Telomere
Telomere Homeostasis
Telomerase
Telomere-Binding Proteins
Telomeric Repeat Binding Protein 1
Telomeric Repeat Binding Protein 2
Cell Aging
In Situ Hybridization, Fluorescence
Dyskeratosis Congenita
Tankyrases
G-Quadruplexes
Chromosomal Instability
Chromosomes, Fungal
Leukocytes
DNA-Binding Proteins
Repetitive Sequences, Nucleic Acid
Saccharomyces cerevisiae Proteins
Saccharomyces cerevisiae
DNA Damage
Genomic Instability
Mutation
Chromosomes
Aging
RNA
Euplotes
Blotting, Southern
DNA
Silent Information Regulator Proteins, Saccharomyces cerevisiae
Base Sequence
Exodeoxyribonucleases
Chromosomes, Human
Chromosome Aberrations
Recombination, Genetic
Aging, Premature
Molecular Sequence Data
Cell Cycle Proteins
Rad52 DNA Repair and Recombination Protein
DNA Repair
RecQ Helicases
Analysis of genomic integrity and p53-dependent G1 checkpoint in telomerase-induced extended-life-span human fibroblasts. (1/4834)
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)A telomere-independent senescence mechanism is the sole barrier to Syrian hamster cell immortalization. (2/4834)
Reactivation of telomerase and stabilization of telomeres occur simultaneously during human cell immortalization in vitro and the vast majority of human cancers possess high levels of telomerase activity. Telomerase repression in human somatic cells may therefore have evolved as a powerful resistance mechanism against immortalization, clonal evolution and malignant progression. The comparative ease with which rodent cells immortalize in vitro suggests that they have less stringent controls over replicative senescence than human cells. Here, we report that Syrian hamster dermal fibroblasts possess substantial levels of telomerase activity throughout their culture life-span, even after growth arrest in senescence. In our studies, telomerase was also detected in uncultured newborn hamster skin, in several adult tissues, and in cultured fibroblasts induced to enter the post-mitotic state irreversibly by serum withdrawal. Transfection of near-senescent dermal fibroblasts with a selectable plasmid vector expressing the SV40 T-antigen gene resulted in high-frequency single-step immortalization without the crisis typically observed during the immortalization of human cells. Collectively, these data provide an explanation for the increased susceptibility of rodent cells to immortalization (and malignant transformation) compared with their human equivalents, and provide evidence for a novel, growth factor-sensitive, mammalian senescence mechanism unrelated to telomere maintenance. (+info)Telomeric repeats on small polydisperse circular DNA (spcDNA) and genomic instability. (3/4834)
Small polydisperse circular DNA (spcDNA) is a heterogeneous population of extrachromosomal circular molecules present in a large variety of eukaryotic cells. Elevated amounts of total spcDNA are related to endogenous and induced genomic instability in rodent and human cells. We suggested spcDNA as a novel marker for genomic instability, and speculated that spcDNA might serve as a mutator. In this study, we examine the presence of telomeric sequences on spcDNA. We report for the first time the appearance of telomeric repeats in spcDNA molecules (tel-spcDNA) in rodent and human cells. Restriction enzyme analysis indicates that tel-spcDNA molecules harbor mostly, if not exclusively, telomeric repeats. In rodent cells, tel-spcDNA levels are higher in transformed than in normal cells and are enhanced by treatment with carcinogen. Tel-spcDNA is also detected in some human tumors and cell lines, but not in others. We suggest, that its levels in human cells may be primarily related to the amount of the chromosomal telomeric sequences. Tel-spcDNA may serve as a unique mutator, through specific mechanisms related to the telomeric repeats, which distinguish it from the total heterogeneous spcDNA population. It may affect telomere dynamics and genomic instability by clastogenic events, alterations of telomere size and sequestration of telomeric proteins. (+info)p53- and ATM-dependent apoptosis induced by telomeres lacking TRF2. (4/4834)
Although broken chromosomes can induce apoptosis, natural chromosome ends (telomeres) do not trigger this response. It is shown that this suppression of apoptosis involves the telomeric-repeat binding factor 2 (TRF2). Inhibition of TRF2 resulted in apoptosis in a subset of mammalian cell types. The response was mediated by p53 and the ATM (ataxia telangiectasia mutated) kinase, consistent with activation of a DNA damage checkpoint. Apoptosis was not due to rupture of dicentric chromosomes formed by end-to-end fusion, indicating that telomeres lacking TRF2 directly signal apoptosis, possibly because they resemble damaged DNA. Thus, in some cells, telomere shortening may signal cell death rather than senescence. (+info)Telomere length dynamics and chromosomal instability in cells derived from telomerase null mice. (5/4834)
To study the effect of continued telomere shortening on chromosome stability, we have analyzed the telomere length of two individual chromosomes (chromosomes 2 and 11) in fibroblasts derived from wild-type mice and from mice lacking the mouse telomerase RNA (mTER) gene using quantitative fluorescence in situ hybridization. Telomere length at both chromosomes decreased with increasing generations of mTER-/- mice. At the 6th mouse generation, this telomere shortening resulted in significantly shorter chromosome 2 telomeres than the average telomere length of all chromosomes. Interestingly, the most frequent fusions found in mTER-/- cells were homologous fusions involving chromosome 2. Immortal cultures derived from the primary mTER-/- cells showed a dramatic accumulation of fusions and translocations, revealing that continued growth in the absence of telomerase is a potent inducer of chromosomal instability. Chromosomes 2 and 11 were frequently involved in these abnormalities suggesting that, in the absence of telomerase, chromosomal instability is determined in part by chromosome-specific telomere length. At various points during the growth of the immortal mTER-/- cells, telomere length was stabilized in a chromosome-specific man-ner. This telomere-maintenance in the absence of telomerase could provide the basis for the ability of mTER-/- cells to grow indefinitely and form tumors. (+info)Telomere loss in somatic cells of Drosophila causes cell cycle arrest and apoptosis. (6/4834)
Checkpoint mechanisms that respond to DNA damage in the mitotic cell cycle are necessary to maintain the fidelity of chromosome transmission. These mechanisms must be able to distinguish the normal telomeres of linear chromosomes from double-strand break damage. However, on several occasions, Drosophila chromosomes that lack their normal telomeric DNA have been recovered, raising the issue of whether Drosophila is able to distinguish telomeric termini from nontelomeric breaks. We used site-specific recombination on a dispensable chromosome to induce the formation of a dicentric chromosome and an acentric, telomere-bearing, chromosome fragment in somatic cells of Drosophila melanogaster. The acentric fragment is lost when cells divide and the dicentric breaks, transmitting a chromosome that has lost a telomere to each daughter cell. In the eye imaginal disc, cells with a newly broken chromosome initially experience mitotic arrest and then undergo apoptosis when cells are induced to divide as the eye differentiates. Therefore, Drosophila cells can detect and respond to a single broken chromosome. It follows that transmissible chromosomes lacking normal telomeric DNA nonetheless must possess functional telomeres. We conclude that Drosophila telomeres can be established and maintained by a mechanism that does not rely on the terminal DNA sequence. (+info)Telomere shortening in mTR-/- embryos is associated with failure to close the neural tube. (7/4834)
Mice genetically deficient for the telomerase RNA (mTR) can be propagated for only a limited number of generations. In particular, mTR-/- mice of a mixed C57BL6/129Sv genetic background are infertile at the sixth generation and show serious hematopoietic defects. Here, we show that a percentage of mTR-/- embryos do not develop normally and fail to close the neural tube, preferentially at the forebrain and midbrain. The penetrance of this defect increases with the generation number, with 30% of the mTR-/- embryos from the fifth generation showing the phenotype. Moreover, mTR-/- kindreds in a pure C57BL6 background are only viable up to the fourth generation and also show defects in the closing of the neural tube. Cells derived from mTR-/- embryos that fail to close the neural tube have significantly shorter telomeres and decreased viability than their mTR-/- littermates with a closed neural tube, suggesting that the neural tube defect is a consequence of the loss of telomere function. The fact that the main defect detected in mTR-/- embryos is in the closing of the neural tube, suggests that this developmental process is among the most sensitive to telomere loss and chromosomal instability. (+info)Generation and characterization of human smooth muscle cell lines derived from atherosclerotic plaque. (8/4834)
The study of atherogenesis in humans has been restricted by the limited availability and brief in vitro life span of plaque smooth muscle cells (SMCs). We describe plaque SMC lines with extended life spans generated by the expression of the human papillomavirus (HPV)-16 E6 and E7 genes, which has been shown to extend the life span of normal adult human aortic SMCs. Resulting cell lines (pdSMC1A and 2) demonstrated at least 10-fold increases in life span; pdSMC1A became immortal. The SMC identity of both pdSMC lines was confirmed by SM22 mRNA expression. pdSMC2 were generally diploid but with various structural and numerical alterations; pdSMC1A demonstrated several chromosomal abnormalities, most commonly -Y, +7, -13, anomalies previously reported in both primary pdSMCs and atherosclerotic tissue. Confluent pdSMC2 appeared grossly similar to HPV-16 E6/E7-expressing normal adult aortic SMCs (AASMCs), exhibiting typical SMC morphology/growth patterns; pdSMC1A displayed irregular cell shape/organization with numerous mitotic figures. Dedifferentiation to a synthetic/proliferative phenotype has been hypothesized as a critical step in atherogenesis, because rat neonatal SMCs and adult intimal SMCs exhibit similar gene expression patterns. To confirm that our pdSMC lines likewise express this apparent plaque phenotype, osteopontin, platelet-derived growth factor B, and elastin mRNA levels were determined in pdSMC1A, pdSMC2, and AASMCs. However, no significant increases in osteopontin or platelet-derived growth factor B expression levels were observed in either pdSMC compared with AASMCs. pdSMC2 alone expressed high levels of elastin mRNA. Lower levels of SM22 mRNA in pdSMC1A suggested greater dedifferentiation and/or additional population doublings in pdSMC1A relative to pdSMC2. Both pdSMC lines (particularly 1A) demonstrated high message levels for matrix Gla protein, previously reported to be highly expressed by human neointimal SMCs in vitro. These results describe 2 novel plaque cell lines exhibiting various features of plaque SMC biology; pdSMC2 may represent an earlier plaque SMC phenotype, whereas pdSMC1A may be representative of cells comprising an advanced atherosclerotic lesion. (+info)A telomere is a region of repetitive DNA sequences found at the end of chromosomes, which protects the genetic data from damage and degradation during cell division. Telomeres naturally shorten as cells divide, and when they become too short, the cell can no longer divide and becomes senescent or dies. This natural process is associated with aging and various age-related diseases. The length of telomeres can also be influenced by various genetic and environmental factors, including stress, diet, and lifestyle.
Telomere homeostasis refers to the balance between the processes that maintain or lengthen telomeres and those that shorten them. Telomeres are the protective caps at the ends of chromosomes, which progressively shorten each time a cell divides due to the inability of conventional DNA polymerase to fully replicate the ends of linear chromosomes.
The maintenance of telomere length is critical for maintaining genomic stability and preventing cellular senescence or apoptosis (programmed cell death). Telomere homeostasis involves several mechanisms, including the enzyme telomerase, which adds DNA repeats to the ends of telomeres, and other protective proteins that bind to telomeres and prevent their degradation.
On the other hand, processes such as oxidative stress, inflammation, and genotoxic agents can cause excessive telomere shortening, leading to cellular dysfunction and aging-related diseases. Therefore, maintaining telomere homeostasis is essential for healthy aging and preventing age-related diseases.
Telomerase is an enzyme that adds repetitive DNA sequences (telomeres) to the ends of chromosomes, which are lost during each cell division due to the incomplete replication of the ends of linear chromosomes. Telomerase is not actively present in most somatic cells, but it is highly expressed in germ cells and stem cells, allowing them to divide indefinitely. However, in many types of cancer cells, telomerase is abnormally activated, which leads to the maintenance or lengthening of telomeres, contributing to their unlimited replicative potential and tumorigenesis.
Telomere-binding proteins are specialized proteins that bind to the telomeres, which are the repetitive DNA sequences found at the ends of chromosomes. These proteins play a crucial role in protecting the structural integrity and stability of chromosomes by preventing the degradation of telomeres during cell division and preventing the chromosomes from being recognized as damaged or broken.
One of the most well-known telomere-binding proteins is called TRF2 (telomeric repeat-binding factor 2), which helps to maintain the structure of the telomere "T-loop" and prevent the activation of DNA repair mechanisms that can lead to chromosomal instability. Another important telomere-binding protein is called POT1 (protection of telomeres 1), which specifically binds to the single-stranded overhang of the telomere and helps to regulate the activity of telomerase, an enzyme that adds DNA repeats to the ends of chromosomes during cell division.
Mutations in telomere-binding proteins have been linked to a variety of human diseases, including premature aging disorders, cancer, and bone marrow failure syndromes. Therefore, understanding the function and regulation of these proteins is an important area of research in molecular biology and genetics.
Telomeric Repeat Binding Protein 1 (TRF1) is a protein that binds to the telomeres, which are the repetitive DNA sequences found at the ends of chromosomes. TRF1 plays a crucial role in the protection and regulation of telomere length. It helps to form a protective cap on the end of the chromosome, preventing it from being recognized as damaged or broken. Additionally, TRF1 is involved in the negative regulation of telomerase, an enzyme that adds repetitive DNA sequences to the ends of chromosomes, thereby controlling the length of the telomeres. Mutations in TRF1 have been associated with certain types of cancer and premature aging disorders.
Telomeric Repeat Binding Protein 2 (TRF2) is a protein that binds to the telomeres, which are the repetitive DNA sequences found at the ends of chromosomes. TRF2 plays a crucial role in protecting the telomeres from being recognized as damaged or broken DNA, which could otherwise lead to chromosomal instability and cellular senescence or apoptosis.
TRF2 is a member of the shelterin complex, a group of proteins that bind to and protect telomeres. TRF2 specifically binds to double-stranded TTAGGG repeats in the telomeric DNA through its N-terminal Myb-like DNA binding domain. By binding to the telomeres, TRF2 helps to prevent the activation of the DNA damage response (DDR) pathway and the subsequent activation of p53-dependent cell cycle checkpoints or apoptosis.
TRF2 has also been shown to play a role in regulating the length of telomeres. It can inhibit the activity of telomerase, an enzyme that adds repetitive DNA sequences to the ends of chromosomes, thereby limiting the extension of telomeres. TRF2 can also promote the formation of t-loops, a higher-order structure in which the 3' overhang of the telomere invades the double-stranded telomeric DNA, forming a displacement loop (D-loop). This helps to protect the telomere from being recognized as a double-strand break and degraded by nucleases.
Mutations in TRF2 have been associated with several human diseases, including premature aging disorders such as dyskeratosis congenita and Hoyeraal-Hreidarsson syndrome, as well as cancer.
Cellular aging, also known as cellular senescence, is a natural process that occurs as cells divide and grow older. Over time, cells accumulate damage to their DNA, proteins, and lipids due to various factors such as genetic mutations, oxidative stress, and epigenetic changes. This damage can impair the cell's ability to function properly and can lead to changes associated with aging, such as decreased tissue repair and regeneration, increased inflammation, and increased risk of age-related diseases.
Cellular aging is characterized by several features, including:
1. Shortened telomeres: Telomeres are the protective caps on the ends of chromosomes that shorten each time a cell divides. When telomeres become too short, the cell can no longer divide and becomes senescent or dies.
2. Epigenetic changes: Epigenetic modifications refer to chemical changes to DNA and histone proteins that affect gene expression without changing the underlying genetic code. As cells age, they accumulate epigenetic changes that can alter gene expression and contribute to cellular aging.
3. Oxidative stress: Reactive oxygen species (ROS) are byproducts of cellular metabolism that can damage DNA, proteins, and lipids. Accumulated ROS over time can lead to oxidative stress, which is associated with cellular aging.
4. Inflammation: Senescent cells produce pro-inflammatory cytokines, chemokines, and matrix metalloproteinases that contribute to a low-grade inflammation known as inflammaging. This chronic inflammation can lead to tissue damage and increase the risk of age-related diseases.
5. Genomic instability: DNA damage accumulates with age, leading to genomic instability and an increased risk of mutations and cancer.
Understanding cellular aging is crucial for developing interventions that can delay or prevent age-related diseases and improve healthy lifespan.
In situ hybridization, fluorescence (FISH) is a type of molecular cytogenetic technique used to detect and localize the presence or absence of specific DNA sequences on chromosomes through the use of fluorescent probes. This technique allows for the direct visualization of genetic material at a cellular level, making it possible to identify chromosomal abnormalities such as deletions, duplications, translocations, and other rearrangements.
The process involves denaturing the DNA in the sample to separate the double-stranded molecules into single strands, then adding fluorescently labeled probes that are complementary to the target DNA sequence. The probe hybridizes to the complementary sequence in the sample, and the location of the probe is detected by fluorescence microscopy.
FISH has a wide range of applications in both clinical and research settings, including prenatal diagnosis, cancer diagnosis and monitoring, and the study of gene expression and regulation. It is a powerful tool for identifying genetic abnormalities and understanding their role in human disease.
Dyskeratosis congenita is a rare genetic disorder that affects the bone marrow's ability to produce blood cells and can also affect other parts of the body, such as the skin, nails, and mucous membranes. It is characterized by the triad of abnormal skin pigmentation, nail dystrophy, and leukoplakia (white patches) in the mouth. People with dyskeratosis congenita are also at an increased risk of developing bone marrow failure, cancer, and pulmonary fibrosis. The disorder is caused by mutations in genes involved in the maintenance of telomeres, which are the protective caps on the ends of chromosomes that shorten as cells divide. These mutations can lead to premature shortening of telomeres and cellular aging, resulting in the symptoms of dyskeratosis congenita.
Tankyrases are a group of proteins that belong to the poly (ADP-ribose) polymerase (PARP) family, specifically PARP5a and PARP5b. They play roles in various cellular processes such as telomere maintenance, Wnt signaling pathway regulation, and protein trafficking. Tankyrases add poly(ADP-ribose) chains to their target proteins, leading to changes in their function, localization, or stability. Dysregulation of tankyrases has been implicated in several diseases, including cancer.
G-Quadruplexes are higher-order DNA or RNA structures that can form in guanine-rich sequences through the stacking of multiple G-tetrads, which are planar arrangements of four guanine bases held together by Hoogsteen hydrogen bonds. These structures are stabilized by monovalent cations, such as potassium, and can play a role in various cellular processes, including transcription, translation, and genome stability. They have been studied as potential targets for the development of new therapeutic strategies in cancer and other diseases.
I apologize for any confusion, but "Oxytricha" is not a medical term. It is actually a genus of ciliate protozoa, which are commonly found in various aquatic environments. These microorganisms are known for their complex cell structure and movement by means of cilia. If you have any questions regarding biology or another topic, I would be happy to try and help!
Chromosomal instability is a term used in genetics to describe a type of genetic alteration where there are abnormalities in the number or structure of chromosomes within cells. Chromosomes are thread-like structures that contain our genetic material, and they usually exist in pairs in the nucleus of a cell.
Chromosomal instability can arise due to various factors, including errors in DNA replication or repair, problems during cell division, or exposure to environmental mutagens. This instability can lead to an increased frequency of chromosomal abnormalities, such as deletions, duplications, translocations, or changes in the number of chromosomes.
Chromosomal instability is associated with several human diseases, including cancer. In cancer cells, chromosomal instability can contribute to tumor heterogeneity, drug resistance, and disease progression. It is also observed in certain genetic disorders, such as Down syndrome, where an extra copy of chromosome 21 is present, and in some rare inherited syndromes, such as Bloom syndrome and Fanconi anemia, which are characterized by a high risk of cancer and other health problems.
Chromosomes in fungi are thread-like structures that contain genetic material, composed of DNA and proteins, present in the nucleus of a cell. Unlike humans and other eukaryotes that have a diploid number of chromosomes in their somatic cells, fungal chromosome numbers can vary widely between and within species.
Fungal chromosomes are typically smaller and fewer in number compared to those found in plants and animals. The chromosomal organization in fungi is also different from other eukaryotes. In many fungi, the chromosomes are condensed throughout the cell cycle, whereas in other eukaryotes, chromosomes are only condensed during cell division.
Fungi can have linear or circular chromosomes, depending on the species. For example, the model organism Saccharomyces cerevisiae (budding yeast) has a set of 16 small circular chromosomes, while other fungi like Neurospora crassa (red bread mold) and Aspergillus nidulans (a filamentous fungus) have linear chromosomes.
Fungal chromosomes play an essential role in the growth, development, reproduction, and survival of fungi. They carry genetic information that determines various traits such as morphology, metabolism, pathogenicity, and resistance to environmental stresses. Advances in genomic technologies have facilitated the study of fungal chromosomes, leading to a better understanding of their structure, function, and evolution.
Leukocytes, also known as white blood cells (WBCs), are a crucial component of the human immune system. They are responsible for protecting the body against infections and foreign substances. Leukocytes are produced in the bone marrow and circulate throughout the body in the bloodstream and lymphatic system.
There are several types of leukocytes, including:
1. Neutrophils - These are the most abundant type of leukocyte and are primarily responsible for fighting bacterial infections. They contain enzymes that can destroy bacteria.
2. Lymphocytes - These are responsible for producing antibodies and destroying virus-infected cells, as well as cancer cells. There are two main types of lymphocytes: B-lymphocytes and T-lymphocytes.
3. Monocytes - These are the largest type of leukocyte and help to break down and remove dead or damaged tissues, as well as microorganisms.
4. Eosinophils - These play a role in fighting parasitic infections and are also involved in allergic reactions and inflammation.
5. Basophils - These release histamine and other chemicals that cause inflammation in response to allergens or irritants.
An abnormal increase or decrease in the number of leukocytes can indicate an underlying medical condition, such as an infection, inflammation, or a blood disorder.
DNA-binding proteins are a type of protein that have the ability to bind to DNA (deoxyribonucleic acid), the genetic material of organisms. These proteins play crucial roles in various biological processes, such as regulation of gene expression, DNA replication, repair and recombination.
The binding of DNA-binding proteins to specific DNA sequences is mediated by non-covalent interactions, including electrostatic, hydrogen bonding, and van der Waals forces. The specificity of binding is determined by the recognition of particular nucleotide sequences or structural features of the DNA molecule.
DNA-binding proteins can be classified into several categories based on their structure and function, such as transcription factors, histones, and restriction enzymes. Transcription factors are a major class of DNA-binding proteins that regulate gene expression by binding to specific DNA sequences in the promoter region of genes and recruiting other proteins to modulate transcription. Histones are DNA-binding proteins that package DNA into nucleosomes, the basic unit of chromatin structure. Restriction enzymes are DNA-binding proteins that recognize and cleave specific DNA sequences, and are widely used in molecular biology research and biotechnology applications.
Repetitive sequences in nucleic acid refer to repeated stretches of DNA or RNA nucleotide bases that are present in a genome. These sequences can vary in length and can be arranged in different patterns such as direct repeats, inverted repeats, or tandem repeats. In some cases, these repetitive sequences do not code for proteins and are often found in non-coding regions of the genome. They can play a role in genetic instability, regulation of gene expression, and evolutionary processes. However, certain types of repeat expansions have been associated with various neurodegenerative disorders and other human diseases.
Saccharomyces cerevisiae proteins are the proteins that are produced by the budding yeast, Saccharomyces cerevisiae. This organism is a single-celled eukaryote that has been widely used as a model organism in scientific research for many years due to its relatively simple genetic makeup and its similarity to higher eukaryotic cells.
The genome of Saccharomyces cerevisiae has been fully sequenced, and it is estimated to contain approximately 6,000 genes that encode proteins. These proteins play a wide variety of roles in the cell, including catalyzing metabolic reactions, regulating gene expression, maintaining the structure of the cell, and responding to environmental stimuli.
Many Saccharomyces cerevisiae proteins have human homologs and are involved in similar biological processes, making this organism a valuable tool for studying human disease. For example, many of the proteins involved in DNA replication, repair, and recombination in yeast have human counterparts that are associated with cancer and other diseases. By studying these proteins in yeast, researchers can gain insights into their function and regulation in humans, which may lead to new treatments for disease.
"Saccharomyces cerevisiae" is not typically considered a medical term, but it is a scientific name used in the field of microbiology. It refers to a species of yeast that is commonly used in various industrial processes, such as baking and brewing. It's also widely used in scientific research due to its genetic tractability and eukaryotic cellular organization.
However, it does have some relevance to medical fields like medicine and nutrition. For example, certain strains of S. cerevisiae are used as probiotics, which can provide health benefits when consumed. They may help support gut health, enhance the immune system, and even assist in the digestion of certain nutrients.
In summary, "Saccharomyces cerevisiae" is a species of yeast with various industrial and potential medical applications.
DNA damage refers to any alteration in the structure or composition of deoxyribonucleic acid (DNA), which is the genetic material present in cells. DNA damage can result from various internal and external factors, including environmental exposures such as ultraviolet radiation, tobacco smoke, and certain chemicals, as well as normal cellular processes such as replication and oxidative metabolism.
Examples of DNA damage include base modifications, base deletions or insertions, single-strand breaks, double-strand breaks, and crosslinks between the two strands of the DNA helix. These types of damage can lead to mutations, genomic instability, and chromosomal aberrations, which can contribute to the development of diseases such as cancer, neurodegenerative disorders, and aging-related conditions.
The body has several mechanisms for repairing DNA damage, including base excision repair, nucleotide excision repair, mismatch repair, and double-strand break repair. However, if the damage is too extensive or the repair mechanisms are impaired, the cell may undergo apoptosis (programmed cell death) to prevent the propagation of potentially harmful mutations.
Genomic instability is a term used in genetics and molecular biology to describe a state of increased susceptibility to genetic changes or mutations in the genome. It can be defined as a condition where the integrity and stability of the genome are compromised, leading to an increased rate of DNA alterations such as point mutations, insertions, deletions, and chromosomal rearrangements.
Genomic instability is a hallmark of cancer cells and can also be observed in various other diseases, including genetic disorders and aging. It can arise due to defects in the DNA repair mechanisms, telomere maintenance, epigenetic regulation, or chromosome segregation during cell division. These defects can result from inherited genetic mutations, acquired somatic mutations, exposure to environmental mutagens, or age-related degenerative changes.
Genomic instability is a significant factor in the development and progression of cancer as it promotes the accumulation of oncogenic mutations that contribute to tumor initiation, growth, and metastasis. Therefore, understanding the mechanisms underlying genomic instability is crucial for developing effective strategies for cancer prevention, diagnosis, and treatment.
A mutation is a permanent change in the DNA sequence of an organism's genome. Mutations can occur spontaneously or be caused by environmental factors such as exposure to radiation, chemicals, or viruses. They may have various effects on the organism, ranging from benign to harmful, depending on where they occur and whether they alter the function of essential proteins. In some cases, mutations can increase an individual's susceptibility to certain diseases or disorders, while in others, they may confer a survival advantage. Mutations are the driving force behind evolution, as they introduce new genetic variability into populations, which can then be acted upon by natural selection.
Chromosomes are thread-like structures that exist in the nucleus of cells, carrying genetic information in the form of genes. They are composed of DNA and proteins, and are typically present in pairs in the nucleus, with one set inherited from each parent. In humans, there are 23 pairs of chromosomes for a total of 46 chromosomes. Chromosomes come in different shapes and forms, including sex chromosomes (X and Y) that determine the biological sex of an individual. Changes or abnormalities in the number or structure of chromosomes can lead to genetic disorders and diseases.
Aging is a complex, progressive and inevitable process of bodily changes over time, characterized by the accumulation of cellular damage and degenerative changes that eventually lead to increased vulnerability to disease and death. It involves various biological, genetic, environmental, and lifestyle factors that contribute to the decline in physical and mental functions. The medical field studies aging through the discipline of gerontology, which aims to understand the underlying mechanisms of aging and develop interventions to promote healthy aging and extend the human healthspan.
RNA (Ribonucleic Acid) is a single-stranded, linear polymer of ribonucleotides. It is a nucleic acid present in the cells of all living organisms and some viruses. RNAs play crucial roles in various biological processes such as protein synthesis, gene regulation, and cellular signaling. There are several types of RNA including messenger RNA (mRNA), ribosomal RNA (rRNA), transfer RNA (tRNA), small nuclear RNA (snRNA), microRNA (miRNA), and long non-coding RNA (lncRNA). These RNAs differ in their structure, function, and location within the cell.
"Euplotes" is a genus of ciliate protozoans, which are single-celled organisms with hair-like structures called cilia. These cilia help the organism move and also aid in feeding. "Euplotes" species are typically found in freshwater or brackish environments and have a complex cell structure with two types of nuclei and specialized organelles for digestion. They are often used as model organisms in studies of cellular differentiation, evolution, and ecology.
Southern blotting is a type of membrane-based blotting technique that is used in molecular biology to detect and locate specific DNA sequences within a DNA sample. This technique is named after its inventor, Edward M. Southern.
In Southern blotting, the DNA sample is first digested with one or more restriction enzymes, which cut the DNA at specific recognition sites. The resulting DNA fragments are then separated based on their size by gel electrophoresis. After separation, the DNA fragments are denatured to convert them into single-stranded DNA and transferred onto a nitrocellulose or nylon membrane.
Once the DNA has been transferred to the membrane, it is hybridized with a labeled probe that is complementary to the sequence of interest. The probe can be labeled with radioactive isotopes, fluorescent dyes, or chemiluminescent compounds. After hybridization, the membrane is washed to remove any unbound probe and then exposed to X-ray film (in the case of radioactive probes) or scanned (in the case of non-radioactive probes) to detect the location of the labeled probe on the membrane.
The position of the labeled probe on the membrane corresponds to the location of the specific DNA sequence within the original DNA sample. Southern blotting is a powerful tool for identifying and characterizing specific DNA sequences, such as those associated with genetic diseases or gene regulation.
Deoxyribonucleic acid (DNA) is the genetic material present in the cells of organisms where it is responsible for the storage and transmission of hereditary information. DNA is a long molecule that consists of two strands coiled together to form a double helix. Each strand is made up of a series of four nucleotide bases - adenine (A), guanine (G), cytosine (C), and thymine (T) - that are linked together by phosphate and sugar groups. The sequence of these bases along the length of the molecule encodes genetic information, with A always pairing with T and C always pairing with G. This base-pairing allows for the replication and transcription of DNA, which are essential processes in the functioning and reproduction of all living organisms.
Silent Information Regulators (SIR) Proteins in Saccharomyces cerevisiae refer to a group of conserved proteins that play a crucial role in the regulation of gene silencing and heterochromatin formation in the genome of this yeast species. The SIR proteins are involved in the maintenance of silent chromatin domains, including telomeres, the mating-type locus (HML/HMR), and rDNA repeats, through the establishment of higher-order chromatin structures that restrict access to the transcriptional machinery.
The core SIR protein complex consists of four components: Sir1p, Sir2p, Sir3p, and Sir4p. Among these, Sir2p is a NAD+-dependent histone deacetylase that specifically targets lysine residues on histones H3 and H4, promoting the formation of compact, repressive chromatin structures. Sir3p and Sir4p are structural components that facilitate the association of the SIR complex with specific DNA sequences and the spreading of silencing across neighboring regions. Sir1p functions as a bridging protein, linking the core SIR complex to specific regulatory elements at telomeres and the mating-type locus.
In summary, Silent Information Regulator Proteins in Saccharomyces cerevisiae are essential for the establishment and maintenance of gene silencing and heterochromatin formation, thereby contributing to genome stability and proper regulation of gene expression in this model eukaryotic organism.
Fungal DNA refers to the genetic material present in fungi, which are a group of eukaryotic organisms that include microorganisms such as yeasts and molds, as well as larger organisms like mushrooms. The DNA of fungi, like that of all living organisms, is made up of nucleotides that are arranged in a double helix structure.
Fungal DNA contains the genetic information necessary for the growth, development, and reproduction of fungi. This includes the instructions for making proteins, which are essential for the structure and function of cells, as well as other important molecules such as enzymes and nucleic acids.
Studying fungal DNA can provide valuable insights into the biology and evolution of fungi, as well as their potential uses in medicine, agriculture, and industry. For example, researchers have used genetic engineering techniques to modify the DNA of fungi to produce drugs, biofuels, and other useful products. Additionally, understanding the genetic makeup of pathogenic fungi can help scientists develop new strategies for preventing and treating fungal infections.
A base sequence in the context of molecular biology refers to the specific order of nucleotides in a DNA or RNA molecule. In DNA, these nucleotides are adenine (A), guanine (G), cytosine (C), and thymine (T). In RNA, uracil (U) takes the place of thymine. The base sequence contains genetic information that is transcribed into RNA and ultimately translated into proteins. It is the exact order of these bases that determines the genetic code and thus the function of the DNA or RNA molecule.
Exodeoxyribonucleases are a type of enzyme that cleave (break) nucleotides from the ends of DNA molecules. They are further classified into 5' exodeoxyribonucleases and 3' exodeoxyribonucleases based on the end of the DNA molecule they act upon.
5' Exodeoxyribonucleases remove nucleotides from the 5' end (phosphate group) of a DNA strand, while 3' exodeoxyribonucleases remove nucleotides from the 3' end (hydroxyl group) of a DNA strand.
These enzymes play important roles in various biological processes such as DNA replication, repair, and degradation. They are also used in molecular biology research for various applications such as DNA sequencing, cloning, and genetic engineering.
Chromosomes are thread-like structures that contain genetic material, i.e., DNA and proteins, present in the nucleus of human cells. In humans, there are 23 pairs of chromosomes, for a total of 46 chromosomes, in each diploid cell. Twenty-two of these pairs are called autosomal chromosomes, which come in identical pairs and contain genes that determine various traits unrelated to sex.
The last pair is referred to as the sex chromosomes (X and Y), which determines a person's biological sex. Females have two X chromosomes (46, XX), while males possess one X and one Y chromosome (46, XY). Chromosomes vary in size, with the largest being chromosome 1 and the smallest being the Y chromosome.
Human chromosomes are typically visualized during mitosis or meiosis using staining techniques that highlight their banding patterns, allowing for identification of specific regions and genes. Chromosomal abnormalities can lead to various genetic disorders, including Down syndrome (trisomy 21), Turner syndrome (monosomy X), and Klinefelter syndrome (XXY).
Nuclear antigens are proteins or other molecules found in the nucleus of a cell that can stimulate an immune response and produce antibodies when they are recognized as foreign by the body's immune system. These antigens are normally located inside the cell and are not typically exposed to the immune system, but under certain circumstances, such as during cell death or damage, they may be released and become targets of the immune system.
Nuclear antigens can play a role in the development of some autoimmune diseases, such as systemic lupus erythematosus (SLE), where the body's immune system mistakenly attacks its own cells and tissues. In SLE, nuclear antigens such as double-stranded DNA and nucleoproteins are common targets of the abnormal immune response.
Testing for nuclear antigens is often used in the diagnosis and monitoring of autoimmune diseases. For example, a positive test for anti-double-stranded DNA antibodies is a specific indicator of SLE and can help confirm the diagnosis. However, it's important to note that not all people with SLE will have positive nuclear antigen tests, and other factors must also be considered in making a diagnosis.
Chromosome aberrations refer to structural and numerical changes in the chromosomes that can occur spontaneously or as a result of exposure to mutagenic agents. These changes can affect the genetic material encoded in the chromosomes, leading to various consequences such as developmental abnormalities, cancer, or infertility.
Structural aberrations include deletions, duplications, inversions, translocations, and rings, which result from breaks and rearrangements of chromosome segments. Numerical aberrations involve changes in the number of chromosomes, such as aneuploidy (extra or missing chromosomes) or polyploidy (multiples of a complete set of chromosomes).
Chromosome aberrations can be detected and analyzed using various cytogenetic techniques, including karyotyping, fluorescence in situ hybridization (FISH), and comparative genomic hybridization (CGH). These methods allow for the identification and characterization of chromosomal changes at the molecular level, providing valuable information for genetic counseling, diagnosis, and research.
Genetic recombination is the process by which genetic material is exchanged between two similar or identical molecules of DNA during meiosis, resulting in new combinations of genes on each chromosome. This exchange occurs during crossover, where segments of DNA are swapped between non-sister homologous chromatids, creating genetic diversity among the offspring. It is a crucial mechanism for generating genetic variability and facilitating evolutionary change within populations. Additionally, recombination also plays an essential role in DNA repair processes through mechanisms such as homologous recombinational repair (HRR) and non-homologous end joining (NHEJ).
Premature aging, also known as "accelerated aging" or "early aging," refers to the physiological process in which the body shows signs of aging at an earlier age than typically expected. This can include various symptoms such as wrinkles, graying hair, decreased energy and mobility, cognitive decline, and increased risk of chronic diseases.
The medical definition of premature aging is not well-established, as aging is a complex process influenced by a variety of genetic and environmental factors. However, certain conditions and syndromes are associated with premature aging, such as Hutchinson-Gilford progeria syndrome, Werner syndrome, and Down syndrome.
In general, the signs of premature aging may be caused by a combination of genetic predisposition, lifestyle factors (such as smoking, alcohol consumption, and poor diet), exposure to environmental toxins, and chronic stress. While some aspects of aging are inevitable, maintaining a healthy lifestyle and reducing exposure to harmful factors can help slow down the aging process and improve overall quality of life.
DNA replication is the biological process by which DNA makes an identical copy of itself during cell division. It is a fundamental mechanism that allows genetic information to be passed down from one generation of cells to the next. During DNA replication, each strand of the double helix serves as a template for the synthesis of a new complementary strand. This results in the creation of two identical DNA molecules. The enzymes responsible for DNA replication include helicase, which unwinds the double helix, and polymerase, which adds nucleotides to the growing strands.
Molecular sequence data refers to the specific arrangement of molecules, most commonly nucleotides in DNA or RNA, or amino acids in proteins, that make up a biological macromolecule. This data is generated through laboratory techniques such as sequencing, and provides information about the exact order of the constituent molecules. This data is crucial in various fields of biology, including genetics, evolution, and molecular biology, allowing for comparisons between different organisms, identification of genetic variations, and studies of gene function and regulation.
Cell cycle proteins are a group of regulatory proteins that control the progression of the cell cycle, which is the series of events that take place in a eukaryotic cell leading to its division and duplication. These proteins can be classified into several categories based on their functions during different stages of the cell cycle.
The major groups of cell cycle proteins include:
1. Cyclin-dependent kinases (CDKs): CDKs are serine/threonine protein kinases that regulate key transitions in the cell cycle. They require binding to a regulatory subunit called cyclin to become active. Different CDK-cyclin complexes are activated at different stages of the cell cycle.
2. Cyclins: Cyclins are a family of regulatory proteins that bind and activate CDKs. Their levels fluctuate throughout the cell cycle, with specific cyclins expressed during particular phases. For example, cyclin D is important for the G1 to S phase transition, while cyclin B is required for the G2 to M phase transition.
3. CDK inhibitors (CKIs): CKIs are regulatory proteins that bind to and inhibit CDKs, thereby preventing their activation. CKIs can be divided into two main families: the INK4 family and the Cip/Kip family. INK4 family members specifically inhibit CDK4 and CDK6, while Cip/Kip family members inhibit a broader range of CDKs.
4. Anaphase-promoting complex/cyclosome (APC/C): APC/C is an E3 ubiquitin ligase that targets specific proteins for degradation by the 26S proteasome. During the cell cycle, APC/C regulates the metaphase to anaphase transition and the exit from mitosis by targeting securin and cyclin B for degradation.
5. Other regulatory proteins: Several other proteins play crucial roles in regulating the cell cycle, such as p53, a transcription factor that responds to DNA damage and arrests the cell cycle, and the polo-like kinases (PLKs), which are involved in various aspects of mitosis.
Overall, cell cycle proteins work together to ensure the proper progression of the cell cycle, maintain genomic stability, and prevent uncontrolled cell growth, which can lead to cancer.
Rad52 is a DNA repair and recombination protein that plays a crucial role in the maintenance of genomic stability in cells. It is highly conserved across various species, including yeast, humans, and other mammals. The primary function of Rad52 is to facilitate the process of homologous recombination (HR), which is a critical DNA repair mechanism that helps to maintain the integrity of the genetic material in the event of double-strand breaks (DSBs) or other types of DNA damage.
Rad52 has several essential roles in HR:
1. Rad52 promotes the formation of ssDNA-Rad51 nucleoprotein filaments: Rad52 interacts with single-stranded DNA (ssDNA) generated during resection of DSBs, facilitating the recruitment and loading of the Rad51 recombinase onto the ssDNA. This Rad51-ssDNA nucleoprotein filament formation is a key step in HR, as it enables the search for homologous sequences and subsequent strand invasion.
2. Rad52 mediates DNA annealing: Rad52 can catalyze the annealing of complementary ssDNA molecules, promoting the reannealing of invaded strands during HR or facilitating the pairing of RPA-coated ssDNA with homologous duplex DNA.
3. Rad52 stimulates D-loop formation and extension: Rad52 can stimulate the extension of D-loops, which are three-stranded structures formed when a single-stranded DNA invades a double-stranded DNA molecule during HR. This process is essential for the subsequent steps of homology search and strand exchange.
4. Rad52 facilitates RPA displacement: Rad52 can displace replication protein A (RPA) from ssDNA, allowing Rad51 to bind and form nucleoprotein filaments. This is a critical step in HR, as RPA inhibits Rad51 binding to ssDNA.
5. Rad52 interacts with other DNA repair proteins: Rad52 interacts with various DNA repair proteins, including BRCA1, BRCA2, and the single-strand binding protein RPA, to coordinate HR and other DNA repair pathways.
In summary, Rad52 is a crucial player in homologous recombination (HR) and DNA damage response. It functions as a mediator of DNA annealing, D-loop formation, and RPA displacement, promoting efficient HR and maintaining genome stability.
DNA repair is the process by which cells identify and correct damage to the DNA molecules that encode their genome. DNA can be damaged by a variety of internal and external factors, such as radiation, chemicals, and metabolic byproducts. If left unrepaired, this damage can lead to mutations, which may in turn lead to cancer and other diseases.
There are several different mechanisms for repairing DNA damage, including:
1. Base excision repair (BER): This process repairs damage to a single base in the DNA molecule. An enzyme called a glycosylase removes the damaged base, leaving a gap that is then filled in by other enzymes.
2. Nucleotide excision repair (NER): This process repairs more severe damage, such as bulky adducts or crosslinks between the two strands of the DNA molecule. An enzyme cuts out a section of the damaged DNA, and the gap is then filled in by other enzymes.
3. Mismatch repair (MMR): This process repairs errors that occur during DNA replication, such as mismatched bases or small insertions or deletions. Specialized enzymes recognize the error and remove a section of the newly synthesized strand, which is then replaced by new nucleotides.
4. Double-strand break repair (DSBR): This process repairs breaks in both strands of the DNA molecule. There are two main pathways for DSBR: non-homologous end joining (NHEJ) and homologous recombination (HR). NHEJ directly rejoins the broken ends, while HR uses a template from a sister chromatid to repair the break.
Overall, DNA repair is a crucial process that helps maintain genome stability and prevent the development of diseases caused by genetic mutations.
RecQ helicases are a group of enzymes that belong to the RecQ family, which are named after the E. coli RecQ protein. These helicases play crucial roles in maintaining genomic stability by participating in various DNA metabolic processes such as DNA replication, repair, recombination, and transcription. They are highly conserved across different species, including bacteria, yeast, plants, and mammals.
In humans, there are five RecQ helicases: RECQL1, RECQL4, RECQL5, BLM (RecQ-like helicase), and WRN (Werner syndrome ATP-dependent helicase). Defects in these proteins have been linked to various genetic disorders. For instance, mutations in the BLM gene cause Bloom's syndrome, while mutations in the WRN gene lead to Werner syndrome, both of which are characterized by genomic instability and increased cancer predisposition.
RecQ helicases possess 3'-5' DNA helicase activity, unwinding double-stranded DNA into single strands, and can also perform other functions like branch migration, strand annealing, and removal of protein-DNA crosslinks. Their roles in DNA metabolism help prevent and resolve DNA damage, maintain proper chromosome segregation during cell division, and ensure the integrity of the genome.
Telomere
Telomere resolvase
Telomere (disambiguation)
Mega-telomere
Telomere-binding protein
Telomere (insect morphology)
Telomere-associated protein RIF1
Alternative Lengthening of Telomeres
Telomeres in the cell cycle
Neal S. Young
Reference genome
Dyskeratosis congenita
Elissa S. Epel
Telomerase
Dicentric chromosome
List of Dance in the Vampire Bund characters
Life Length
Blue jellyfish
Immortal DNA strand hypothesis
POT1
Systems biology
D-loop
Induced stem cells
Danazol
Breakage-fusion-bridge cycle
Non-coding DNA
Minichromosome
Antagonistic pleiotropy hypothesis
Long non-coding RNA
Flower mantis
Telomere - Wikipedia
Telomere-to-Telomere
Telomere and telomerase in stem cells | British Journal of Cancer
Genome Damage Drives Telomere-Induced Cellular Aging
Chronic stress of cancer causes accelerated telomere shortening | ScienceDaily
How Telomeres Work | HowStuffWorks
Telomere Shortening
Telomere chromatin establishment and its maintenance during mammalian development
Telomere Growth Predicts Reduced Chance of Death from Heart Disease - ScienceBlog.com
Inhibition of the Alternative Lengthening of Telomeres (ALT) Pathway
NHANES 1999-2000: Telomere Mean and Standard Deviation (Surplus) Data Documentation, Codebook, and Frequencies
telomeres Archives - SENS Research Foundation
telomeres | Blogs | CDC
Telomeres, Second Edition
C-Circles, an ALT Plan for Telomere Restoration | SGD
Magnesium Deficiency Shortens Telomeres in Human Cells
DDRNA-based cancer therapy targeted telomeres | DDRNA | Project | Fact sheet | H2020 | CORDIS | European Commission
Telomere lengths in plants are correlated with flowering time variation | bioRxiv
Telomere shortening in smokers with and without COPD | European Respiratory Society
The Telomere Effect: A Revolutionary Approach to Living Younger, Healthier, Longer by Elizabeth Blackburn | Goodreads
"Atrx deficiency induces telomere dysfunction, endocrine defects, and reduced life span" by L. Ashley...
Enzymedica® | Telomere Plus™ | Increase Telomerase Activity
Research reveals that large non-coding RNA in mammals play an important role in telomere maintenance
Examining the Cross-sectional Association Between Neighborhood Conditions, Discrimination, and Telomere Length in a...
Association between dementia risk, size of white blood cell telomeres | Nepalnews
Frontiers | Short Telomere Length Is Related to Limitations in Physical Function in Elderly European Adults
RCSB PDB - 1PH1: CRYSTAL STRUCTURE OF THE OXYTRICHA NOVA TELOMERE END-BINDING PROTEIN COMPLEXED WITH NONCOGNATE SSDNA...
Telomere trade-offs - The Evolution and Medicine Review
Telomere Length And Hospital Stay In Patients With Schizophrenia - Database Football
Increased telomere length2
- For example, telomere length is positively linked with nutritional status in human and animal studies ( see a review ), possibly through the effects of various nutrients on reducing inflammation and oxidative stress, and a study in 2013 found that lifestyle changes (a plant-based diet, moderate exercise, stress reduction and weekly group support) increased telomere length by about 10% in men with prostate cancer. (meresearch.org.uk)
- Results suggest that WF inhalation increased telomere length without affecting telomerase in whole brain. (cdc.gov)
Ends of chromosomes8
- Just as aglets prevent a shoelace from unraveling or fraying, telomeres are structures on the ends of chromosomes that protect the chromosome from deteriorating, breaking apart or joining with other chromosomes, which can lead to mutations. (sciencedaily.com)
- Short telomeres - the protective caps on the ends of chromosomes - have been previously linked to increased risk of death from heart disease. (scienceblog.com)
- Telomeres specialized structures found at the ends of chromosomes are essential for maintaining the integrity of chromosomes and their faithful duplication during cell division. (cshlpress.com)
- Telomeres are the tips at the ends of chromosomes that protect our DNA. (enzymedica.com)
- The DNA still seemed to look normal, until the researchers focused on the caps that protect the ends of chromosomes, called telomeres. (labroots.com)
- Telomeres are tandem nucleotide repeats that protect the ends of chromosomes from erosion during cell division. (datadryad.org)
- Telomeres are repetitive DNA sequences located at the ends of chromosomes , playing a vital role in maintaining chromosomal integrity and stability. (bvsalud.org)
- all genes associated with this syndrome (ie, DKC1 , TERT, TERC, NOP10 ) encode proteins in the telomerase complex responsible for maintaining telomeres at the ends of chromosomes regarding shortening length, protection, and replication. (medscape.com)
Longer telomeres7
- A 2007 dermatology study conducted at King's College London indicates that people with more moles often have longer telomeres. (howstuffworks.com)
- In reality, some people are born with longer telomeres than others. (howstuffworks.com)
- The longer the telomere, the more cell divisions can take place over a lifetime - and more moles were linked to longer telomeres . (stackexchange.com)
- There are a several different claims in the article: moles are correlated with: skin cells that divide more often, better bone density, and longer telomeres. (stackexchange.com)
- Researchers have correlated higher vitamin D levels with longer telomeres in humans. (mindbodygreen.com)
- It is not understood why there are variations of telomere length but if you had a choice, you would want to be born with longer telomeres. (bellenews.com)
- Heterogeneity among studies and their publication bias were further assessed by the χ(2)-based Q statistic test and Egger's test, respectively.The results showed that shorter telomeres were significantly associated with cancer risk (OR = 1.35, 95% CI = 1.14-1.60), compared with longer telomeres. (duke.edu)
Relative telomere length5
- From each sample, relative telomere length was measured using real-time PCR. (meresearch.org.uk)
- Telomere length was determined as relative telomere length (RTL) by comparison with an internal cell line control (1301 cells) 4 . (ersjournals.com)
- This hypothesis awaits confirmation in a prospective study measuring changes in relative telomere length over time. (huffpost.com)
- A series of epidemiological studies have examined the association between shortened telomeres and risk of cancers, but the findings remain conflicting.A dataset composed of 11,255 cases and 13,101 controls from 21 publications was included in a meta-analysis to evaluate the association between overall cancer risk or cancer-specific risk and the relative telomere length. (duke.edu)
- Furthermore, the results also indicated that the association between the relative telomere length and overall cancer risk was statistically significant in studies of Caucasian subjects, Asian subjects, retrospective designs, hospital-based controls and smaller sample sizes. (duke.edu)
Shorter23
- Each time a cell divides, however, the telomeres become shorter. (howstuffworks.com)
- Even now, your telomeres may grow shorter with each cell division, burning down ever closer to the point of guttering out. (howstuffworks.com)
- We do know, however, that telomeres are shorter than usual in patients with diseases like cancer, osteoporosis and the cardiovascular disorders, even when the effect of ageing is taken into account. (meresearch.org.uk)
- Recently, evidence has come to light that telomeres are also shorter than normal in people with ME/CFS. (meresearch.org.uk)
- Based on adjusted group means, telomere length was shorter by 593 and 508 base pairs in the CFS and 'fatigue' groups, respectively, compared with the controls. (meresearch.org.uk)
- Drawing from this scientific body of knowledge, they share lists of foods and suggest amounts and types of exercise that are healthy for our telomeres, mind tricks you can use to protect yourself from stress, and information about how to protect your children against developing shorter telomeres, from pregnancy through adolescence. (goodreads.com)
- We examined whether adverse neighborhood conditions, alone or in conjunction with discrimination, associate with shorter leukocyte telomere length among a predominantly AA cohort. (rand.org)
- Less walkable neighborhoods were associated with shorter telomeres. (rand.org)
- Higher air pollution (PM 2.5 ) was associated with shorter telomeres among those experiencing greater discrimination. (rand.org)
- Shorter telomeres on the ends of white blood cell chromosomes were discovered to be associated with an increased risk of dementia. (nepalnews.com)
- However, whether patients with schizophrenia also have shorter telomeres remains inconclusive, because the results of previous studies investigating an association between leukocyte telomere length and schizophrenia have been largely inconsistent. (databasefootball.com)
- Telomeres become shorter with age, oxidation and chemical insults. (huffpost.com)
- Most Tetrahymena are immortal, Blackburn explained, and they have lots of telemorase, but the mutant had shorter and shorter telomeres over time, so its cells started to die. (lindau-nobel.org)
- As we get older, our telomeres get shorter and can directly impact our body health and how we age. (antiaging-systems.com)
- As we age, our telomeres naturally get shorter due to cell replication and the natural wear and tear of everyday life. (antiaging-systems.com)
- Our telomeres get shorter with every cell division until they eventually become too small to protect the chromosomes. (antiaging-systems.com)
- as our telomeres get shorter, we experience the effects of aging[ 1 ]. (antiaging-systems.com)
- Telomere length can also impact overall health, as shorter telomeres can increase our risk for age-related diseases like cancer and heart disease [ 2 ] and even shorten our lifespan. (antiaging-systems.com)
- As we get older, our telomeres naturally get shorter, increasing the risk of age-related diseases and impacting overall wellness. (antiaging-systems.com)
- Shorter telomeres were found in older women, Latinas, particularly those who were Mexican-born, and those with higher education. (confex.com)
- There was a dose-response relationship between higher educational attainment and shorter telomeres (p-trend = 0.006). (confex.com)
- Women who chose an affirmative or neutral response to the statement, I would move from this neighborhood if I could , had shorter telomeres (p=0.02) than women who disagreed with this statement. (confex.com)
- Our results also demonstrated significantly shorter telomere lengths in NSCLC patients compared to controls (p = 0.0004). (bvsalud.org)
Alternative Lengtheni2
- Cancer cells overcome this replicative senescence in one of two ways: through activating telomerase, an enzyme that extends telomeres, or using another process called the alternative lengthening of telomeres (ALT) pathway. (massgeneral.org)
- However, it turns out that cells lacking functional telomerase have a backup plan to restore telomere length by "alternative lengthening of telomeres" (ALT). (yeastgenome.org)
Shorten8
- Researchers know that telomeres shorten and deteriorate with aging, but they are learning that stress also affects telomere length. (sciencedaily.com)
- Since telomeres shorten with each cell division, it pays to start out ahead. (howstuffworks.com)
- Telomeres naturally shorten with age. (cdc.gov)
- Telomeres are complex DNA-protein structures located at the end of eukaryotic chromosomes, which shorten with age in all replicating somatic cells 3 , 4 . (ersjournals.com)
- In somatic cells such as leukocytes, telomeres gradually shorten with each cell division because of low telomerase activity. (databasefootball.com)
- In the next stage of their research, the Glasgow scientists will look at what causes telomeres to shorten - including inherited and environmental factors - to make it possible to predict life expectancy more accurately. (bellenews.com)
- Telomeres have been implicated in senescence and mortality because they tend to shorten with stress, growth and age. (datadryad.org)
- Every time a cell divides, the telomeres shorten a bit. (msdmanuals.com)
Leukocyte8
- The researchers measured patients' leukocyte telomere length at the start of the study and again five years later, and then examined whether the difference between these measurements predicted which patients were most likely to die over the next four years. (scienceblog.com)
- Socioeconomic status, health behavior, and leukocyte telomere length in the National Health and Nutrition Examination Survey, 1999-2000. (cdc.gov)
- Here, we investigate the association of leukocyte telomere length with schizophrenia with the quantitative polymerase chain reaction method in independent Japanese cohorts consisting of 1,241 patients with schizophrenia and 1,042 controls, which we believe is the largest ever as an independent sample set of telomere studies in schizophrenia. (databasefootball.com)
- Correlations between leukocyte telomere length and age in patients with schizophrenia and healthy controls. (databasefootball.com)
- The red and blue dashed lines show non-linear relationships between leukocyte telomere length and age in patients with schizophrenia and healthy controls, respectively. (databasefootball.com)
- Black lines represent the mean leukocyte telomere length in each group. (databasefootball.com)
- The researchers also measured the length of their leukocyte telomeres. (huffpost.com)
- Is leukocyte telomere length (LTL) associated with alterations in cardiovascular structure and function? (cdc.gov)
Long telomeres4
- On one hand, Noah might have been born with rather long telomeres, while Batty drew the proverbial shortest straw. (howstuffworks.com)
- While short telomeres do lead to health problems, long telomeres lead to health problems of their own. (cdc.gov)
- Far from extending life, long telomeres appear to cause cancer and a blood disorder known as CHIP, a condition that increases the risk of blood cancers and heart disease. (cdc.gov)
- Mice have long telomeres and senesce just fine. (cdc.gov)
Lengthen telomeres4
- At present, scientists are exploring interventions to lengthen telomeres. (meresearch.org.uk)
- By activating the enzyme telomerase to lengthen telomeres, we can support cellular health and age gracefully. (enzymedica.com)
- Studies have shown taking telomerase activation supplements can help lengthen telomeres, which can help slow down the aging process and reduce the risk of age-related diseases [ 3 ]. (antiaging-systems.com)
- Less understood are a newly recognized group of cancer-prone syndromes that are associated with mutations that lengthen telomeres. (cdc.gov)
Extend telomeres2
- Furthermore, it was predicted that a specialized DNA polymerase (originally called a tandem-DNA-polymerase) could extend telomeres in immortal tissues such as germ line, cancer cells and stem cells. (wikipedia.org)
- In contrast to the RNA-directed DNA synthesis by telomerase, ALT relies on recombination and replication of telomere DNA to extend telomeres. (massgeneral.org)
Rate of telomere3
- In the new study, Whooley and colleagues asked whether the rate of telomere change - rather than absolute telomere length - might be a better predictor of health span in heart disease patients. (scienceblog.com)
- To test this hypothesis, the rate of telomere shortening was compared with age in circulating lymphocytes harvested from smokers with and without COPD. (ersjournals.com)
- This makes telomeres a telling marker for how a body will age: After studying telomere length across multiple species, a research team out of Spain found that the rate of telomere decay over time could accurately predict the life span of that species. (mindbodygreen.com)
Somatic8
- In somatic cells, the activity of telomerase, a reverse transcriptase that can elongate telomeric repeats, is usually diminished after birth so that the telomere length is gradually shortened with cell divisions, and triggers cellular senescence. (nature.com)
- Thus, even in stem cells, except for embryonal stem cells and cancer stem cells, telomere shortening occurs during replicative ageing, possibly at a slower rate than that in normal somatic cells. (nature.com)
- In most human somatic cells except for stem cells and lymphocytes, telomerase activity is diminished after birth so that telomere length shortens with each cell division. (nature.com)
- Systematic analysis of telomere length and somatic alterations in 31 cancer types. (sens.org)
- Telomere length shortens with age in all replicating somatic cells. (ersjournals.com)
- The steady shortening of telomeres with each replication in somatic cells is linked to cellular aging, genetic instability, and tumor formation. (news-medical.net)
- This epigenetic protection of fly telomeres has been essentially studied in somatic cells where capping proteins such as HOAP or HP1 are essential in preventing chromosome end-to-end fusions. (ens-lyon.fr)
- While HipHop is involved in telomere capping in somatic cells, K81 hasspecialized in the protection of telomeres in post-meiotic male germ cells. (ens-lyon.fr)
Lengths2
- Overall, telomere lengths were found to be significantly longer in the healthy controls than in the Fukuda 1994 CFS patients or in the group of 'fatigue' patients, and these differences remained significant after statistical adjustment for differences between groups. (meresearch.org.uk)
- The study - which used zebra finches, one of Australia's most common bird species - is the first to measure telomere lengths at regular intervals through an entire life. (bellenews.com)
Dysfunctional telomeres3
- It cannot help in determining the cellular threshold for the number of dysfunctional telomeres that causes cells to stop dividing due to persistent DNA damage response signaling. (genengnews.com)
- Telomerase is the enzyme that repairs shortened or dysfunctional telomeres, and various telomerase-activating drugs are under development, with some success as recent work on blood disorders has shown ( read more ). (meresearch.org.uk)
- In humans, Mendelian defects in several of these factors can result in abnormally short or dysfunctional telomeres, causing a group of rare heterogeneous premature-ageing diseases, termed telomeropathies, short-telomere syndromes or telomere biology disorders (TBDs). (cdc.gov)
Leucocyte8
- They went on to evaluate potential correlations between leucocyte telomere length and dementia risk, including Alzheimer's disease and vascular dementia, as well as total and regional brain volumes, using data from the UK Biobank. (nepalnews.com)
- The length of leucocyte telomeres was determined by analysing blood samples collected at the time of enrollment. (nepalnews.com)
- The data analysis found a substantial link between leucocyte telomere length and the risk of dementia. (nepalnews.com)
- Participants with the shortest leucocyte telomeres were 14 per cent more likely to be diagnosed with dementia and 28 per cent more likely to be diagnosed with Alzheimer's disease after controlling for gender and age. (nepalnews.com)
- Nevertheless, the researchers conclude, "We found that leucocyte telomere length acts as an aging biomarker associated with the risk of dementia. (nepalnews.com)
- Furthermore, we also observed linear associations of leucocyte telomere length with total and regional brain structure. (nepalnews.com)
- The present study aims to explore the potential influence of leucocyte telomere length (LTL) on both a single indicator and a composite construct of physical functioning in a large European population of elderly men and women across diverse geographical locations. (frontiersin.org)
- Our GWAS confirmed 11 genetic loci previously associated with leucocyte telomere length (LTL) and two novel loci in SCNN1D and PITPNM1. (cdc.gov)
Linked with shortened telomeres1
- Recently, another study in the journal PLoS ONE showed that stress from phobic anxieties -- like being afraid of spiders, social situations, or the like -- is linked with shortened telomeres. (huffpost.com)
Correlation between telomere length2
- As expected, there was a correlation between telomere length and age in the total sample. (meresearch.org.uk)
- There was no correlation between telomere length and growth in either sex, suggesting that our results are a consequence of divergent selection on life histories of males and females. (datadryad.org)
Proteins7
- Telomere, a complex of guanine-rich repeat sequences and associated proteins, caps and protects every eukaryotic chromosome end against chromosomal fusion, recombination, and terminal DNA degradation ( Blackburn, 2001 ). (nature.com)
- To prevent degradation by exonucleases or processing as damaged DNA, the telomere 3′ single-strand overhang folds back into the D-loop of duplex telomeric DNA to form a protective 'T-loop', which is reinforced with TRF2 and other telomeric DNA-binding proteins named Shelterin ( de Lange, 2005 ). (nature.com)
- In a study published on-line on August 27 in Molecular Cell, the Wistar scientists, led by Lieberman, describe how they discovered the telomere proteins that interact with TERRA and the processes by which they do so. (news-medical.net)
- Telomeres consist of tandem repeats of TTAGGG and DNA binding proteins that form a cap to protect chromosomal termini from the loss of genetic material. (databasefootball.com)
- We thus propose that the maintenance of capping proteins at Drosophila sperm telomeres is crucial for the transmission of telomere identity to the diploid zygote. (ens-lyon.fr)
- We therefore focus on elucidating the roles of the telomere binding proteins in this process. (lu.se)
- A TELOMERE cap complex consisting of telomere-specific proteins in association with telomeric DNA such as telomeric dsDNA-sDNA junction. (bvsalud.org)
Chromosome8
- In 1975-1977, Elizabeth Blackburn, working as a postdoctoral fellow at Yale University with Joseph G. Gall, discovered the unusual nature of telomeres, with their simple repeated DNA sequences composing chromosome ends. (wikipedia.org)
- Telomerase can add telomeric repeats onto the chromosome ends, and prevents the replication-dependent loss of telomere and cellular senescence in highly proliferative cells of the germline and in the majority of cancers ( Blasco, 2005 ). (nature.com)
- Telomeres are a protective nucleoprotein structure at each chromosome end. (cdc.gov)
- Previously she was a biological researcher at the University of California, San Francisco, who studied the telomere, a structure at the end of chromosomes that protects the chromosome. (goodreads.com)
- This is because telomeres eventually 'run out' after a certain number of cell divisions, resulting in the loss of vital genetic information from the cell's chromosome with future divisions. (news-medical.net)
- At the end of each chromosome is a telomere, which acts as a protective cap. (antiaging-systems.com)
- A critical function of telomeres is to prevent the ligation of chromosome ends by DNA repair enzymes. (ens-lyon.fr)
- Telomeres play a key role in the maintenance of chromosome integrity and stability, and telomere shortening is involved in initiation and progression of malignancies. (duke.edu)
Important role in telomere1
- Moreover, we observed that components of the shelterin complex, Trf1 and Trf2, play an important role in telomere end protection, and their regulation may be responsible for the increase in telomere length. (cdc.gov)
Oxidative stress2
- Given that ME Research UK-funded work has found high levels of oxidative stress and associated arterial stiffness to be a feature in ME/CFS patients ( read more ), it may be that telomere shortening is intimately linked with ongoing inflammatory processes. (meresearch.org.uk)
- [ 18 ] Loss of DKC1 has been reported to induce oxidative stress independent of telomere shortening. (medscape.com)
Senescence11
- A critical length of telomere repeats is required to ensure proper telomere function and avoid the activation of DNA damage pathways that result in replicative senescence or cell death. (nature.com)
- A team of cancer scientists led by Francis Rodier, PhD, a professor at the University of Montréal, has updated the current model of cellular senescence by providing evidence that the aging-related arrest of DNA replication is caused by irreversible damage to the genome rather than simply by an erosion of telomeres. (genengnews.com)
- The study is reported in an article in the journal Nucleic Acids Research, titled, " Homologous recombination-mediated irreversible genome damage underlies telomere-induced senescence . (genengnews.com)
- The new multistep model for entry into telomere-mediated senescence presented in the current study reconciles observations of senescence-associated genomic instability with observations that telomere breaks are largely irreparable and that cells can tolerate telomere-induced DNA damage foci (TIF) during an unstable "pre-senescent" state. (genengnews.com)
- This updated model offers a new basis for stress- or age-associated genome damage and indicates, cells that escape telomere-mediated senescence harbor irreparable genome damage. (genengnews.com)
- The telomere plays a key role in the continuous duplication of proliferating cells, and its erosion eventually leads to a cell's senescence. (massgeneral.org)
- Length-independent telomere damage drives post-mitotic cardiomyocyte senescence. (sens.org)
- Telomeres and Cell Senescence - Size Matters Not. (sens.org)
- Telomere length is, therefore, a marker of cell ageing and senescence 5 . (ersjournals.com)
- Progerin induced senescence, lamin B1 loss, DNA damage, and telomere shortening are prevented by TERT in primary and HGPS fibroblasts, control experiments. (elifesciences.org)
- Numerous factors localize at telomeres to regulate their length, structure and function, to avert replicative senescence or genome instability and cell death. (cdc.gov)
Affects telomere length1
- However, it is still unclear whether lead exposure affects telomere length. (bmj.com)
Maintain telomere length2
- TA65® capsules - plant based compound to help maintain telomere length, or rebuild where necessary. (antiaging-systems.com)
- Although most cancer cells activate telomerase to maintain telomere length, about 10% of tumors use an alternative telomere lengthening mechanism, the so-called ALT mechanism. (lu.se)
Short telomere syndromes2
- Telomere shortening is a well-characterized cellular aging mechanism, and short telomere syndromes cause age-related disease. (evmedreview.com)
- Short telomere syndromes are the most prevalent premature aging disorders, with prominent phenotypes affecting the lung and hematopoietic system. (cdc.gov)
Diseases10
- As shortened telomeres are also found in a range of other chronic diseases, including cancer ( read more ), diabetes, Alzheimer's disease and Parkinson's disease, the phenomenon is most likely associated with chronic illness per se , rather than with ME/CFS in particular. (meresearch.org.uk)
- Telomeres and telomerase as therapeutic targets to prevent and treat age-related diseases. (meresearch.org.uk)
- When telomeres are not properly controlled, the resulting chromosomal alterations can induce genomic instability and ultimately the development of human diseases, such as cancer. (nih.gov)
- Researchers, journalists, and inquiring minds want to know more about telomeres, which seem to hold clues to human aging and age-related diseases. (cdc.gov)
- Chapters in this volume cover telomere structure and function in a range of organisms, focusing on how they are maintained, their roles in cell division and gene expression, and how deficiencies in these structures contribute to cancers and other diseases and even aging. (cshlpress.com)
- Since this RNA also facilitates the formation of DNA at telomeres-a process that can protect aging cells and destabilize tumor cells-manipulating its expression may be useful in treating cancer and other diseases. (news-medical.net)
- Many of the diseases of ageing, including cancers, are associated with the shortening of telomeres,' Blackburn said. (lindau-nobel.org)
- Even the risk factors for these diseases increases with short telomeres. (lindau-nobel.org)
- Dr. Park's book offers a clear and friendly account of the role of telomeres in causing age-related diseases and the enormous potential of telomerase to prevent and cure age-related diseases by reversing human aging at the genetic level. (rechargebiomedical.com)
- Objectives Critically shortening of telomere length caused by various factors including environmental pollutants results in genome instability and age-associated diseases. (bmj.com)
Structures6
- Telomeres are specialized structures that evolved to protect the end of linear chromosomes from the action of the cell DNA damage machinery. (nih.gov)
- Telomeres Increasingly Develop Aberrant Structures in Aging Humans. (sens.org)
- Telomeres are complex DNA-protein structures located at the end of eukaryotic chromosomes. (ersjournals.com)
- To explore the mechanisms of sequence-specific ssDNA recognition, we determined the crystal structures of 10 different non-cognate ssDNAs complexed with the Oxytricha nova telomere end-binding protein (OnTEBP) and evaluated their corresponding binding affinities (PDB ID codes 1PH1-1PH9 and 1PHJ). (rcsb.org)
- Consider telomeres little helmets for your DNA: These protein structures cap off both sides of our chromosomes to protect them from damage and decay over time. (mindbodygreen.com)
- The telomeres are the DNA-protein structures at the ends of eukaryotic chromosomes, which serve to protect and stabilize the genome. (lu.se)
Telomerase activity4
- The regulation of telomere length and telomerase activity is a complex and dynamic process that is tightly linked to cell cycle regulation in human stem cells. (nature.com)
- Thus, telomerase activity and telomere maintenance are associated with the immortality of cancer cells, germ-line cells, and embryonic stem (ES) cells. (nature.com)
- Basically, given the difference of telomere and telomerase activity in human and mouse cells, the telomere and telomerase status in stem cell populations is different between humans and mice ( Harrington, 2004 ). (nature.com)
- We are using the yeast model organism Saccharomyces castellii, which has telomere traits and telomerase activity that are highly similar to human cells. (lu.se)
Genetic14
- Telomeres are a widespread genetic feature most commonly found in eukaryotes. (wikipedia.org)
- Recently, the importance of telomere maintenance in human stem cells has been highlighted by studies on dyskeratosis congenital, which is a genetic disorder in the human telomerase component. (nature.com)
- In fact, the cell division caused by telomere dysfunction is so unstable that it ends up creating genetic defects. (genengnews.com)
- Telomeres (in white) cap the ends of human chromosomes, protecting the genetic information from damage. (howstuffworks.com)
- While many factors contribute to aging and illness, Dr. Elizabeth Blackburn discovered a biological indicator called telomerase, the enzyme that replenishes telomeres, which protect our genetic heritage. (goodreads.com)
- A team of researchers from The Wistar Institute have shown that a large non-coding RNA in mammals and yeast plays a central role in helping maintain telomeres, the tips of chromosomes that contain important genetic information and help regulate cell division. (news-medical.net)
- Genetic from Mendel to the Era of According to his theory of telomeres are represented by tandem repeats, which create a buffer that determines the number of divisions that a certain cell clone can undergo. (slideshare.net)
- Genetic from Mendel to the Era of Elizabeth Blackburn and her graduate student Carol Greider then went looking for the mechanism that maintains telomeres, and on Christmas day, 1984, discovered the first evidence for the enzyme telomerase. (slideshare.net)
- Associations between telomere attrition, genetic variants in telomere maintenance genes, and non-small cell lung cancer risk in the Jammu and Kashmir population of North India. (bvsalud.org)
- Genetic variations within telomere maintenance genes may influence the risk of developing NSCLC. (bvsalud.org)
- The present study aimed to evaluate the genetic associations of select variants within telomere maintenance genes in a population from Jammu and Kashmir, North India , and to investigate the relationship between telomere length and NSCLC risk . (bvsalud.org)
- We employed the cost -effective and high-throughput MassARRAY MALDI -TOF platform to assess the genetic associations of select variants within telomere maintenance genes in a population from Jammu and Kashmir, North India . (bvsalud.org)
- This study highlights the crucial interplay between genetic variation in telomere maintenance genes , telomere attrition, and NSCLC risk in the Jammu and Kashmir population of North India . (bvsalud.org)
- Telomeres are used to move the cell's genetic material in preparation for cell division. (msdmanuals.com)
Researchers3
- Controlling for these and other factors, the researchers found that those whose telomeres shortened over five years were 32 percent more likely to die during the next four years than those whose telomeres stayed the same, and those who experienced telomere lengthening were 56 percent less likely to die. (scienceblog.com)
- The researchers also point out several limitations: Because telomere length was only assessed once, it was unable to determine whether changes over time increased dementia risk. (nepalnews.com)
- The longer a person's telomeres, researchers found, the greater the risk of cancer and other disorders, challenging a popular hypothesis about the chromosomal roots of vitality. (cdc.gov)
Role of telomere2
- An article in this week's NEJM provides some of the best evidence yet for the role of telomere length in the trade-off between slowing aging and the risk of cancer. (evmedreview.com)
- Discuss the potential role of telomere biology in maternal and child health outcomes. (confex.com)
Function of telomeres1
- The mystery of the function of telomeres had been solved. (lindau-nobel.org)
Regulation of telomere1
- However, little is known about regulation of telomere biology during pregnancy. (confex.com)
Cellular12
- Telomeres, guanine-rich tandem DNA repeats of the chromosomal end, provide chromosomal stability, and cellular replication causes their loss. (nature.com)
- Our current understanding of cellular aging rests upon the uncapping of the repetitive, non-protein-coding extremities of our linear chromosomes called telomeres. (genengnews.com)
- Genetically, we were able to reproduce the phenomenon of cellular aging in the laboratory and ensured that all the telomeres of a population of cells became dysfunctional," said PhD student Marc-Alexandre Olivier, co-first author of the study with former colleague Sabrina Ghadaouia, PhD, currently pursuing postdoctoral studies in England. (genengnews.com)
- It remains unknown whether telomere shortening is simply a sign of 'cellular age' or whether it contributes to the ageing process more directly. (meresearch.org.uk)
- On top of that, the ingredients in Telomere Plus-including astragalus root, broccoli seed, rhodiola extract and vitamin D3-give us a whole range of additional benefits, from immune support to enhancing the body's stress tolerance, cellular protection and boosted enzyme activity. (enzymedica.com)
- Sequence-specific protein recognition of single-stranded nucleic acids is critical for many fundamental cellular processes, such as DNA replication, DNA repair, transcription, translation, recombination, apoptosis and telomere maintenance. (rcsb.org)
- The risk of these phenotypes was mediated by extended cellular longevity and by the capacity to maintain telomeres over time. (evmedreview.com)
- The shortening of telomeres to a critical length leads to genomic instability and cellular apoptosis. (databasefootball.com)
- It seems that vitamin D , a hormone that's essential for a number of processes in the body, works by increasing the activity of telomerase 4 , the building blocks of telomeres that protect cellular DNA from aging. (mindbodygreen.com)
- Telomere length is a biomarker of cellular aging and predictor of chronic disease. (confex.com)
- Alterations in telomere length are indicative of cellular aging and, possibly, neurodegeneration. (cdc.gov)
- Normal cellular ageing involves the shortening of telomeres in each cell division. (lu.se)
Genome4
- He had just observed that the ends of the irradiated chromosomes, different from the other genome, did not present alterations such as deletions or inversions, thanks to the presence of a protective cap that he called "terminal gene" and afterwards "telomere", from the greek terms "telos" (end) and "meros" (part) (Müller HJ. (wikipedia.org)
- The model also suggests that strategies targeted at repairing telomeres in pre-senescent cells could eradicate telomere-induced DNA damage foci and low-level DNA damage response while preventing further irreversible damage to the genome. (genengnews.com)
- TERRA is a major component in helping protect the genome at a very sensitive place, the telomeres,' said senior author Paul M. Lieberman, Ph.D., a professor in Wistar's Gene Expression and Regulation Program. (news-medical.net)
- Without telomeres, our genome would be vulnerable to damage and dysfunction. (antiaging-systems.com)
Attrition2
- Telomere attrition was also accelerated in cell populations from magnesium-deficient cultures. (wellnessresources.com)
- Title : Association of chronic fatigue syndrome with premature telomere attrition Personal Author(s) : Rajeevan, Mangalathu S.;Murray, Janna;Oakley, Lisa;Lin, Jin-Mann S.;Unger, Elizabeth R. (cdc.gov)
Whose telomeres5
- Now, research by scientists at UC San Francisco and the Veterans Affairs Medical Center in San Francisco has found that change in telomere length over time is also important: heart disease patients whose telomeres shrank over time had a worse short-term prognosis than those whose telomeres stayed stable, and those whose average telomere length grew over the course of the study had a higher chance of survival. (scienceblog.com)
- Overall, one quarter of patients had died by the end of the study, but only 12 percent of patients whose telomeres had lengthened during the five-year observation period were among this group. (scienceblog.com)
- In contrast, 39 percent of patients whose telomeres had shrunk in the five-year observation period died within the next four years. (scienceblog.com)
- However, those whose telomeres shortened over the course of the study also showed higher abdominal fat, worse kidney function, and lower overall fitness. (scienceblog.com)
- The results hold huge implications for humans, whose telomeres work in the same way. (bellenews.com)
Telomeric3
- The length of telomeric repeats is dynamically regulated and can be affected by changes in the telomere chromatin structure. (nih.gov)
- Dr. Zou and his team postulated that such cancer cell lines were those without active telomerase, relying instead on the ALT pathway, which lengthens telomeres through recombination with telomeric DNA sequences from the same or other chromosomes. (massgeneral.org)
- TERRA associates with telomeric factors, but its precise function and mechanism of localization at telomeres had been largely unknown. (news-medical.net)
Protect telomeres2
- Among the research-vetted ways to protect telomeres, the authors cite avoiding smoking, getting at least 150 minutes of moderate exercise or 75 minutes of vigorous exercise per week, and maintaining a healthy, low-fat diet. (scienceblog.com)
- The New York Times bestselling book coauthored by the Nobel Prize winner who discovered telomerase and telomeres' role in the aging process and the health psychologist who has done original research into how specific lifestyle and psychological habits can protect telomeres, slowing disease and improving life. (goodreads.com)
Longest telomeres2
- Human beings with the highest vitamin D levels have the longest telomeres, and people with the lowest vitamin D levels have the [shortest] telomeres," Gundry told mbg co-CEO Jason Wachob , referring to research in the Archives of Medical Science 2 and the Journal of Nutrition 3 on the association between telomere length and vitamin D levels. (mindbodygreen.com)
- But one bird in the group with the longest telomeres survived to almost nine years old. (bellenews.com)
Lengthens telomeres2
- The botanicals in Telomere Plus have been shown to increase the activity of telomerase, a naturally-occurring enzyme that lengthens telomeres and protects them from shortening. (enzymedica.com)
- The naturally-occurring enzyme telomerase lengthens telomeres and keeps them from shortening, and the botanicals in Telomere Plus activate the telomerase in our bodies so that it can give us the whole-body benefits. (enzymedica.com)
Recombination3
- ALT employs recombination via extrachromosomal telomere elements called C-circles. (yeastgenome.org)
- This pairing requires the SAGA / TREX2 complex and, once paired, the recombination between C-circles and telomeres appears to be effected by Rad59 p, the paralog of Rad52 p. (yeastgenome.org)
- They also showed the circles interact with the SAGA/TREX2 complex, which favors telomere recombination. (yeastgenome.org)
Longevity4
- In older people with stable heart disease, longevity can vary widely, but a number of studies have suggested that telomere length appears to be a good predictor of a patient's likely health span - their number of healthy years of life remaining. (scienceblog.com)
- A new study in the journal PLoS ONE shows the impact job stress has on certain sections of our DNA called telomeres, which have been linked in research with longevity. (huffpost.com)
- When combined with a healthy diet and regular exercise , taking a vitamin D supplement can help keep telomeres in tiptop shape and promote longevity from the inside out. (mindbodygreen.com)
- By understanding what telomeres are and how they work, we can take measures to help lengthen our telomeres and promote longevity. (antiaging-systems.com)
Stability1
- A balance between elongation and trimming regulates telomere stability in stem cells. (sens.org)
Abnormally short1
- And abnormally short telomeres seem to make humans more susceptible to conditions such as bone marrow failure, pulmonary fibrosis, liver disease, and gastrointestinal disease over time. (mindbodygreen.com)
Enzyme telomerase1
- Blackburn, Carol Greider, and Jack Szostak were awarded the 2009 Nobel Prize in Physiology or Medicine for the discovery of how chromosomes are protected by telomeres and the enzyme telomerase. (wikipedia.org)
Linear chromosomes1
- Telomeres are non-coding, repetitive sequences located at the termini of linear chromosomes to act as buffers for those coding sequences further behind. (wikipedia.org)
Humans2
- Telomeres don't shrink significantly in healthy humans for decades due to an enzyme called telomerase , which partially repairs and lengthens them after each shortening. (howstuffworks.com)
- Telomeres and the natural lifespan limit in humans. (sens.org)
Yeast1
- The telomerase ribonucleoprotein complex is the primary means by which yeast cells maintain telomeres. (yeastgenome.org)
Length assay2
- This inconsistency may be partially due to the relatively small sample sizes in each study and heterogeneity caused by various uncontrolled confounders (e.g., duration of illness or hospitalization, lifetime antipsychotic dose, and telomere length assay methods). (databasefootball.com)
- Indeed, only one study has recruited more than 1,000 patients with schizophrenia (and a sufficient sample of controls), although this was a meta-analysis, including different telomere length assay protocols. (databasefootball.com)
Protective4
- Discovered in 1938 by gen-eticist Hermann J. Müller, telomeres (Greek for 'end part') are essentially protective caps composed of short DNA sequences on the tips of chromosomes. (howstuffworks.com)
- Also, statins seem to have a protective role against telomere shortening, and lifestyle factors may have an important role to play. (meresearch.org.uk)
- It also shows, rather surprisingly, that a substantial number of people had telomere lengthening, and that this appeared to be protective. (scienceblog.com)
- Because some really villainous free radicals have the power to tear away at your telomeres (protective tips of your DNA critical for aging), they ultimately have the power to tear away at your DNA, too. (susansmithjones.com)
20171
- 2017). Data from: Age-related sex differences in body condition and telomere dynamics of red-sided garter snakes [Dataset]. (datadryad.org)
Significantly1
- In contrast to never-smokers, telomere length significantly decreased with age in smokers. (ersjournals.com)
Repetitive1
- Showcasing a revolutionary new way to think about aging and health, Dr. Ed Park's entertaining and insightful new book introduces readers to Telomeres - repetitive DNA sequences that play a vital role in aging and health. (rechargebiomedical.com)
Shortest1
- The birds with the shortest telomeres did tend to die first - from as early as seven months after the start of the trial. (bellenews.com)
Homeostasis2
- Therefore, proper establishment, regulation, and maintenance of the telomere chromatin structure are required for cell homeostasis. (nih.gov)
- Another gene implicated in DKC, TINF2 , encodes a key component of the protein shelterin, which plays a role in telomere homeostasis. (medscape.com)
Mechanism4
- As stem cells have elongated proliferative capacity, they should have a mechanism that maintains telomere length through many cell divisions. (nature.com)
- So far, the mechanism of telomere lengthening is unknown, the authors say. (scienceblog.com)
- The mechanism that limits cell division involves a structure called a telomere. (msdmanuals.com)
- In cancer cells, the telomerase enzyme elongates telomeres, providing a mechanism for a continued unlimited cell division. (lu.se)
Tandem2
- According to his theory of marginotomy DNA sequences at the ends of telomeres are represented by tandem repeats, which create a buffer that determines the number of divisions that a certain cell clone can undergo. (wikipedia.org)
- Drosophila telomeres are unusual as they lack short tandem repeats. (ens-lyon.fr)
Genetics2
Gene5
- We examined the clinical and molecular features of aging and cancer in persons carrying heterozygous loss-of-function mutations in the telomere-related gene POT1 and noncarrier relatives. (evmedreview.com)
- Results PWBTL averaged 1.76 (telomere/single-copy gene of albumin, T/S) in 144 battery plant workers. (bmj.com)
- Our findings suggest that TERT and POT1 gene variants, along with telomere length, may serve as potential biomarkers and therapeutic targets for NSCLC in this population . (bvsalud.org)
- Telomere length, DNA-methylation, gene expression of Trf1, Trf2, ATM, and APP, protein expression of p-Tau, a-synuclein, and presenilin 1 and 2 were assessed in whole brain tissue at 12 wk after WF exposure ended. (cdc.gov)
- A heterozygous mutation was found on the conserved telomere maintenance component 1 gene ( CTC1 ). (medscape.com)
POT12
- In contrast to noncarrier relatives, who had the typical telomere shortening with age, POT1 mutation carriers maintained telomere length over the course of 2 years. (evmedreview.com)
- POT1 mutations associated with long telomere length conferred a predisposition to a familial clonal hematopoiesis syndrome that was associated with a range of benign and malignant solid neoplasms. (evmedreview.com)
Epigenetic3
- Epigenetic maintenance of telomere identity in Drosophila: buckle up for the sperm ride. (ens-lyon.fr)
- Home / Teams / Epigenetics and Zygote Formation - B. Loppin / Publications / Epigenetic maintenance of telomere identity in Drosophila: buckle up for the sperm ride. (ens-lyon.fr)
- These findings suggest a possible correlation between epigenetic modifications, telomere length alteration, and neurodegeneration because of the presence of factors in serum after WF exposure that may cause extra-pulmonary effects as well as the translocation of potentially neurotoxic metals associated with WF to the central nervous system (CNS). (cdc.gov)
Replication5
- The processes that maintain telomeres employ replication protein A (RPA), a single-stranded DNA binding protein. (massgeneral.org)
- Dr. Zou and his team had previously investigated the role for RPA at telomeres3 and found that it associated transiently with telomeres during S phase of DNA replication. (massgeneral.org)
- And indeed the team found that in cells that use the ALT pathway, RPA binds persistently to telomeres, not detaching after replication. (massgeneral.org)
- ATRX-deficient neu-roprogenitors exhibited higher incidence of telomere fusions and increased sensitivity to replication stress-inducing drugs. (bepress.com)
- A telomere, which looks like a shoelace cap, is intended to keep chromosomes from fraying or unravelling during replication. (nepalnews.com)
Damage2
- We show that the Atrx-null embryonic mouse brain accumulates replicative damage at telomeres and pericentro-meric heterochromatin, which is exacerbated by loss of p53 and linked to ATM activation. (bepress.com)
- So between DNA getting attacked by free radicals (which can be produced by harmful UV exposure) and decreasing NADs unable to adequately, efficiently repair the DNA damage caused by destroyed telomeres. (susansmithjones.com)
Critically1
- Often, when telomeres reach a critically short length, the cell dies in a process called apoptosis. (huffpost.com)