repair, or in certain viruses. It can also be artificially produced in the laboratory for various purposes, such as in the process of DNA sequencing. In the medical field, single-stranded DNA is often used in diagnostic tests and as a tool for genetic research.
Transcription factors are proteins that regulate gene expression by binding to specific DNA sequences and controlling the transcription of genetic information from DNA to RNA. They play a crucial role in the development and function of cells and tissues in the body. In the medical field, transcription factors are often studied as potential targets for the treatment of diseases such as cancer, where their activity is often dysregulated. For example, some transcription factors are overexpressed in certain types of cancer cells, and inhibiting their activity may help to slow or stop the growth of these cells. Transcription factors are also important in the development of stem cells, which have the ability to differentiate into a wide variety of cell types. By understanding how transcription factors regulate gene expression in stem cells, researchers may be able to develop new therapies for diseases such as diabetes and heart disease. Overall, transcription factors are a critical component of gene regulation and have important implications for the development and treatment of many diseases.
RecQ helicases are a family of DNA helicases that play important roles in maintaining genome stability. They are named after the first discovered member of the family, the RecQ protein in Escherichia coli. RecQ helicases are involved in a variety of cellular processes, including DNA repair, telomere maintenance, and prevention of genomic instability. They use the energy from ATP hydrolysis to unwind double-stranded DNA, allowing other proteins to access and repair damaged or damaged DNA. Mutations in RecQ helicase genes have been linked to several human diseases, including Werner syndrome, Bloom syndrome, and Rothmund-Thomson syndrome. These conditions are characterized by premature aging, increased cancer risk, and other symptoms related to genomic instability. In the medical field, RecQ helicases are of interest as potential therapeutic targets for diseases related to genomic instability, such as cancer. Additionally, they are being studied as potential biomarkers for early detection of cancer and other diseases.
N-Glycosyl Hydrolases (NGHs) are a group of enzymes that hydrolyze (break down) the glycosidic bonds in complex carbohydrates, also known as glycans. These enzymes play important roles in various biological processes, including cell signaling, protein folding, and immune response. In the medical field, NGHs are of particular interest due to their involvement in diseases such as cancer, diabetes, and infectious diseases. For example, some NGHs are overexpressed in cancer cells, leading to increased cell proliferation and invasion. In diabetes, NGHs are involved in the breakdown of glycans in the body, which can lead to hyperglycemia (high blood sugar levels). In infectious diseases, NGHs are produced by pathogens to evade the host immune system. NGHs are also being studied as potential therapeutic targets for various diseases. For example, inhibitors of NGHs have been developed as potential treatments for cancer and diabetes. Additionally, NGHs are being investigated as potential biomarkers for disease diagnosis and prognosis.
Telomeric Repeat Binding Protein 2 (TRBP2) is a protein that plays a role in the maintenance of telomeres, which are the protective caps at the ends of chromosomes. TRBP2 is a member of the TRBP family of proteins, which are involved in the regulation of RNA interference (RNAi) and the processing of small interfering RNAs (siRNAs). In addition to its role in telomere maintenance, TRBP2 has been implicated in a number of other cellular processes, including the regulation of gene expression and the response to DNA damage. In the medical field, TRBP2 has been studied in the context of various diseases, including cancer, where it has been shown to be involved in the development and progression of the disease.
DNA, or deoxyribonucleic acid, is a molecule that carries genetic information in living organisms. It is composed of four types of nitrogen-containing molecules called nucleotides, which are arranged in a specific sequence to form the genetic code. Neoplasm refers to an abnormal growth of cells in the body, which can be either benign (non-cancerous) or malignant (cancerous). Neoplasms can occur in any part of the body and can be caused by a variety of factors, including genetic mutations, exposure to carcinogens, and hormonal imbalances. In the medical field, DNA and neoplasms are closely related because many types of cancer are caused by mutations in the DNA of cells. These mutations can lead to uncontrolled cell growth and the formation of tumors. DNA analysis is often used to diagnose and treat cancer, as well as to identify individuals who are at increased risk of developing the disease.
Cisplatin is a chemotherapy drug that is commonly used to treat various types of cancer, including ovarian, testicular, bladder, and lung cancer. It works by binding to the DNA of cancer cells, which prevents them from dividing and growing. Cisplatin is usually administered intravenously and can cause a range of side effects, including nausea, vomiting, hair loss, and damage to the kidneys and hearing. It is important to note that cisplatin is not effective for all types of cancer and may not be suitable for everyone. The use of cisplatin should be determined by a healthcare professional based on the individual's specific medical needs and circumstances.
Free radicals are highly reactive molecules that contain an unpaired electron in their outermost shell. In the medical field, free radicals are often associated with oxidative stress, which occurs when there is an imbalance between the production of free radicals and the body's ability to neutralize them. Free radicals can be produced naturally by the body as a result of normal metabolic processes, or they can be generated by external factors such as exposure to environmental pollutants, radiation, or certain medications. When free radicals react with healthy cells, they can damage cellular components such as DNA, proteins, and lipids, leading to a variety of health problems, including cancer, cardiovascular disease, and neurodegenerative disorders. To counteract the harmful effects of free radicals, the body has developed a number of antioxidant defenses, including enzymes and non-enzymatic antioxidants such as vitamins C and E. However, when the production of free radicals exceeds the body's ability to neutralize them, antioxidants may not be sufficient to prevent oxidative damage, and additional measures may be necessary to reduce the risk of disease.
Xeroderma Pigmentosum (XP) is a rare genetic disorder that affects the body's ability to repair damage caused by ultraviolet (UV) radiation from the sun. People with XP are highly sensitive to sunlight and are at an increased risk of developing skin cancer, particularly in areas of the skin that are exposed to the sun. XP is caused by mutations in one of several genes that are involved in the repair of DNA damage. These mutations can be inherited from one or both parents, and they can result in a range of symptoms, including: - Sensitivity to sunlight: People with XP are highly sensitive to UV radiation and may develop sunburns or other skin reactions after only a few minutes of exposure to sunlight. - Skin abnormalities: People with XP may develop unusual skin growths, such as freckles, moles, and skin tags, and may also have a higher risk of developing skin cancer. - Eye problems: People with XP may develop eye problems, such as cataracts and damage to the retina, which can lead to vision loss. - Other symptoms: Some people with XP may also have developmental delays, learning difficulties, and other neurological problems. Treatment for XP typically involves avoiding exposure to sunlight and using protective measures, such as sunscreen and protective clothing, to minimize the risk of skin damage. In some cases, people with XP may also need to take medications to help prevent skin cancer or to treat symptoms such as eye problems.
Chromosome aberrations refer to changes or abnormalities in the structure or number of chromosomes in a cell. These changes can occur naturally during cell division or as a result of exposure to mutagens such as radiation or certain chemicals. Chromosome aberrations can be classified into several types, including deletions, duplications, inversions, translocations, and aneuploidy. These changes can have significant effects on the function of the affected cells and can lead to a variety of medical conditions, including cancer, genetic disorders, and birth defects. In the medical field, chromosome aberrations are often studied as a way to understand the genetic basis of disease and to develop new treatments.
Superoxide Dismutase (SOD) is an enzyme that plays a critical role in protecting cells from damage caused by reactive oxygen species (ROS), such as superoxide radicals. ROS are naturally produced by cells as a byproduct of metabolism, but in excess, they can cause oxidative stress and damage to cellular components, including DNA, proteins, and lipids. SOD catalyzes the dismutation of superoxide radicals into molecular oxygen and hydrogen peroxide, which are less reactive and less harmful to cells. There are several different forms of SOD, including copper-zinc SOD (CuZnSOD), manganese SOD (MnSOD), and iron SOD (FeSOD), which are found in different cellular compartments and have different substrate specificities. In the medical field, SOD is of interest because of its potential therapeutic applications in treating a variety of diseases and conditions that are associated with oxidative stress, including cancer, neurodegenerative diseases, cardiovascular disease, and aging. SOD supplements are also sometimes used as dietary supplements to enhance the body's natural antioxidant defenses. However, the efficacy and safety of SOD supplements have not been well-established, and more research is needed to fully understand their potential benefits and risks.
DNA-directed DNA polymerase, also known as DNA polymerase, is an enzyme that plays a crucial role in DNA replication. It is responsible for synthesizing new DNA strands by adding nucleotides to the growing chain, using the original DNA strand as a template. In the medical field, DNA-directed DNA polymerase is often studied in the context of genetic diseases and cancer. Mutations in the genes encoding DNA polymerases can lead to errors in DNA replication, which can result in genetic disorders such as xeroderma pigmentosum and Cockayne syndrome. Additionally, DNA polymerase is a target for some anti-cancer drugs, which work by inhibiting its activity and preventing the replication of cancer cells. Overall, DNA-directed DNA polymerase is a critical enzyme in the process of DNA replication and plays a significant role in both normal cellular function and disease.
In the medical field, "Disease Models, Animal" refers to the use of animals to study and understand human diseases. These models are created by introducing a disease or condition into an animal, either naturally or through experimental manipulation, in order to study its progression, symptoms, and potential treatments. Animal models are used in medical research because they allow scientists to study diseases in a controlled environment and to test potential treatments before they are tested in humans. They can also provide insights into the underlying mechanisms of a disease and help to identify new therapeutic targets. There are many different types of animal models used in medical research, including mice, rats, rabbits, dogs, and monkeys. Each type of animal has its own advantages and disadvantages, and the choice of model depends on the specific disease being studied and the research question being addressed.
Doxorubicin is an anthracycline chemotherapy drug that is used to treat a variety of cancers, including breast cancer, ovarian cancer, and leukemia. It works by interfering with the production of DNA and RNA, which are essential for the growth and division of cancer cells. Doxorubicin is usually administered intravenously, and its side effects can include nausea, vomiting, hair loss, and damage to the heart and kidneys. It is a powerful drug that can be effective against many types of cancer, but it can also have serious side effects, so it is typically used in combination with other treatments or in low doses.
Camptothecin is a natural alkaloid compound that is derived from the Chinese tree Camptotheca acuminata. It has been used in the medical field as an anti-cancer drug due to its ability to inhibit the activity of topoisomerase I, an enzyme that is essential for DNA replication and repair. This inhibition leads to the formation of DNA double-strand breaks, which can cause cell death and prevent the growth and spread of cancer cells. Camptothecin and its derivatives have been used to treat various types of cancer, including ovarian, lung, and colorectal cancer. However, they can also cause significant side effects, such as nausea, vomiting, and diarrhea, and may interact with other medications.
In the medical field, neoplasms refer to abnormal growths or tumors of cells that can occur in any part of the body. These growths can be either benign (non-cancerous) or malignant (cancerous). Benign neoplasms are usually slow-growing and do not spread to other parts of the body. They can cause symptoms such as pain, swelling, or difficulty moving the affected area. Examples of benign neoplasms include lipomas (fatty tumors), hemangiomas (vascular tumors), and fibromas (fibrous tumors). Malignant neoplasms, on the other hand, are cancerous and can spread to other parts of the body through the bloodstream or lymphatic system. They can cause a wide range of symptoms, depending on the location and stage of the cancer. Examples of malignant neoplasms include carcinomas (cancers that start in epithelial cells), sarcomas (cancers that start in connective tissue), and leukemias (cancers that start in blood cells). The diagnosis of neoplasms typically involves a combination of physical examination, imaging tests (such as X-rays, CT scans, or MRI scans), and biopsy (the removal of a small sample of tissue for examination under a microscope). Treatment options for neoplasms depend on the type, stage, and location of the cancer, as well as the patient's overall health and preferences.
Glutathione is a naturally occurring antioxidant that is produced by the body. It is a tripeptide composed of three amino acids: cysteine, glycine, and glutamic acid. Glutathione plays a crucial role in protecting cells from damage caused by free radicals, which are unstable molecules that can damage cells and contribute to the development of diseases such as cancer, heart disease, and neurodegenerative disorders. In the medical field, glutathione is often used as a supplement to support the immune system and protect against oxidative stress. It is also used in the treatment of certain conditions, such as liver disease, HIV/AIDS, and cancer. However, more research is needed to fully understand the potential benefits and risks of glutathione supplementation.
Fanconi Anemia Complementation Group D2 Protein (FANCD2) is a protein that plays a crucial role in the maintenance of genomic stability in cells. It is involved in the repair of DNA damage, particularly double-strand breaks, which can occur due to various factors such as radiation, chemotherapy, or errors during DNA replication. FANCD2 is a component of the Fanconi Anemia (FA) pathway, a complex network of proteins that respond to DNA damage and help prevent the accumulation of mutations that can lead to cancer. The FA pathway is activated in response to DNA damage, and FANCD2 is one of the key proteins that is modified and recruited to sites of DNA damage. Mutations in the FANCD2 gene can cause Fanconi Anemia, a rare genetic disorder characterized by bone marrow failure, congenital abnormalities, and an increased risk of cancer. Individuals with Fanconi Anemia have defects in their ability to repair DNA damage, leading to the accumulation of mutations and an increased risk of cancer. In addition to its role in the FA pathway, FANCD2 has also been implicated in other cellular processes, including cell cycle checkpoint control, DNA repair, and telomere maintenance. Understanding the function of FANCD2 and its role in maintaining genomic stability is important for developing new treatments for cancer and other diseases.
Catalase is an enzyme that is found in almost all living organisms, including humans. It is primarily responsible for breaking down hydrogen peroxide (H2O2), a toxic byproduct of cellular metabolism, into water (H2O) and oxygen (O2). In the medical field, catalase is often used as a diagnostic tool to measure the activity of this enzyme in various tissues and fluids, such as blood, urine, and liver tissue. Abnormal levels of catalase activity can be indicative of certain medical conditions, such as liver disease, kidney disease, and certain types of cancer. Catalase is also used in various medical treatments, such as in the treatment of certain types of cancer, where it is used to increase the production of reactive oxygen species (ROS) to kill cancer cells. Additionally, catalase is used in some wound healing products to help break down hydrogen peroxide and reduce inflammation.
Chromosomal instability (CIN) is a condition in which cells have an increased tendency to experience errors during cell division, leading to the formation of abnormal chromosomes or aneuploidy. This can result in the production of cells with too many or too few chromosomes, which can lead to a variety of health problems, including cancer. CIN can be caused by a variety of factors, including genetic mutations, exposure to certain chemicals or radiation, and certain viral infections. It is often associated with the development of cancer, as the abnormal chromosomes produced by CIN can lead to the uncontrolled growth and division of cells. There are several different types of CIN, including constitutional chromosomal instability (CCI), which is present from birth and is associated with a higher risk of cancer, and acquired chromosomal instability (ACI), which is caused by environmental factors and is associated with a higher risk of cancer in adulthood. Treatment for CIN depends on the underlying cause and the specific symptoms and health problems associated with the condition. In some cases, treatment may involve medications or other therapies to help manage symptoms or prevent the development of cancer. In other cases, surgery or other interventions may be necessary to remove abnormal cells or tumors.
DNA, Mitochondrial refers to the genetic material found within the mitochondria, which are small organelles found in the cells of most eukaryotic organisms. Mitochondrial DNA (mtDNA) is a small circular molecule that is separate from the nuclear DNA found in the cell nucleus. Mitochondrial DNA is maternally inherited, meaning that a person inherits their mtDNA from their mother. Unlike nuclear DNA, which is diploid (contains two copies of each gene), mtDNA is haploid (contains only one copy of each gene). Mutations in mitochondrial DNA can lead to a variety of inherited disorders, including mitochondrial disorders, which are a group of conditions that affect the mitochondria and can cause a range of symptoms, including muscle weakness, fatigue, and neurological problems.
CDC2 Protein Kinase is a type of enzyme that plays a crucial role in cell division and the regulation of the cell cycle. It is a serine/threonine protein kinase that is activated during the G2 phase of the cell cycle and is responsible for the initiation of mitosis. CDC2 is also involved in the regulation of DNA replication and the maintenance of genomic stability. In the medical field, CDC2 Protein Kinase is often studied in the context of cancer research, as its dysregulation has been linked to the development and progression of various types of cancer.
In the medical field, "aging, premature" refers to the process of aging that occurs at an earlier age than is typical for a person of a given species. This can be caused by a variety of factors, including genetics, environmental factors, and lifestyle choices. Premature aging can manifest in a variety of ways, including physical changes such as wrinkles, gray hair, and a loss of muscle mass and bone density. It can also affect the body's ability to function properly, leading to conditions such as cardiovascular disease, diabetes, and osteoporosis. In some cases, premature aging may be caused by genetic mutations or other inherited conditions, such as Werner syndrome or Hutchinson-Gilford progeria syndrome. In other cases, it may be caused by environmental factors, such as exposure to toxins or radiation. Treatment for premature aging may involve lifestyle changes, such as exercise and a healthy diet, as well as medical interventions, such as hormone replacement therapy or medications to manage specific conditions. In some cases, stem cell therapy may also be used to help repair damaged tissues and organs.
In the medical field, RNA, Messenger (mRNA) refers to a type of RNA molecule that carries genetic information from DNA in the nucleus of a cell to the ribosomes, where proteins are synthesized. During the process of transcription, the DNA sequence of a gene is copied into a complementary RNA sequence called messenger RNA (mRNA). This mRNA molecule then leaves the nucleus and travels to the cytoplasm of the cell, where it binds to ribosomes and serves as a template for the synthesis of a specific protein. The sequence of nucleotides in the mRNA molecule determines the sequence of amino acids in the protein that is synthesized. Therefore, changes in the sequence of nucleotides in the mRNA molecule can result in changes in the amino acid sequence of the protein, which can affect the function of the protein and potentially lead to disease. mRNA molecules are often used in medical research and therapy as a way to introduce new genetic information into cells. For example, mRNA vaccines work by introducing a small piece of mRNA that encodes for a specific protein, which triggers an immune response in the body.
Methylnitronitrosoguanidine (MNNG) is a chemical compound that is classified as a mutagen and carcinogen. It is a nitrosamine that is commonly used in scientific research to study the effects of mutagens on DNA and to induce mutations in cells. In the medical field, MNNG is not used as a therapeutic agent, but it has been used in some experimental cancer treatments. However, due to its carcinogenic properties, the use of MNNG in cancer treatment is generally not recommended.
DNA topoisomerases, type I, are a class of enzymes that play a crucial role in regulating DNA topology during various cellular processes, such as DNA replication, transcription, and recombination. These enzymes are responsible for relaxing or tightening the supercoiled structure of DNA, which is essential for maintaining the proper functioning of the genome. Type I topoisomerases work by creating a temporary break in one strand of DNA, allowing the other strand to pass through the break, and then resealing the break. This process is known as "catalytic cleavage and religation" and is essential for maintaining the proper topology of the DNA double helix. In the medical field, type I topoisomerases are important targets for the development of anti-cancer drugs, as they are often overexpressed in cancer cells and are involved in the regulation of cell proliferation and survival. Inhibitors of type I topoisomerases can cause DNA damage and cell death, making them potential therapeutic agents for the treatment of various types of cancer.
Fungal proteins are proteins that are produced by fungi. They can be found in various forms, including extracellular proteins, secreted proteins, and intracellular proteins. Fungal proteins have a wide range of functions, including roles in metabolism, cell wall synthesis, and virulence. In the medical field, fungal proteins are of interest because some of them have potential therapeutic applications, such as in the treatment of fungal infections or as vaccines against fungal diseases. Additionally, some fungal proteins have been shown to have anti-cancer properties, making them potential targets for the development of new cancer treatments.
Serine is an amino acid that is a building block of proteins. It is a non-essential amino acid, meaning that it can be synthesized by the body from other compounds. In the medical field, serine is known to play a role in various physiological processes, including the production of neurotransmitters, the regulation of blood sugar levels, and the maintenance of healthy skin and hair. It is also used as a dietary supplement to support these functions and to promote overall health. In some cases, serine may be prescribed by a healthcare provider to treat certain medical conditions, such as liver disease or depression.
Rad52 is a protein that plays a role in DNA repair and recombination in cells. It is involved in the homologous recombination pathway, which is a mechanism for repairing DNA damage such as double-strand breaks. Rad52 helps to recognize and align homologous DNA sequences, which are necessary for the repair process to occur. In the medical field, mutations in the RAD52 gene can lead to increased susceptibility to certain types of cancer, such as breast and ovarian cancer. Additionally, Rad52 has been studied as a potential target for cancer therapy.
In the medical field, carrier proteins are proteins that transport molecules across cell membranes or within cells. These proteins bind to specific molecules, such as hormones, nutrients, or waste products, and facilitate their movement across the membrane or within the cell. Carrier proteins play a crucial role in maintaining the proper balance of molecules within cells and between cells. They are involved in a wide range of physiological processes, including nutrient absorption, hormone regulation, and waste elimination. There are several types of carrier proteins, including facilitated diffusion carriers, active transport carriers, and ion channels. Each type of carrier protein has a specific function and mechanism of action. Understanding the role of carrier proteins in the body is important for diagnosing and treating various medical conditions, such as genetic disorders, metabolic disorders, and neurological disorders.
Fanconi Anemia (FA) is a rare genetic disorder that affects the body's ability to repair damaged DNA. It is characterized by a range of symptoms, including bone marrow failure, which can lead to anemia, infections, and an increased risk of developing cancer. FA is caused by mutations in one of 19 different genes, and it is inherited in an autosomal recessive pattern, meaning that an individual must inherit two copies of the mutated gene (one from each parent) in order to develop the disorder. There is currently no cure for FA, but treatments are available to manage the symptoms and complications of the disease.
In the medical field, RecA recombinases are a type of enzyme that play a crucial role in DNA repair and recombination. RecA proteins are involved in the process of homologous recombination, which is a mechanism for repairing DNA damage or creating genetic diversity. During homologous recombination, RecA proteins bind to single-stranded DNA and recruit other proteins to form a complex called a nucleoprotein filament. This filament searches for a homologous double-stranded DNA molecule, which is used as a template for repairing the damaged or mutated DNA. RecA recombinases are also involved in the process of genetic recombination, which is the exchange of genetic material between two different DNA molecules. This process can lead to the creation of new genetic combinations and is an important mechanism for evolution. In addition to their role in DNA repair and recombination, RecA recombinases have also been implicated in various diseases, including cancer and bacterial infections. For example, mutations in the RecA gene have been associated with increased susceptibility to certain types of cancer, and some bacteria have evolved mechanisms to evade the immune system by using RecA proteins to manipulate their own DNA.
E2F1 transcription factor is a protein that plays a crucial role in regulating the cell cycle and cell proliferation. It is a member of the E2F family of transcription factors, which are involved in controlling the expression of genes that are necessary for cell cycle progression and DNA replication. E2F1 is activated during the G1 phase of the cell cycle, when the cell is preparing to divide. It binds to specific DNA sequences in the promoter regions of target genes, such as those involved in DNA replication and cell cycle progression, and promotes their transcription. In this way, E2F1 helps to coordinate the various events that occur during the cell cycle and ensure that the cell divides properly. Abnormal regulation of E2F1 has been implicated in a number of diseases, including cancer. For example, overexpression of E2F1 has been observed in many types of cancer, and it is thought to contribute to the uncontrolled proliferation of cancer cells. Conversely, loss of E2F1 function has been associated with impaired cell cycle progression and reduced cell proliferation, which may contribute to the development of certain types of cancer. Overall, E2F1 transcription factor plays a critical role in regulating the cell cycle and cell proliferation, and its dysregulation has been implicated in a number of diseases, including cancer.
Multiprotein complexes are groups of two or more proteins that interact with each other to form a functional unit in the cell. These complexes can be involved in a wide range of cellular processes, including signal transduction, gene expression, metabolism, and protein synthesis. Multiprotein complexes can be transient, meaning they assemble and disassemble rapidly in response to changes in the cellular environment, or they can be stable and persist for longer periods of time. Some examples of well-known multiprotein complexes include the proteasome, the ribosome, and the spliceosome. In the medical field, understanding the structure and function of multiprotein complexes is important for understanding how cells work and how diseases can arise. For example, mutations in genes encoding proteins that make up multiprotein complexes can lead to the formation of dysfunctional complexes that contribute to the development of diseases such as cancer, neurodegenerative disorders, and metabolic disorders. Additionally, drugs that target specific components of multiprotein complexes are being developed as potential treatments for these diseases.
Ubiquitin-conjugating enzymes, also known as E2 enzymes, are a family of enzymes that play a crucial role in the ubiquitin-proteasome system (UPS) in the medical field. The UPS is a major pathway for the degradation of proteins in cells, and it is involved in a wide range of cellular processes, including cell cycle regulation, signal transduction, and protein quality control. E2 enzymes are responsible for transferring ubiquitin, a small protein that is covalently attached to target proteins, from an E1 enzyme to a target protein. This process is essential for the formation of polyubiquitin chains, which serve as a signal for the degradation of the target protein by the proteasome. In the medical field, the UPS is involved in the regulation of many diseases, including cancer, neurodegenerative disorders, and autoimmune diseases. Dysregulation of the UPS has been implicated in the development and progression of these diseases, and targeting the UPS has become an important strategy for the development of new therapies. E2 enzymes are therefore of great interest in the medical field, as they play a central role in the UPS and are involved in the regulation of many important cellular processes. Understanding the function and regulation of E2 enzymes is essential for developing new therapies for diseases that are associated with dysregulation of the UPS.
Cell transformation, neoplastic refers to the process by which normal cells in the body undergo genetic changes that cause them to become cancerous or malignant. This process involves the accumulation of mutations in genes that regulate cell growth, division, and death, leading to uncontrolled cell proliferation and the formation of tumors. Neoplastic transformation can occur in any type of cell in the body, and it can be caused by a variety of factors, including exposure to carcinogens, radiation, viruses, and inherited genetic mutations. Once a cell has undergone neoplastic transformation, it can continue to divide and grow uncontrollably, invading nearby tissues and spreading to other parts of the body through the bloodstream or lymphatic system. The diagnosis of neoplastic transformation typically involves a combination of clinical examination, imaging studies, and biopsy. Treatment options for neoplastic transformation depend on the type and stage of cancer, as well as the patient's overall health and preferences. Common treatments include surgery, radiation therapy, chemotherapy, targeted therapy, and immunotherapy.
Caspase 3 is an enzyme that plays a central role in the process of programmed cell death, also known as apoptosis. It is a cysteine protease that cleaves specific proteins within the cell, leading to the characteristic morphological and biochemical changes associated with apoptosis. In the medical field, caspase 3 is often studied in the context of various diseases and conditions, including cancer, neurodegenerative disorders, and cardiovascular disease. It is also a target for the development of new therapeutic strategies, such as drugs that can modulate caspase 3 activity to either promote or inhibit apoptosis. Caspase 3 is activated by a variety of stimuli, including DNA damage, oxidative stress, and the activation of certain signaling pathways. Once activated, it cleaves a wide range of cellular substrates, including structural proteins, enzymes, and transcription factors, leading to the disassembly of the cell and the release of its contents. Overall, caspase 3 is a key player in the regulation of cell death and has important implications for the development and treatment of many diseases.
Malondialdehyde (MDA) is a toxic compound that is produced as a byproduct of lipid peroxidation, a process that occurs when lipids (fats) in cells are damaged by free radicals or other reactive molecules. MDA is a highly reactive molecule that can bind to proteins, DNA, and other cellular components, causing damage and potentially leading to cell death. In the medical field, MDA is often used as a biomarker of oxidative stress and inflammation. Oxidative stress occurs when there is an imbalance between the production of reactive oxygen species (ROS) and the body's ability to neutralize them. Inflammation is a normal response to injury or infection, but chronic inflammation can contribute to the development of a wide range of diseases, including cancer, cardiovascular disease, and neurodegenerative disorders. MDA levels can be measured in blood, urine, or other body fluids, and elevated levels of MDA have been associated with a variety of health problems, including aging, diabetes, and certain types of cancer. Therefore, MDA is an important biomarker for monitoring the health status of individuals and for identifying potential risk factors for disease.
Ascorbic acid, also known as vitamin C, is a water-soluble vitamin that is essential for human health. It is a powerful antioxidant that helps protect cells from damage caused by free radicals, which are unstable molecules that can damage cells and contribute to the development of chronic diseases such as cancer, heart disease, and diabetes. In the medical field, ascorbic acid is used to prevent and treat scurvy, a disease caused by a deficiency of vitamin C. It is also used to treat certain types of anemia, as well as to boost the immune system and improve wound healing. Ascorbic acid is available over-the-counter as a dietary supplement and is also used in some prescription medications. However, it is important to note that high doses of ascorbic acid can cause side effects such as diarrhea, nausea, and stomach cramps, and may interact with certain medications. Therefore, it is important to consult with a healthcare provider before taking ascorbic acid supplements.
Proto-oncogenes are normal genes that are involved in regulating cell growth and division. When these genes are mutated or overexpressed, they can become oncogenes, which can lead to the development of cancer. Proto-oncogenes are also known as proto-oncogene proteins.
Escherichia coli (E. coli) is a type of bacteria that is commonly found in the human gut. E. coli proteins are proteins that are produced by E. coli bacteria. These proteins can have a variety of functions, including helping the bacteria to survive and thrive in the gut, as well as potentially causing illness in humans. In the medical field, E. coli proteins are often studied as potential targets for the development of new treatments for bacterial infections. For example, some E. coli proteins are involved in the bacteria's ability to produce toxins that can cause illness in humans, and researchers are working to develop drugs that can block the activity of these proteins in order to prevent or treat E. coli infections. E. coli proteins are also used in research to study the biology of the bacteria and to understand how it interacts with the human body. For example, researchers may use E. coli proteins as markers to track the growth and spread of the bacteria in the gut, or they may use them to study the mechanisms by which the bacteria causes illness. Overall, E. coli proteins are an important area of study in the medical field, as they can provide valuable insights into the biology of this important bacterium and may have potential applications in the treatment of bacterial infections.
DNA primers are short, single-stranded DNA molecules that are used in a variety of molecular biology techniques, including polymerase chain reaction (PCR) and DNA sequencing. They are designed to bind to specific regions of a DNA molecule, and are used to initiate the synthesis of new DNA strands. In PCR, DNA primers are used to amplify specific regions of DNA by providing a starting point for the polymerase enzyme to begin synthesizing new DNA strands. The primers are complementary to the target DNA sequence, and are added to the reaction mixture along with the DNA template, nucleotides, and polymerase enzyme. The polymerase enzyme uses the primers as a template to synthesize new DNA strands, which are then extended by the addition of more nucleotides. This process is repeated multiple times, resulting in the amplification of the target DNA sequence. DNA primers are also used in DNA sequencing to identify the order of nucleotides in a DNA molecule. In this application, the primers are designed to bind to specific regions of the DNA molecule, and are used to initiate the synthesis of short DNA fragments. The fragments are then sequenced using a variety of techniques, such as Sanger sequencing or next-generation sequencing. Overall, DNA primers are an important tool in molecular biology, and are used in a wide range of applications to study and manipulate DNA.
Indirect DNA damage
DNA damage (naturally occurring)
DNA damage-binding protein
DNA damage theory of aging
G2-M DNA damage checkpoint
DNA damage-inducible transcript 3
Free radical damage to DNA
DNA repair-deficiency disorder
DNA-(apurinic or apyrimidinic site) lyase
Bioremediation of radioactive waste
Biotin carboxyl carrier protein
DNA methylation in cancer
Cell cycle withdrawal
Causes of cancer
Could Shift Work Damage Your DNA? - HealthStatus
Omega-3 may protect against DNA damage in vascular cells: Study
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Quantifying DNA damage on paper sensors via controlled template-independent DNA polymerization - Chemical Science (RSC...
An age-related increase in resistance to DNA damage-induced apoptotic cell death is associated with development of DNA repair...
Subject: DNA damage and DNA repair | Search Results | Academic Commons
Can Schlafen 11 Help to Stratify Ovarian Cancer Patients Treated with DNA-Damaging Agents? | Lékařská fakulta Masarykovy...
Inhibition of protein synthesis in apoptosis: differential requirements by the tumor necrosis factor alpha family and a DNA...
Bone marrow aspirate, trephine and immunophenotyping showed no evidence of infiltration by myeloma - DNA Damage Signalling...
Assessing DNA Damage Responses Using B Lymphocyte Cultures<...
Sweeteners may damage DNA and increase cancer risk - MJ
Benzoyl peroxide-induced damage to DNA and its components - Staff
Fanconi anemia: MedlinePlus Genetics
Health Effects of Radiation | Radiation | NCEH | CDC
NAT10 regulates the repair of UVB-induced DNA damage and tumorigenicity. | Toxicol Appl Pharmacol;477: 116688, 2023 10 15. ...
Stress-induced DNA damage biomarkers: applications and limitations - Archive ouverte HAL
Nanoparticle News, Research - Page 93
Kiwifruit as a modulator of DNA damage and DNA repair. - NextBio article
UV radiation damage and bacterial DNA repair systems - Fingerprint - Bar-Ilan University
DNA annealing by Redβ is insufficient for homologous recombination and the additional requirements involve intra- and inter...
Mediterranean Diet Cuts Some Breast Cancer Risk by 40%
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The importance of XRCC2 in RAD51-related DNA damage repair. - Department of Oncology
Chromogenic Escherichia coli reporter strain for screening DNA damaging agents | AMB Express | Full Text
Ataxia-Telangiectasia: Practice Essentials, Pathophysiology, Epidemiology
Premature senescence of mesothelial cells is associated with non-telomeric DNA damage - Fingerprint - Mayo Clinic
DNA Double-Stranded Breaks News, Articles | The Scientist Magazine®
- Despite the central role of cellular metabolism in maintaining genome integrity, there has been no systematic, unbiased study on how metabolic perturbations affect the DNA damage and repair process. (technologynetworks.com)
- The researchers observed that cellular respiratory enzymes, a major source of reactive oxygen species, relocated from the mitochondria to the nucleus in response to DNA damage. (technologynetworks.com)
- PRDX1 was also found to repair the damage by regulating the cellular availability of aspartate, a raw material that is critical for synthesising nucleotides, the building blocks of DNA. (technologynetworks.com)
- Human mediator of DNA damage checkpoint 1 (hMDC1) is an essential component of the cellular response to DNA double strand breaks. (ox.ac.uk)
- A study published online May 15 in Nature sheds new light on a cellular process designed to destroy faulty DNA in the mitochondria before it is passed on to developing reproductive cells. (wng.org)
- DNA, as we know, is a script of proper cellular life. (timeskipper.com)
- As our DNA replicates, the cellular machinery involved in the process makes mistakes, leading to changes in the DNA sequence. (longevityfacts.com)
- Investigation of the cellular responses to these DNA breaks has established important insights into B cell development and, more broadly, has provided fundamental advances into the molecular mechanisms of DNA damage response pathways. (wustl.edu)
- This chapter describes methods for generating these cellular systems, inducing and quantifying DSBs, and assessing DNA damage programs. (wustl.edu)
- 8-hydroxy-2'-deoxyguanosine (8-OHdG or 8-oxo-dG) is an oxidized derivative of deoxyguanosine and is generated by hydroxyl radicals, singlet oxygen, and one-electron oxidants in cellular DNA. (gentaur.be)
- A variety of environmental stresses like chemicals, UV and ionizing radiation and organism's endogenous processes such as replication stress and metabolism can lead to the generation of reactive oxygen and nitrogen species (ROS/RNS) that can attack cellular vital components like DNA, proteins and lipid membranes. (hal.science)
- Instead, this caspase activity leads to DNA damage that, in turn, promotes genomic instability , cellular transformation, and tumorigenesis . (bvsalud.org)
- Further study of reactive oxygen species was conducted using analysis of cellular H2O2 generation, lipid peroxidation of cellular membranes and DNA damage. (cdc.gov)
- Without vigilant repair, cancer would run rampant, and now scientists at the University of Pittsburgh and Carnegie Mellon University have gotten a glimpse of how one protein in particular keeps DNA damage in check. (cmu.edu)
- According to a study published today in Nature Structural and Molecular Biology , a protein called UV-DDB - which stands for ultraviolet-damaged DNA-binding - is useful beyond safeguarding against the sun. (cmu.edu)
- Elledge had found that Rnr2 protein levels increased when yeast cells were grown in the presence of agents that damaged DNA. (the-scientist.com)
- He found that RNR2 RNA levels increased dramatically, even more than the protein levels, upon exposure of cells to DNA damage and that mutations in RNR2 resulted in hypersensitivity to DNA damage. (the-scientist.com)
- Studying RNR2' s regulatory elements, he found those that were necessary to induce the production of higher protein levels in response to DNA damage and identified factors that bind these DNA elements to mediate the response of RNR2 to DNA damage. (the-scientist.com)
- The oversight is understandable since DNA does not appear on nutrition labels in the same manner as protein, carbohydrates, fat, vitamins, and minerals. (jpost.com)
- Jeffrey, I. W. , Bushell, M. , Tilleray, V. J. , Morley, S. and Clemens, M. J. (2002) Inhibition of protein synthesis in apoptosis: differential requirements by the tumor necrosis factor alpha family and a DNA-damaging agent for caspases and the double-stranded RNA-dependent protein kinase. (gla.ac.uk)
- In contrast, treatment of cells with the DNA-damaging agent etoposide inhibits protein synthesis equally well in the presence of a pan-specific caspase inhibitor and in the presence or absence of PKR. (gla.ac.uk)
- Rabbit polyclonal to Parp.Poly(ADP-ribose) polymerase-1 (PARP-1), also designated PARP, is a nuclear DNA-bindingzinc finger protein that influences DNA repair, DNA replication, modulation of chromatin structure,and apoptosis. (2011globalhealth.org)
- DNA nuclease/helicase 2 (DNA2), a multi-functional protein protecting the high fidelity of genomic transmission, plays critical roles in DNA replication and repair processes. (longevityfacts.com)
- Meanwhile, Tarn's group found that co-phase separation between non-coding RNA and RNA binding protein Y14 may contribute to the repair of DNA damage. (sinica.edu.tw)
- 8-OHdG also participates in epigenetic regulation of gene activation/repression by inhibiting the binding affinity of MBD protein to the CpG sites of DNA. (gentaur.be)
Types of DNA lesions2
- This PAT assay provides a low-cost, high throughput and easy to use method for quantifying the absolute levels of various types of DNA lesions, thus making it well-suited for drug development, genotoxicity testing, and environmental toxicology. (rsc.org)
- In this review we describe the most accepted chemical pathways for DNA damage induction and the different types of DNA lesions, i.e., single, complex DNA lesions etc. that can be used as DNA damage biomarkers. (hal.science)
- Elledge's idea that eukaryotic cells sense the progress of DNA replication and transform that information into a DNA-damage response was new. (the-scientist.com)
- Those results led him to study how cells monitor roadblocks to replication and DNA damage, such as nicks and double-stranded breaks, and how the cell handles that information. (the-scientist.com)
- Moreover, DNA2 potentially participates in controlling the cell cycle by repairing the DNA replication faults at main checkpoints. (longevityfacts.com)
- As a modified nucleoside base, 8-OHdG is considered important not only because of its abundance but also because of its mutagenic potential through G-to-T transversion mutations upon replication of DNA. (gentaur.be)
- In addition, we suggest the use of DNA repair gene products as biomarkes for identification of different types of stresses i.e., radiation, oxidative, or replication stress, based on bioinformatic approaches and meta-analysis of literature data. (hal.science)
- The FA pathway sends certain proteins to the area of damage, which trigger DNA repair so DNA replication can continue. (medlineplus.gov)
- on opposite strands of DNA are abnormally attached or linked together, which stops the process of DNA replication. (medlineplus.gov)
- The activation of these two proteins brings DNA repair proteins to the area of the ICL so the cross-link can be removed and DNA replication can continue. (medlineplus.gov)
- The ICLs stall DNA replication, ultimately resulting in either abnormal cell death due to an inability make new DNA molecules or uncontrolled cell growth due to a lack of DNA repair processes. (medlineplus.gov)
- The potential heart health benefits of omega-3s may be linked (in part at least) to their ability to protect the DNA in the cells lining blood vessels, according to a study from Japanese researchers. (nutraingredients.com)
- As in the DNA tightrope experiment, UV-DDB rushed to the scene, and when it wasn't available, cells were more sensitive to oxidative stress. (cmu.edu)
- His first experimental results contained a serendipitous artifact that laid the foundation for a scientific career studying how eukaryotic cells deal with damage to their DNA. (the-scientist.com)
- While it's too soon to say this occurs in humans - the study only observed heat-damaged DNA component uptake and increased DNA injury in lab-grown cells and mice - the findings could have important implications for dietary choices and public health. (jpost.com)
- In contrast, key components of DNA known as nucleotides that are made available through the normal breakdown of biomolecules - for instance, during digestion - are readily incorporated into the DNA of cells, suggesting a plausible and potentially significant pathway for damaged food DNA to inflict damage on other DNA downstream in consumers, the team wrote. (jpost.com)
- The image illustrates the location of DNA damage (in the nucleus of these four cells - green) and the colocalization of PRDX1 (in red, same place). (technologynetworks.com)
- Cells are thought to delicately balance their energy needs and avoid damaging DNA by containing metabolic activity outside the nucleus and within the cytoplasm and mitochondria. (technologynetworks.com)
- If DNA damage occurs anyway, cells pause momentarily and carry out repairs, synthesising new building blocks and filling in the gaps. (technologynetworks.com)
- These experiments revealed that cells order the enzyme PRDX1, an antioxidant enzyme also normally found in mitochondria, to travel to the nucleus and scavenge reactive oxygen species present to prevent further damage. (technologynetworks.com)
- New research shows God designed an intricate system within our cells to prevent developing egg cells from inheriting harmful, mutant DNA. (wng.org)
- During our lives, DNA molecules in cells are being constantly damaged by various factors. (timeskipper.com)
- Accumulation of these damages leads to impaired function of our cells. (timeskipper.com)
- And while cells protect DNA to the best of their ability, these are affected by free radicals more than 10,000 times per day causing naturally occurring DNA damages, which unfortunately we cannot avoid. (timeskipper.com)
- Some of them can interact with DNA , bind to it, and thus make it unreadable for the cells. (timeskipper.com)
- One way would be to equip our cells with Vitamin D. There are two clinical trials showing that Vitamin D stimulates DNA repair in humans. (timeskipper.com)
- They isolated B cells from the blood and treated them with hydrogen peroxidase, to inflict oxidative damage on DNA. (timeskipper.com)
- The results showed that DNA repair in young and centenarian cells works at a similar pace, while old cells are slower. (timeskipper.com)
- DNA repair mechanisms in the old cells had 40% lower levels of activity before peroxidase treatment, compared to the young and centenarian cells. (timeskipper.com)
- After treatment, the activity of DNA repair mechanisms in young and centenarian cells was rapidly upregulated, while it was only moderately upregulated in the old cells. (timeskipper.com)
- Development of B cells requires the programmed generation and repair of double-stranded DNA breaks in antigen receptor genes. (wustl.edu)
- In the new study, when researchers exposed human blood cells to sucralose-6-acetate, they found that it caused breaks in DNA. (medicaljournal.xyz)
- They also found that sucralose-6-acetate - and sucralose itself - damaged the junctions that hold together the cells that line the human intestines, causing the gut to become leaky. (medicaljournal.xyz)
- The EpiQuik™ 8-OHdG DNA Damage Quantification Direct Kit (Fluorometric) is a complete set of optimized buffers and reagents to fluorometrically detect and quantify oxidative DNA damage (8-OHdG) directly using DNA isolated from any species such as mammals, plants, fungi, bacteria, and viruses in a variety of forms including, but not limited to, cultured cells, fresh and frozen tissues, paraffin-embedded tissues, and body fluid samples. (gentaur.be)
- Highly convenient assay with direct use of DNA isolated from cells or tissues, without the need for DNA digestion or hydrolysis. (gentaur.be)
- The currently used competitive ELISA methods are also not conveniently applicable for cell/tissue 8-OHdG detection because they are less accurate and have an inability to use intact DNA isolated from cells or tissues directly. (gentaur.be)
- Radiation can damage the DNA in our cells. (cdc.gov)
- Berberine may damage DNA in some cells. (msdmanuals.com)
- They engineered the insects to carry a mix of both good and bad mitochondrial DNA, which they designed to fluoresce so they could observe the process in real time. (wng.org)
- DNA2 is also involved in the stability of mitochondrial DNA and the maintenance of telomeres. (longevityfacts.com)
- Limited mitochondrial permeabilization causes DNA damage and genomic instability in the absence of cell death. (bvsalud.org)
- That uptake directly places damage in the consumer's DNA, potentially triggering genetic mutations that may eventually lead to cancer and other diseases. (jpost.com)
- Antioxidant enzymes are deployed to mop up reactive oxygen species at their source before they reach DNA, a defensive strategy that protects the roughly 3 billion nucleotides from suffering potentially catastrophic mutations. (technologynetworks.com)
- But the DNA in a mother's mitochondria can develop harmful mutations and lead to genetic diseases in her offspring. (wng.org)
- Distinguished Research Fellow Woan-Yuh Tarn in the Institute of Biomedical Sciences, Academia Sinica found that the long non-coding RNA HOTAIRM1 brings mRNA surveillance factors to the DNA damage sites, which degrade the transcripts induced by double-strand breaks. (sinica.edu.tw)
- Taking advantage of this finding, we proposed a paper-assisted TdT (PAT) assay for absolute quantification of alkylated DNA lesions (N7-methylguanine), DNA deamination (cytosine-to-uracil) and DNA oxidation (8-oxo-7,8-dihydroguanine) by combining various DNA glycosylases. (rsc.org)
- Based on the type of DNA lesions detected one can hypothesize on the most probable mechanisms involved in the formation of these lesions for example in the case of UV and ionizing radiation (e.g. (hal.science)
- Importantly, we observed that TdT efficiently incorporates fluorescently labeled dUTP on to 3′-OH ends of DNA strands in a strictly controllable manner on cellulose paper, in comparison to its distributive mode of DNA synthesis in solution. (rsc.org)
- DNA damage aging theory claims: the accumulation of unrepaired corruptions in DNA is the reason we grow old. (timeskipper.com)
- According to the DNA Damage Theory of Aging, the process of aging is caused by the accumulation of unrepaired DNA damage. (longevityfacts.com)
- There is little disagreement among scientists that this accumulation of DNA damage is a significant cause of aging. (longevityfacts.com)
- This new evidence points to UV-DDB being a scout for general DNA damage and an overseer of the molecular repair crew that fixes it. (cmu.edu)
- For the first time, Van Houten's team witnessed this molecular tango along a "tightrope" of DNA slung between two silica beads, using real-time, single-molecule imaging. (cmu.edu)
- A research team led by Sara Sdelci at the Centre for Genomic Regulation (CRG) in Barcelona and Joanna Loizou at the CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences in Vienna and the Medical University of Vienna addressed this challenge by carrying out various experiments to identify which metabolic enzymes and processes are essential for a cell's DNA damage response. (technologynetworks.com)
- Direct detection of 8-OHdG using intact DNA, which eliminates interference from high molecular weight compounds, such as carbohydrates and proteins that are often seen in competitive 8-OHdG assays. (gentaur.be)
- Directly affecting the DNA molecule, causing rearrangements in its structure and changes in interactions of atoms. (timeskipper.com)
- So many, in fact, that a group of researchers led by Pan-Pan Jia at the Chinese Academy of Sciences, felt it necessary to publish a review that summarizes the role of an important DNA repair molecule called DNA2. (longevityfacts.com)
- The characteristics of its genome--a aplastic anemia, hemorrhage, and lymphoid depletion) and single, closed molecule of circular, negative-sense DNA increased death in young chicken ( 11 ). (cdc.gov)
- Increased intakes of niacin (vitamin B3) from the diet may protect against DNA damage in people exposed to ionizing radiation such as pilots, says a new study. (nutraingredients.com)
- Among them, much attention has been focused on DNA since DNA damage plays a role in several biological disorders and aging processes. (hal.science)
- These outcomes correlated with nFe2O3 dissolution, increased intracellular iron, and genotoxicity, as well as significant changes in pathways related to DNA damage repair and autophagic processes. (cdc.gov)
- We investigated the presence of HGyV DNA in 1, VP2, and VP3) that encode proteins of 465, 231, and blood samples of 301 persons in Italy using specifi c PCRs. (cdc.gov)
- Many studies link the consumption of charred and fried foods to DNA damage and attribute the harm to certain small molecules that form so-called reactive species in the body. (jpost.com)
- For those reactive species to cause DNA damage, they must physically encounter DNA in a cell to trigger a deleterious chemical reaction - probably a rare event. (jpost.com)
- These reactions also create reactive oxygen species, dangerous by-products like hydrogen peroxide which damage the building blocks of DNA in the same way oxygen and water corrode metal and form rust. (technologynetworks.com)
- Surprisingly, inducing DNA damage resulted in reactive oxygen species being generated and accumulating inside the nucleus. (technologynetworks.com)
- Indirectly affecting DNA by turning other molecules into Reactive Oxygen Species, which then interact with DNA, causing rearrangements and…well, you get the picture. (timeskipper.com)
- Toxins such as free radicals, also called reactive oxygen species (ROS) or radiation can also damage DNA. (longevityfacts.com)
- Permanent DNA damage leads to loss of function, inflammation, chronic illness and participates significantly in our eventual demise. (longevityfacts.com)
Lack of DNA repair1
- Is it possible that this lowered level could contribute to lack of DNA repair which could contribute to cancer and other diseases? (healthstatus.com)
- The reason we survive is due to DNA repair mechanisms. (timeskipper.com)
- There are several mechanisms of detection and reversion of DNA damages, working round the clock in every cell. (timeskipper.com)
- Following this rough treatment, they measured the characteristics of the DNA repair mechanisms. (timeskipper.com)
- Scientists have made headway in understanding our DNA repair mechanisms and have found potential ways to mitigate some of its effects. (longevityfacts.com)
- Research has shown that our DNA repair mechanisms decline as we get older. (longevityfacts.com)
- Unless we are lucky to be among the tiny percentage of centenarians who are blessed with superb DNA repair mechanisms, the odds are that unrepaired DNA damage will strike us down with chronic diseases before we reach our goal. (longevityfacts.com)
- Our body has its DNA repair mechanisms, but this, like many other things in our body, falters with age. (longevityfacts.com)
- If we could somehow keep our body's DNA repair mechanisms in good working order, we would be well on our way to reaching the age of 120. (longevityfacts.com)
- Most of the time, our body's DNA repair mechanisms fix the damage, but errors slip through and accumulate as we age. (longevityfacts.com)
- The deterioration of our DNA repair machinery is a primary cause of aging, as our failing repair mechanisms allow temporary errors to become permanent. (longevityfacts.com)
- The high frequency of DNA damage necessitates effective repair mechanisms. (sinica.edu.tw)
Theory of Aging2
- DNA Damage Theory of Aging says that aging is mainly due to faulty DNA Repair. (longevityfacts.com)
- Although there is a minority of researchers who disagree with the theory, the DNA Damage Theory of Aging is backed up by a great deal of experimental evidence over the past several decades. (longevityfacts.com)
- The EpiQuik™ 8-OHdG DNA Damage Quantification Direct Kit (Fluorometric) contains all reagents necessary for the quantification of Oxidative DNA damage (8-OHdG). (gentaur.be)
- The direct fluorometric quantification of DNA samples replaces obsolete or inferior methods and eliminates the need for DNA digestion/denaturation, radioactivity, extraction, or chromatography. (gentaur.be)
- DNA is the cell's "instruction manual" that controls a cell's normal growth and function. (cdc.gov)
- When UV-DDB finds damage, it acts like a foreman to help the DNA repair crew get in, fix the faulty bases and detach quickly. (cmu.edu)
- When telomeres (green) undergo damage (bottom row), UV-DDB (red) rushes to the scene (yellow). (cmu.edu)
- But what has never been documented before our study is the potentially large quantities of heat-damaged DNA available for uptake into a consumer's own DNA. (jpost.com)
- However, the amount of this chemical in a single serving of a sucralose-containing beverage could be high enough to potentially damage DNA, the authors of the new study pointed out. (medicaljournal.xyz)
- As a start to designing those gene-targeting tools, Elledge, now a professor of genetics at Harvard Medical School, began by trying to clone the mammalian homolog of recA , a bacterial gene required for DNA repair via recombination. (the-scientist.com)
- The new promising marker Schlafen 11 seems to correlate with sensitivity or resistance to DNA-damaging agents, including platinum compounds or PARP inhibitors in various types of cancer. (muni.cz)
- 1 There is potential that lower melatonin in night-shift workers could lead to a body's decreased ability to repair its DNA. (healthstatus.com)
- For years, researchers have continued to identify DNA repair pathways, and the activity seems to have increased in the summer of 2017, leading to many published articles on the subject. (longevityfacts.com)
- It identifies DNA damage so that another crew can come in and patch and seal it," said study senior author Bennett Van Houten , Ph.D., professor of pharmacology and chemical biology at the Pitt School of Medicine and UPMC Hillman Cancer Center . (cmu.edu)
- Working at night resulted in lower melatonin levels and a less of the chemical which repairs DNA in the urine. (healthstatus.com)
- A study from researchers at North Carolina State University suggests that a chemical formed from one artificial sweetener might also damage our DNA. (medicaljournal.xyz)
- These results indicate that the radical generation and the damage caused by them is not only a function of surface area but is also influenced by changing chemical and other characteristics due to particle size. (cdc.gov)
- Evidence is mounting that RNA plays an important role in DNA repair. (sinica.edu.tw)
- Fortunately, we can avoid DNA damage and stimulate DNA repair to achieve longevity. (timeskipper.com)
- It was published in ACS Central Science under the title "Possible Genetic Risks from Heat-Damaged DNA in Food. (jpost.com)
- However, those small molecules produced in typical cooking number many thousands of times less than the amount of DNA occurring naturally in foods, Kool said. (jpost.com)
- Extract DNA from cell or tissue samples using a commercial DNA Extraction kit or other desired method. (antibodies-online.com)
- Researchers have warned manufacturers of functional foods and supplements to keep polyphenol doses low, following conclusions that low concentrations protect but high concentrations may damage DNA. (nutraingredients.com)
- The researchers discovered that a perfectly timed drop in mitofusin levels triggers the sorting of good from bad DNA. (wng.org)
- Researchers are piecing together the DNA repair puzzle. (longevityfacts.com)
- Scientists revealed that damaged DNA in overheated food can be absorbed during digestion and incorporated into the DNA of those who consume it. (jpost.com)
- As shown for the first time, Stanford scientists and their collaborators at the National Institute of Standards and Technology (NIST), the University of Maryland, and Colorado State University revealed that components of heat-marred DNA can be absorbed during digestion and incorporated into the DNA of those who eat such food. (jpost.com)
- Nutrition and diet have again been linked to the quality of male sperm, with a new study revealing that high micronutrient intakes is 'strongly' associed with improved sperm DNA quality in older men. (nutraingredients.com)
- DNA High-Binding Plate : One 96-well strip plate. (antibodies-online.com)
- CDP-DNA standards or unknown DNA samples are first heat denatured before being adsorbed onto a 96-well DNA high-binding plate. (antibodies-online.com)
- Note: Samples with high concentrations of CPD may be further diluted 2-4 fold in 4 μg/mL Reduced DNA. (antibodies-online.com)
- Add 50 μL of unknown DNA samples or CPD-DNA standards to the wells of the DNA High- Binding plate. (antibodies-online.com)
- Due to the high roughness and porous nature of cellulose paper, we attribute this controllable DNA polymerization to the pore confinement effect on the catalytic behaviour of TdT. (rsc.org)
- TH34 is a potent HDAC6/8/10 inhibitor that induces DNA damage-mediated cell death in human high-grade neuroblastoma cell lines. (csnpharm.cn)
- These changes were consistent with the need for DNA damage repair because of high metabolic rates during flight. (cdc.gov)
- Daily folic acid supplements could improve DNA stability and reduce the risk of certain cancers linked to faults in the genetic code, suggests new research. (nutraingredients.com)
- We have shown that cooking can damage DNA in food and have discovered that consumption of this DNA may be a source of genetic risk," said chemistry Prof. Eric Kool. (jpost.com)
- Daily supplements of astaxanthin - the pigment that gives salmon its pink colour - may protect DNA from damage and boost the immune response in healthy young women, says a new study. (nutraingredients.com)
- Can Schlafen 11 Help to Stratify Ovarian Cancer Patients Treated with DNA-Damaging Agents? (muni.cz)
- In addition to DNA damage, new studies have found that sucralose can lead to leaky gut lining and increase the activity of genes related to inflammation and cancer. (medicaljournal.xyz)
- RÉSUMÉ Des données de plus en plus nombreuses indiquent que les antioxydants alimentaires ont des effets favorables sur la réduction du risque de cancer. (who.int)
- When DNA is damaged, a cell can begin growing out of control and create a cancer tumor. (cdc.gov)
- DNA damage, aging, and cancer. (medscape.com)
- Three to four cups of a 'special' coffee rich in green coffee bean compounds and roast products may protect oxidative damage to DNA and help reduce body fat, say new results published today. (nutraingredients.com)
- In the time it takes you to read this sentence, every cell in your body suffers some form of DNA damage. (cmu.edu)
- Although this study hasn't proven the relationship between the chemicals the body produces and DNA its a very good estimate of results. (healthstatus.com)
- Acetaldehyde damages your DNA and prevents your body from repairing the damage. (cdc.gov)