TY - JOUR. T1 - Regulation of telomeric repeat binding factor 1 binding to telomeres by casein kinase 2-mediated phosphorylation. AU - Mi, Kyung Kim. AU - Mi, Ran Kang. AU - Hyung, Wook Nam. AU - Bae, Young Seuk. AU - Yu, Sam Kim. AU - In, Kwon Chung. PY - 2008/5/16. Y1 - 2008/5/16. N2 - Telomere maintenance is essential for continued cell proliferation and chromosome stability. Telomeres are maintained by telomerase and a collection of associated proteins. The telomeric protein telomeric repeat binding factor 1 (TRF1) negatively regulates telomere length by inhibiting access of telomerase at telomere termini. Here we report that TRF1 interacts with the βsubunit of casein kinase 2 (CK2) and serves as a substrate for CK2. CK2-mediated phosphorylation is required for the efficient telomere binding of TRF1 in vitro and in vivo. Inhibition of CK2 by the CK2 inhibitor 5,6-dichloro-1-β-D- ribofuranosyl-benzimidazole decreased the ability of TRF1 to bind telomeric DNA. The resulting telomere-unbound ...

View mouse Terf2ip Chr8:112011398-112020528 with: phenotypes, sequences, polymorphisms, proteins, references, function, expression

Uncapped telomeres activate a p53-mediated DNA damage response to elicit cellular senescence. In turn, p53 negatively modulates telomere capping by promoting ubiquitin-mediated degradation of the TRF2 shelterin component. The telomere-capping complex shelterin protects functional telomeres and prevents the initiation of unwanted DNA-damage-response pathways. At the end of cellular replicative lifespan, uncapped telomeres lose this protective mechanism and DNA-damage signalling pathways are triggered that activate p53 and thereby induce replicative senescence. Here, we identify a signalling pathway involving p53, Siah1 (a p53-inducible E3 ubiquitin ligase) and TRF2 (telomere repeat binding factor 2; a component of the shelterin complex). Endogenous Siah1 and TRF2 were upregulated and downregulated, respectively, during replicative senescence with activated p53. Experimental manipulation of p53 expression demonstrated that p53 induces Siah1 and represses TRF2 protein levels. The p53-dependent

Is predicted to contribute to telomerase activity. Predicted to be involved in protein localization to chromosome, telomeric region; regulation of telomere maintenance; and telomere maintenance. Predicted to localize to shelterin complex. Is expressed in several structures, including gill; heart; liver; nervous system; and pleuroperitoneal region. Orthologous to human TERF2 (telomeric repeat binding factor 2 ...

Acts both as a regulator of telomere function and as a transcription regulator. Involved in the regulation of telomere length and protection as a component of the shelterin complex (telosome). In contrast to other components of the shelterin complex, it is dispensible for telomere capping and does not participate in the protection of telomeres against non-homologous end-joining (NHEJ)-mediated repair. Instead, it is required to negatively regulate telomere recombination and is essential for repressing homology-directed repair (HDR), which can affect telomere length. Does not bind DNA directly: recruited to telomeric double-stranded 5-TTAGGG-3 repeats via its interaction with TERF2. Independently of its function in telomeres, also acts as a transcription regulator: recruited to extratelomeric 5-TTAGGG-3 sites via its association with TERF2 or other factors, and regulates gene expression. When cytoplasmic, associates with the I-kappa-B-kinase (IKK) complex and acts as a regulator of the NF-kappa-B

POT1 is one of the six core components of the human telomeric protein complex (reviewed in de Lange, 2005). This complex is composed of TRF1, TRF2, TIN2, TPP1 (previously known as PIP1, PTOP, or TINT1), Rap1, and POT1, which are thought to fulfill the two main functions of telomeres: the recruitment and regulation of telomerase, and the protection of chromosome ends. Defects in telomere protection activate the DNA damage response, leading to a DNA damage signal and inappropriate DNA repair reactions at chromosome ends. The cell cycle arrest resulting from telomere dysfunction is thought to be responsible for the finite lifespan of human cells lacking telomerase.. The current challenge is to understand how the telomeric complex protects chromosome ends from being recognized as sites of DNA damage. One approach is to define which repair and signaling pathways are repressed at natural chromosome ends by studying the events at dysfunctional telomeres. This approach has shown that chromosome ends are ...

TRF1 antibody [3H11] (telomeric repeat binding factor (NIMA-interacting) 1) for ELISA, ICC/IF, WB. Anti-TRF1 mAb (GTX80331) is tested in Human samples. 100% Ab-Assurance.

In human cells, homologous recombination (HR) provides an accurate mechanism for the repair of DNA double-strand breaks caused by replication fork breakdown or DNA damaging agents. HR also plays a role in the maintenance of eukaryotic telomeres; cells defective in the recombinational repair proteins RAD51D or RAD54 exhibit telomere shortening and end-to-end chromosome fusions. Here we discuss the way in which HR contributes to telomere protection and elongation in mammalian cells. Understanding the mechanisms by which HR promotes telomere maintenance has important implications for genomic stability and tumorigenesis.

a) Mammalian telomeres consist of tandem repeats of the TTAGGG sequence that are bound by the shelterin-telosome protein complex. Adjacent to telomeres are the subtelomeric regions, which are also rich in repetitive DNA. (b) In addition to shelterin, mammalian telomeres also contain nucleosomes that show histone modifications characteristic of heterochromatin domains. In addition, subtelomeric DNA is heavily methylated. These chromatin modifications at telomeres and subtelomeres have been shown to negatively regulate telomere length and telomere recombination. TriM, trimethyl. Image and legend from Telomere length, stem cells and aging.. You can also have a look at the diagrams related to telomere extension in my 2011 blog entry The epigenetic regulation of telomeres.. Shortened telomeres is only one of a number of factors that can contribute to cellular senescence, and may often be a downstream effect of such factors.. Apostles of telomere-extending would lead us to believe that cell ...

Studies revealed that NBS1 plays important roles in maintaining genome stability, but the underlying mechanism is controversial and elusive. Our study using clinical samples showed that NBS1 was involved in ATM/ATR-dependent pathways. NBS1 deficiency severely affected the phosphorylation of ATM/ATR as well as their downstream targets. The inefficiency in activating ATM/ATR-dependent pathways led to multiple defects in cellular responses towards DNA damage, such as inefficiency in inhibiting DNA synthesis and resistance to DNA-damaging agent. Accelerated telomere shortening was also observed in NBS fibroblasts, consistent with an earlier onset of cellular replicative senescence in vitro. This abnormality may be due to the shelterin protein TRF2 which was found upregulated in NBS fibroblasts. Prevalent telomeric fusions and cellular aneuploidy were also observed in NBS fibroblasts. Collectively, our study suggests a possible mechanism that NBS1 deficiency simultaneously affects ATM/ATR-dependent ...

Telomeres serve to protect the ends of chromosomes, and failure to maintain telomeres can lead to dramatic genomic instability. Human TPP1 was identified as a protein which interacts with components o

I love writing and blogging! I like looking for information on the latest movies, music and entertainment, celebrity news. Im also working on The Munroe Series - 14 Novels in the Romance, Mystery, Paranormal Category. The Calamity Girl - 2 Novels in Womens Fiction, Mystery, Romance. Young Adult Novels two of them about magic, witches, fairies and giants and I love going to the movies, dancing, socializing with friends and spending time with my loved ones and my dog ...

TY - JOUR. T1 - Solution structure of the arabidopsis thaliana telomeric repeat-binding protein DNA binding domain. T2 - A new fold with an additional C-terminal helix. AU - Sue, Shih Che. AU - Hsiao, Hsin Hao. AU - Chung, Ben C.P.. AU - Cheng, Ying Hsien. AU - Hsueh, Kuang Lung. AU - Chen, Chung Mong. AU - Ho, Chia Hsing. AU - Huang, Tai Huang. PY - 2006/2/10. Y1 - 2006/2/10. N2 - The double-stranded telomeric repeat-binding protein (TRP) AtTRP1 is isolated from Arabidopsis thaliana. Using gel retardation assays, we defined the C-terminal 97 amino acid residues, Gln464 to Val560 (AtTRP1464-560), as the minimal structured telomeric repeat-binding domain. This region contains a typical Myb DNA-binding motif and a C-terminal extension of 40 amino acid residues. The monomeric AtTRP1464-560 binds to a 13-mer DNA duplex containing a single repeat of an A. thaliana telomeric DNA sequence (GGTTTAG) in a 1:1 complex, with a KD∼10-6-10-7 M. Nuclear magnetic resonance (NMR) examination revealed that the ...

The results described in this study provided evidences that SYUIQ5, a Gquadruplex ligand, potently inhibited the proliferation and induced telomere DNA damage and autophagy in CNE2 and HeLa cancer cells in vitro. TRF2 delocalized from telomeres after SYUIQ5 treatment and was further degraded by proteasomes. In addition, overexpression of TRF2 prevented SYUIQ5-mediated cell death. ATM was also activated and involved in SYUIQ-5-induced telomere DNA damage response and autophagy. Furthermore, ATG5 knockdown attenuated the cytotoxicity of SYUIQ-5 in CNE2 and HeLa cells.. Telomeres are capable of forming guanine quadruplex (G4) structures on the G-rich strand, and the ligands that interact with G-quadruplex are recognized as promising anticancer agents by interfering with telomere conformation and telomere elongation. These compounds were first evaluated as telomerase inhibitors and induced telomere shortening and senescence. Recently, it was observed that G-quadruplex ligands induced a short-term ...

Telomeres, which are found at the end of eukaryotic linear chromosomes, are essential for chromosome maintenance and genomic stability (1). Mammalian telomeres are composed of repetitive d-(TTAGGG) sequences and telomere-specific shelterin complex proteins, which protect the chromosome ends from being recognized as DNA damage and preventing end-to-end chromosomal fusions (2). The shelterin proteins (TRF1, TRF2, POT1, TIN2, TPP1, and RAP1) form a protective complex that is present at telomeres throughout the cell cycle (3). Because of the end-replication problem, oxidative damage and other replication-associated end-processing events, telomeres progressively shorten with each round of DNA replication in normal somatic cells (4). The ribonucleoprotein enzyme complex telomerase counteracts telomere shortening by adding hexameric telomeric DNA (TTAGGG) repeats to the end of linear chromosomes in cancer cells but only partially counteracts progressive telomere shortening in some normal human ...

Mammalian telomeres are inherently heterochromatic. While enhanced telomere maintenance is evident in malignant cancers, some cancers appear to maintain telomeres by neither the common telomerase nor the alternative telomere repeat recombination mechanisms. Specifically, the roles of epigenetic modifications in telomere protection are largely unknown in human cancers. I have combined newly developed cellular and molecular approaches to show that in some cancer cell types, experimentally enhanced heterochromatinization localized specifically at telomeres reduced damage-induced foci at telomeres, suggesting augmentation of telomere stability. These results lead to the intriguing hypothesis that manipulating the epigenetic status at telomeres may be exploited to elicit damage at the telomeres of cancer cells as a novel approach to fight cancer. My current work in progress focuses on identifying novel chromatin modifiers that weaken telomere protection by modulating telomere compaction. It is ...

The involvement of TRF2 and the shelterin complex in telomere protection and maintenance has been extensively studied in telomerase-positive tumor cell lines. However, the role of TRF2 in ALT cells has not been investigated in depth. For this reason, we used a number of approaches, ranging from RNAi to functional inhibition, to manipulate TRF2 function in ALT cells. Colony formation experiments clearly show that RNAi-mediated TRF2 knockdown results in a marked decrease in the number of colonies, thus implicating an effect on either apoptosis or cell cycle, or both. Nevertheless, we find that apoptosis is not induced in TRF2-depleted cells or in cells expressing the dominant-negative ΔBΔM mutant in transient, and only moderately in stable settings. In a previous study, the ALT cell line SAOS2 was shown to be resistant to the cytotoxic effects of TRF2 inactivation, and this was ascribed to the absence of p53 (Karlseder et al., 1999). However, we show here that U2OS cells, which, unlike SAOS2, ...

Human telomeres are composed of long arrays of TTAGGG repeats that form a nucleoprotein complex required for the protection and replication of chromosome ends.

Human telomeres associate with shelterin, a six-protein complex that protects chromosome ends from being recognized as sites of DNA damage. The shelterin subunit TRF2 (telomeric repeat-binding factor 2) protects telomeres by facilitating their organization into the protective capping structure. We have reported previously that the DNA-PKcs (DNA-dependent protein kinase catalytic subunit)-interacting protein KIP associates with telomerase through an interaction with hTERT (human telomerase...

We were interested in characterizing proteins involved in telomere-membrane interactions in human sperm. To this end, nuclear membranes were partially solubilized by treatment with 0.5% Triton X-100 in buffer containing 100 mM NaCl. Earlier FISH data (Zalensky et al. 1995) demonstrated that such treatment destroyed association of human sperm telomeres with nuclear membrane. Usual methods for telomere-binding protein isolation involve nuclei extraction with salt buffers of higher molarity (e.g., 0.6 M KCl). Surprisingly, a Triton extract of human sperm was active in binding ds(TTAGGG) DNA, and this telomere-binding activity appeared to be identical to hSTBP previously described in 0.5 M NaCl nuclear extracts (Zalensky et al. 1997) as judged by a characteristic gel-retardation pattern (Fig. 1 a). The pretreatment of crude Triton-soluble hSTBP (hSTBPTR) with 6 M Urea, DNAase, and RNAase does not influence ds(TTAGGG) binding, at the same time activity is sensitive to temperature, and destroyed by ...

Telomeres are regions of tandem arrays of TTAGGG repeats and associated proteins located at chromosomal ends that allow cells to distinguish chromosome ends from double-strand breaks and protect chromosomes from end-to-end fusion, recombination and degradation (Houben et al., 2008). Telomeres are not linear structures, telomeric DNA is maintained in a loop structure due to many key proteins. This structure serves to protect the ends of chromosomes (Neidle and Parkinson 2003).Telomeres are subjected to shortening at each cycle of cell division due to incomplete synthesis of the lagging strand during DNA replication owing to the inability of DNA polymerase to completely replicate the ends of chromosome DNA (end-replication problem) (Muraki et al., 2012). Therefore, they assume to limit the number of cell cycles and act as a mitotic clock (Olovnikov, 1996). Shortened telomeres cause decreased proliferative potential, thus triggering senescence (Blackburn et al., 2006).Telomere length (TL) is highly

Yeast telomeric DNA is assembled into a nonnucleosomal chromatin structure known as the telosome, which is thought to influence the transcriptional repression of genes placed in its vicinity, a phenomenon called telomere position effect (TPE). The product of the RAP1 gene, Rap1p, is a component of the telosome. We show that the fraction of cells exhibiting TPE can be substantially reduced by expressing large amounts of a deletion derivative of Rap1p that is unable to bind DNA, called Rap1 delta BBp, or by introducing extra telomeres on a linear plasmid, presumably because both compete in trans with telomeric chromatin for factor(s) important for TPE. This reduction in TPE, observed in three different strains, was demonstrated for two different genes, each assayed at a different telomere. In contrast, the addition of internal tracts of telomeric DNA on a circular plasmid had very little effect on TPE. The product of the SIR3 gene, Sir3p, appears to be limiting for TPE. Overexpression of Sir3p ...

ZBTB48 binds through the last of its 11 zinc fingers directly to telomeric DNA (TTAGGG, in red) as well as subtelomeric variant repeats (TTGGG/TCAGGG, grey), which represent the protective caps at the end of chromosomes. In addition, it binds to the promoter sequences (dark blue) of specific target genes including mitochondrial fission process 1, MTFP1. In the absence of ZBTB48 (right panel) telomeres become longer whereas the expression of ZBTB48 target genes is strongly reduced. For instance, ZBTB48 KO (knock-out) cells loose the expression of MTFP1 leading to defects in the mitochondrial network with mitochondria clustering around the nucleus instead of being widely spread throughout the cell.

Telomeres are DNA tandem repeats associated with six proteins located at chromosome ends. Telomere shortening happens after each replication round in the majority of huma..

In recent years Hsp90 is available to connect to several telomeric proteins at various phases of cell cycle. in an ATP dependent manner with several cochaperones and provides the maturation of the target protein at a near native state [4]. In budding yeast there are two isoforms of Hsp90; Hsc82 (human ortholog of Hsp90β) which is constitutively expressed in the cell and Hsp82 (human ortholog of Hsp90α) which is induced whenever cells are exposed to any kind of stressed condition. It is known that expression of either one of the two isoforms of Hsp90 is required for yeast viability [5]. The two isoforms share 97% sequence identity and they comprise (1-2) % of the total cytosolic proteins. Hsp90 level is significantly increased in the cell upon exposure to stress including temperature nonphysiological pH nutrient deprivation and malignancy [6]. Recent studies possess unraveled novel jobs of Hsp90 where Hsp90 and its own cochaperone p23 get excited about stabilization SU-5402 of different ...

A relatively new area of interest concerns the HS1.2 region of immunoglobulin. Although this region is not active in Ig production, it is conserved and several DNA regions have been shown to interact with specific proteins, thus suggesting a functional/regulative role for this region. In collaboration with prof. D. Frezza (University of Rome Tor Vergata) and prof. A. Pastore (Kings College of London, UK), we have shown that some DNA sequences belonging to the promotor regions with which these proteins interact can form an intramolecular quadruplex structure (Figure 3). Quadruplex DNA is not found only at telomeric edge of chromosomes but it is also frequently found in regulative regions of DNA. Thus, our studies suggest a functional, still unknown, role for this region. The solution structure of these structures is planned for the future ...

The linear nature of eukaryotic chromosomes necessitates protection of their physical ends, the telomeres, because the DNA-repair machinery can misconstrue the ends as double-stranded DNA breaks. Thus, protection is crucial for avoiding an unwarranted DNA-damage response that could have catastrophic …

Get Apollo Hospitals Enterprises latest Quarterly Results, Financial Statements and Apollo Hospitals Enterprises detailed profit and loss accounts.

J Ye, C Lenain, S Bauwens, A Rizzo, A Saint-Léger, A Poulet, D Benarroch, F Magdinier, J Morere, S Amiard, E Verhoeyen,S Britton, P Calsou, B Salles, A Bizard, M Nadal, E Salvati, L Sabatier, Y Wu, A Biroccio, A Londoño-Vallejo, MJ Giraud-Panis and E Gilson* (2010) TRF2 and Apollo cooperate with Topoisomerase 2a to protect human telomeres from replicative damage, Cell, 142: 230-242; IF= 32, ...

Apollo Endeavour - See the full details of the Apollo Endeavour campervan. Check out rental prices and let our expert reservation team answer all your questions about a campervan holiday.

Conical sauté pan Apollo with lid 20 cm: |p|Conical sauté pan with lid from the Apollo series by Demeyere. Made from 7-ply material up to the edge.|/p| |p|Ø 20 cm. Height 7.5 cm. Volume: 2 liters|/p| - Shop online on BetterKitchen.eu

From time to time we may update the firmware in our test equipment to bring you a better experience. You can find the latest version of available firmware for your Apollo Series Test Lead Set below ...

Looduslik Eesti filtreeritud terviseturba šampoon sisaldab bioaktiivseid aineid ja mineraale, mis puhastavad ja toidavad juuksejuuri sügavuti. Tulemuseks tugevamad ja elujõulisemad juuksed. Šampoonis sisalduv argaaniaõli aitab siluda katkiseid juukseotsi,

Telomeres, the physical ends of chromosomes, play an important role in preserving genomic integrity. This protection is supported by telomere binding proteins collectively known as the shelterin complex. The shelterin complex protects chromosome ends by suppressing DNA damage response and acting as a regulator of telomere length maintenance by telomerase, an enzyme that elongates telomeres. Telomere dysfunction manifests in different forms including chromosomal end-to-end fusion, telomere shortening and p53-dependent apoptosis and/or senescence. An important shelterin-associated protein with critical role in telomere protection in human and mouse cells is the catalytic subunit of DNA-protein kinase (DNA-PKcs). DNA-PKcs deficiency in mouse cells results in elevated levels of spontaneous telomeric fusion, a marker of telomere dysfunction, but does not cause telomere length shortening. Similarly, inhibition of DNA-PKcs with chemical inhibitor, IC86621, prevents chromosomal end protection through mechanism

High Mobility Group AT-hook protein 2 (HMGA2) is a non-histone chromatin binding protein expressed in stem cells, cancer cells but not in normal human somatic cells. The presence of HMGA2 in cancer correlates with advanced neoplastic disease and poor prognosis. HMGA2 plays important roles in Base Excision Repair (BER) and at replication forks. HMGA2 is present at mammalian metaphase telomeres and its loss induces chromosomal aberrations. However, the functional role of HMGA2 at telomeres remains elusive. We hypothesized a protective role of HMGA2 that guards telomeres and modulates DNA damage repair signaling pathways. Employing different HMGA2+ human tumor cell models, we investigated the HMGA2-mediated functions that contribute to chemoresistance in glioblastoma (GB). This study presents a novel interaction of HMGA2 with telomeric protein TRF2 (Telomere Repeat-Binding Factor 2). This interaction retains TRF2 at telomeres, thus capping the telomeres and reducing telomere-dysfunction induced ...

Almost 12 years ago, an evolutionary theory based on intergenerational telomere erosion was introduced [8] and was widely covered by the press [11, 12]. In 2011, based on published data on human telomere length inheritance, I refined my theoretical framework and located the source of human intergenerational telomere erosion in the female germline [6, 7, 10]. According to this model, telomeres in the testes of elderly males are longer than those in young males because the seniors are members of a previous generation (=birth-cohort effect) and therefore skipped, on average, one female-based intergenerational telomere loss. In 2014, I further developed the model of telomere-driven macroevolution and presented a complete biological framework for the old European model of saltatory evolution of nonadaptive characters [6].. In agreement with this theoretical model, a high-profile study, published in the August issue of Aging Cell in 2015, finally confirmed the long-awaited birth-cohort effect on ...

1221 Telomeres lie at the end of chromosomes and contain the repeat sequence 5′-TTAGGG-3′. At the very ends of each telomeric DNA there is a single-stranded, 3′ overhang of between 50 and 500 bases in the G-rich strand, the so-called G-tail. The G-tail length and telomere binding proteins are essential for formation of t-loop and chromosome maintenance. Dominant negative telomere binding protein TRF2 induces the dissociation of TRF2 binding from telomeres and the destruction of t-loop accompanied by G-tail shortening. Recently, we have developed G-tail telomere HPA, a new technique to measure telomeric G-tail (Nature Methods, 2005). This method has the advantage of being simple to perform, accurate and highly sensitive for G-tails as short as 20 nucleotides. In addition, this assay is specific and quantitative for G-tails, and can be used for large-scale screening to understand diseases associated with ageing and telomere dysfunction. Using this assay, we have measured G-tail length in ...

The lab studies telomeres, protective elements at the ends of chromosomes that are critical for genome integrity and shorten with cell division. de Lange seeks to understand how telomeres are protected by a protein complex called shelterin, how they are replicated and maintained, and how telomere loss contributes to genome instability in cancer. The lab also studies DNA double-strand break repair with emphasis on the function of two critical DNA repair proteins, BRCA1 and 53BP1. Research in the de Lange lab focuses on human and mouse telomeres, which are made up of long arrays of double-stranded TTAGGG repeats that end in a single-stranded 3′ overhang. The lab identified a six-subunit protein complex, which they named shelterin, that specifically binds to telomeres. Using genetic approaches, de Lange and her colleagues determined the fate of telomeres lacking one or more of the six shelterin subunits. The results showed that cells lacking shelterin perceive their natural chromosome ends as ...

Previous work from the de Lange lab showed that TRF2, a shelterin protein that binds to the duplex part of the telomere, is crucial for telomere protection. Without TRF2, telomeres activate a DNA damage signal and are repaired by the same pathways that act on DNA breaks. TRF2 brings a second shelterin protein, POT1, to the telomeres. Because POT1 binds to single-stranded telomeric DNA present at the very end of the chromosomes, the de Lange lab asked how POT1 contributes to the protection of telomeres.. We had previously removed TRF2 from mouse cells and seen many dramatic phenotypes, says de Lange, all of the telomeres ligate together; there is a massive DNA damage response and the cells basically die. We argued that if the function of TRF2 was to bring POT1 to the DNA, then we should observe the same phenotype if we removed POT1.. To determine if this was the case, graduate student Dirk Hockemeyer, the first author of the paper, decided to remove the POT1 gene from mice. Humans have one ...

The telomeres that cap the ends of eukaryotic chromosomes serve a dual part in protecting the chromosome ends and in intracellular signaling for regulating cell proliferation. by DNA-binding protein that subsequently associate with various other signaling protein/complexes to attain telomere-end length and security control. The distance of telomeric DNA is normally maintained with the enzyme telomerase, but additionally, six telomere-associated proteins - TRF1, TRF2, Container1, RAP1, TIN2 and TPP1 in mammalian cells - have already been shown to type a complicated referred to as the telosome, or shelterin complicated, that is needed for telomere function [1-10]. Right here we will briefly review the structure of the telosome, its part in telomere maintenance, and its contacts with intracellular signaling pathways. Telomere repeat element-1 (TRF1) and -2 (TRF2) are related proteins that share a number of sequence and organizational similarities, and along with safety of telomeres-1 (POT1), they ...

POT1 and TPP1 are part of the shelterin complex and are essential for telomere length regulation and maintenance. Naturally occurring mutations of the telomeric POT1-TPP1 complex are implicated in familial glioma, melanoma and chronic lymphocytic leukaemia. Here we report the atomic structure of the interacting portion of the human telomeric POT1-TPP1 complex and suggest how several of these mutations contribute to malignant cancer. The POT1 C-terminus (POT1C) forms a bilobal structure consisting of an OB-fold and a holiday junction resolvase domain. TPP1 consists of several loops and helices involved in extensive interactions with POT1C. Biochemical data shows that several of the cancer-associated mutations, partially disrupt the POT1-TPP1 complex, which affects its ability to bind telomeric DNA efficiently. A defective POT1-TPP1 complex leads to longer and fragile telomeres, which in turn promotes genomic instability and cancer.. ...

In response to metabolic or environmental stress, cells activate powerful defense mechanisms to prevent the formation and accumulation of toxic protein aggregates. The main orchestrator of this cellular response is HSF1 (heat shock factor 1), a transcription factor involved in the up-regulation of protein-coding genes with protective roles. It has become very clear that HSF1 has a broader function than initially expected. Indeed, our previous work demonstrated that, upon stress, HSF1 activates the transcription of a non-coding RNA, named Satellite III, at pericentromeric heterochromatin. Here, we observe that the function of HSF1 extends to telomeres and identify subtelomeric DNA as a new genomic target of HSF1. We show that the binding of HSF1 to subtelomeric regions plays an essential role in the upregulation of non-coding TElomeric Repeat containing RNA (TERRA) transcription upon heat shock. Importantly, our data show that telomere integrity is impacted by heat shock and that telomeric DNA ...

Author Summary Telomeres are protein-DNA structures that protect the ends of eukaryotic chromosomes. A failure in this protective structure can lead to chromosomal instabilities and contribute to cancer and aging. The protective nature of telomeres relies on complex interactions between repetitive telomeric DNA and associated proteins. One major question is how telomeric proteins, including telomere-associated nucleosomes, are modified in order to achieve this protection. In this study, we have discovered that Arabidopsis telomeric nucleosomes contain a unique mixture of both active and inactive chromatin marks. Additionally, the telomeric DNA itself is modified by methylation of cytosines within the telomeric repeat. Regulation of DNA methylation is achieved by telomeric repeat-containing small RNAs, which are derived from the processing of telomeric transcripts by the RNA-dependent DNA methylation pathway. From these data, we infer that the formation of a proper telomere structure is partly regulated

The ends of eukaryotic chromosomes are capped by telomeres which consist of tandem G-rich DNA repeats stabilized by the shelterin protein complex. Telomeres shorten progressively in most normal cells due to the end replication problem. In more than 85% of cancers however, the telomere length is maintained by telomerase; a reverse transcriptase that adds telomeric TTAGGG repeats using its integral RNA template. The strong association between telomerase activity and malignancy in many cancers suggests that telomerase activity could serve as a diagnostic marker. We demonstrate single-molecule, real-time telomerase extension activity observed digitally as the telomeric repeats are added to a substrate. The human telomerase complex pulled down from mammalian cells displays extension activity dependent on dNTP concentration. In complex with the processivity factor, POT1-TPP1, telomerase adds repeats at an accelerated rate and yields longer products. Our assay provides a unique detection platform that ...

We have previously shown, that in plant cells, similarly to human, animal and protozoan cells, telomeres are maintained by telomerase, the specialised ribonucleoprotein complex of reverse-transcriptase activity. Our subsequent studies revealed the con

Binds to the hairpin form of the viral telomeric sequence. Might direct genome encapsidation into the virus particle (By similarity).

Telomeres belong to the key functional elements of eukaryotic chromosomes. Like all the other parts of the genome, they exist and function as complexes of DNA with histones and various nonhistone proteins, including specific telomere-binding proteins.

TY - GEN. T1 - Therapeutic applications and mechanisms underlying the activity of immunosuppressive oligonucleotides. AU - Klinman, Dennis M.. AU - Tross, Debbie. AU - Klaschik, Sven. AU - Shirota, Hidekazu. AU - Sato, Takeshi. N1 - Copyright: Copyright 2018 Elsevier B.V., All rights reserved.. PY - 2009/9/1. Y1 - 2009/9/1. N2 - Synthetic oligodeoxynucleotides (ODN) capable of neutralizing or inhibiting immune responses have been described. This review will focus on the properties of phosphorothioate ODN that mimic the immunosuppressive activity of the repetitive TTAGGG motifs present in mammalian telomeres. These TTAGGG multimers block the production of pro-inflammatory and T helper type 1 cytokines elicited when immune cells are activated by a wide variety of Toll-like receptor ligands, polyclonal activators, and antigens. Several mechanisms contribute to the suppressive activity of such ODN. Ongoing microarray studies indicate that suppressive ODN interfere with the phosphorylation of ...

PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.

Summary Telomeres are the nucleoprotein structures at the ends of linear chromosomes and maintain the genomic integrity through multiple cell divisions. Telomeres protect the chromosome ends from degradation, end-to-end fusion and abnormal recombi

Telomeres usually contain some version of tandem copies of sequences like 5-CCCCAA-3 on one strand and 5-TTGGGG on the complementary strand. The GT-rich strand comprises the 3-end and **sticks out** longer than the CA strand (and forms a loop, sealing the end). Specifically for human telomeres, there are 300-8,000 sets of repeats of the sequence CCCTAA /TTAGGG, then a 100-200 nucleotide extension of single-stranded TTAGGG repeats, hence the comment that telomeres have high GT content. But why? The best way to understand this beautiful system is to watch the very simple but very revealing short animation in the link above called telomere animation of how telomerase works at the telomere (see especially step 5 and later). Note that it is all about the requirements of polymerase for a free 3 -OH (and a ss DNA template strand)! It might also help to scan quickly through the very good article from Nature Network listed above as well ...

Telomeres usually contain some version of tandem copies of sequences like 5-CCCCAA-3 on one strand and 5-TTGGGG on the complementary strand. The GT-rich strand comprises the 3-end and **sticks out** longer than the CA strand (and forms a loop, sealing the end). Specifically for human telomeres, there are 300-8,000 sets of repeats of the sequence CCCTAA /TTAGGG, then a 100-200 nucleotide extension of single-stranded TTAGGG repeats, hence the comment that telomeres have high GT content. But why? The best way to understand this beautiful system is to watch the very simple but very revealing short animation in the link above called telomere animation of how telomerase works at the telomere (see especially step 5 and later). Note that it is all about the requirements of polymerase for a free 3 -OH (and a ss DNA template strand)! It might also help to scan quickly through the very good article from Nature Network listed above as well ...

We studied the expression of four telomere-associated proteins (TRF1, TRF2, POT1, and RAP1 genes) in normal and tumor tissues of lung cancer patients and observed significant down-regulation of TRF1 in tumor samples and no significant difference in expression between tumor and normal tissues for TRF2, POT1, and RAP1 (Table 3). The down-regulation of TRF1 in tumor tissue was consistent when we used GAPDH alone, 18S rRNA alone, β-actin alone (data not shown) or the geometric mean of three genes as internal control. In previous published studies, controversial data were presented for these telomeric genes in cancer. Some studies suggested that TRF1 and TRF2 were down-regulated in tumor tissues (21-26), whereas others showed that TRF1 or TRF2 was up-regulated (27-30). Different tumor type and tumor stage may account for some of these differences. One study showed that tumor stage and telomere length might also influence POT1 expression in cancer (31). Their data indicated that in stage I/II gastric ...

Now the Redux state-layer is paired with the React view-layer just as the Apollo Client state-layer was paired before. We then wrap our entire application tree with the ApolloProvider, so we can make a query, mutation or subscription from any component. This generates a component that we will use to display a form to collect and save data with the GraphQL service. Apollo Client gives you a way to specify the optimisticResponse option, that will be used to update active queries immediately, in the same way that the servers mutation response will. Apollo is an awesome GraphQL client package and if you look at … ⚙️ When client-side JavaScript is available and we do not go through a page render after a mutation, it might be handy to refetch some GraphQL queries. The Apollo Client library has a range of benefits: 1. Apollo Client is a convenient client library for working with GraphQL. graphql-tag is integrated into apollo-boost, but not included in apollo-client. React Apollo - Client ...

Complete information for ACD gene (Protein Coding), ACD, Shelterin Complex Subunit And Telomerase Recruitment Factor, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium

Apollo Sugar is a disease management clinic focused on providing high quality, integrated care across its clinics for people with diabetes. ASCL is a Subsidiary of Apollo Health & Lifestyle, the arm of the Apollo Hospitals Group that is driving its rapid growth in primary and secondary healthcare. In India, Diabetes afflicts over 65 million citizens, and in addition to this over 77 million people have been diagnosed as being pre-diabetic. These numbers are still growing significantly

The protein-DNA complexes that compose the end of mammalian chromosomes-telomeres-serve to stabilize linear genomic DNA and are involved in cellular and organismal aging. One mechanism that protects telomeres from premature degradation is the formation of structures called t-loops, in which the sing …

Apollo Gleneagles Hospital Kolkata is a leading multi-specialty hospital with a capacity of 510 beds and outstanding medical facilities and healthcare services.

Apollo Hospital Chennai is a pioneer super-specialty tertiary hospital with a capacity of 560 beds, 220+ doctors offering outstanding healthcare services.

Apollo's journey towards medical excellence with a human touch continues as Indore will adorn the global Apollo map on 7th October, 2014.

Apollo accelerates the growth and success of your entire sales org with the first truly reliable, scalable revenue engine and account-based sales platform.

Apollo accelerates the growth and success of your entire sales org with the first truly reliable, scalable revenue engine and account-based sales platform.

Get all the latest news & events updates of Apollo Hospital Chennai including awards won, upcoming events, reports & analysis etc. Visit our website to know more.

Berthold Technologies offers the Apollo 11, an instrument characterized by long-time proven and continuously optimized optics as well as a modern LED light source. Up to 6 filters can be used with the instrument enabling the performance of all important applications.

Apollo Hospitals Dhaka is the only JCI Accredited 425-bed multi-disciplinary super-specialty tertiary care hospital in Bangladesh.

The connection between Telomeres and health grows closer every day, with newer research showing how it may aid in the battles against aging and cancer.

Product Name:1-(3-Chloropropyl)imidazole CAS Number:53710-78-4 Catalouge Number:OR471035 Purity: Commodity Code:2933299090 MDL Number:MFCD09728547 Notes: Synonyms:

Instead of treating POTS symptomatically, we look for (and treat) the underlying medical issues causing POTS. Serving Colleyville TX and surrounding areas.

Neti pots have been proven effective for thousands of years, but they still come with unique dangers that can be easily avoided with proper care.

TOKYはデザイン性の高いオリジナル鉢・セレクト鉢の販売をするお店です。多肉植物・サボテンをそれぞれの個性に合わせた鉢に仕立てたものの提案もしています。