...Two independent papers in the December 1st issue of G&D detail how hum...The human RecQ family of helicases consists of 5 members: WRN BLM RE...Dr. Alexander Mazin (Drexel University College of Medicine) and collea...In a separate paper Drs. Guangbin Luo (Case Western Reserve Univerist...,Human,RecQ,helicases,,homologous,recombination,and,genomic,instability,biological,biology news articles,biology news today,latest biology news,current biology news,biology newsletters
Bloom syndrome is a rare genetic disorder characterized by severe growth retardation and cancer predisposition. The disease is caused by a loss of function of the Bloom syndrome protein (BLM), a member of the RecQ family of DNA helicases. Here we report on the first 3D structure of a BLM fragment, a solution structure of the C-terminal helicase-and-ribonuclease D-C-terminal (HRDC) domain from human BLM. The structure reveals unique features of BLM HRDC that are distinct from the HRDC domain of Werner syndrome protein. In particular, BLM HRDC retains many acidic residues exposed to the solvent, which makes the domain surface extensively electronegative. Consistent with this, fluorescence polarization assays showed an inability of isolated BLM HRDC to interact with DNA substrates. Analyses employing ultracentrifugation, gel-filtration, CD spectroscopy and dynamic light scattering showed that the BLM HRDC domain exists as a stable monomer in solution. The results show that BLM HRDC is a compact, ...
The RecQ helicase family is a group of highly conserved DNA unwinding enzymes critical in guarding genome stability in all kingdoms of life. Human RecQ homologs...
高い抗原親和性、特異性と安定した品質を兼ね備えたアブカムのウサギ・モノクローナル抗体 RabMAb® ab247955 交差種: Hu 適用: WB
Complete information for RECQL5 gene (Protein Coding), RecQ Like Helicase 5, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Principal Investigator:KONDO Naomi, Project Period (FY):1998 - 2002, Research Category:Grant-in-Aid for Scientific Research on Priority Areas
Mouse polyclonal antibody raised against a full-length human RECQL protein. RECQL (NP_002898.2, 1 a.a. ~ 649 a.a) full-length human protein. (H00005965-B01P) - Products - Abnova
Genetic information processingDNA metabolismDNA replication, recombination, and repairATP-dependent DNA helicase, RecQ family (TIGR00614; EC 3.6.4.12; HMM-score: 39) ...
Patients with Werners syndrome (WS) exhibit pleiotropic properties characteristic of premature ageing, including the greying and loss of hair, cataract formation, osteoporosis, atherosclerosis, diabetes, hypogonadism and scleroderma (Epstein et al., 1966). Cultured WS cells display a limited capacity to proliferate and a prolonged S‐phase (Martin et al., 1970). Moreover, WS cells exhibit evidence of genomic instability exemplified by chromosomal breaks, multiple large deletions, translocations and altered telomere dynamics (Fukuchi et al., 1989).. The gene mutated in WS, WRN, encodes a member of the RecQ family of DNA helicases. This family also includes the human RECQL, RECQ4, RECQ5 and BLM proteins, as well as the Saccharomyces cerevisiae Sgs1 protein (Chakraverty and Hickson, 1999). Mutations in the BLM gene lead to Blooms syndrome. Cells defective in BLM also exhibit genomic instability, the hallmark being an increased level of sister chromatid exchanges (German, 1993). In addition, BS ...
Bloom syndrome helicase (BLM) has key roles in homologous recombination repair, telomere maintenance, and DNA replication. Germ-line mutations in the BLM gene causes Bloom syndrome, a rare disorder characterized by premature aging and predisposition to multiple cancers, including breast cancer. The clinicopathologic significance of BLM in sporadic breast cancers is unknown. We investigated BLM mRNA expression in the Molecular Taxonomy of Breast Cancer International Consortium cohort (n = 1,950) and validated in an external dataset of 2,413 tumors. BLM protein level was evaluated in the Nottingham Tenovus series comprising 1,650 breast tumors. BLM mRNA overexpression was significantly associated with high histologic grade, larger tumor size, estrogen receptor-negative (ER(-)), progesterone receptor-negative (PR(-)), and triple-negative phenotypes (ps , 0.0001). BLM mRNA overexpression was also linked to aggressive molecular phenotypes, including PAM50.Her2 (P , 0.0001), PAM50.Basal (P , 0.0001), ...
Rothmund-Thomson syndrome (RTS) is a rare genetic disease that affects many parts of the body, particularly the skin which is typically normal at birth. The first sign of this disease is a rash that starts on the cheeks between ages three months and six months as erthema, swelling, and blistering on the face and subsequently spreads to the buttocks and extremities. The rash evolves over months to years into the chronic pattern of reticulated hypo- and hyperpigmentation, punctate atrophy, and telangiectases. These skin problems persist for life, and are collectively known as poikiloderma. This disease is also characterized by sparse hair, eyebrows, and eyelashes, slow growth and small stature, abnormalities of the teeth and nails, juvenile cataract, skeletal abnormalities (mainly osteopenia and defects of the radial ray: thumb appendages, hypoplasia or aplasia of the thumbs, or radial aplasia), gastrointestinal problems in infancy such as chronic diarrhea and vomiting, premature aging and ...
Reactivité: Humain, Souris Hôte: Lapin Clone: Polyclonal Conjugué: HRP | Commandez Blm/Blooms Syndrome Protein Blm lanticorps (ABIN1712183).
What is Werner syndrome?Werner syndrome, also called progeria, is a hereditary condition associated with premature aging and an increased risk of cancer and other diseases. Signs of Werner syndrome usually develop in the childhood or teenage years. A person with Werner syndrome does not have the usual growth spurt typical of a teenager and tends to be shorter than others.
Accumulation of lipid-laden foam cells of monocyte origin plays an important role in atherogenesis. Therefore, for determination of the mechanism of accelerated atherogenesis in Werners syndrome, studies were carried out on the metabolism of acetylated low density lipoprotein (LDL) by monocyte-derived macrophages from patients with this syndrome. These macrophages showed abnormally high activities for degradation and uptake of 125I-acetylated LDL, incorporation of 14C-oleate into cellular cholesteryl ester in the presence of acetylated LDL, and accumulation of cholesteryl ester derived from internalized 3H-cholesteryl linoleate-labeled acetylated LDL. However, these macrophages showed normal binding of 125I-acetylated LDL. These results indicate that in monocyte-derived macrophages of patients with Werners syndrome, the uptake, lysosomal hydrolysis, and re-esterification of free cholesterol are enhanced with no change in the receptor binding of acetylated LDL. As a result, these macrophages ...
BLM (ENST00000355112.8) at chr15:90717346-90816166 - Homo sapiens BLM RecQ like helicase (BLM), transcript variant 4, mRNA. (from RefSeq NM_001287248) BLM (ENST00000648453.1) at chr15:90717363-90815342 - Bloom syndrome RecQ like helicase (from HGNC BLM) BLM (ENST00000560821.1) at chr15:90808771-90815629 - Bloom syndrome RecQ like helicase (from HGNC BLM) BLM (ENST00000560559.1) at chr15:90790289-90794357 - Bloom syndrome RecQ like helicase (from HGNC BLM) BLM (ENST00000560509.5) at chr15:90717394-90815333 - Homo sapiens BLM RecQ like helicase (BLM), transcript variant 3, mRNA. (from RefSeq NM_001287247) BLM (ENST00000560136.5) at chr15:90762396-90811327 - Bloom syndrome RecQ like helicase (from HGNC BLM) BLM (ENST00000559724.5) at chr15:90717404-90815328 - The sequence shown here is derived from an Ensembl automatic analysis pipeline and should be considered as preliminary data. (from UniProt H0YLV8) BLM (ENST00000559426.5) at chr15:90762364-90769181 - Bloom syndrome RecQ like helicase (from ...
Participates in DNA replication and repair. Exhibits a magnesium-dependent ATP-dependent DNA-helicase activity that unwinds single- and double-stranded DNA in a 3-5 direction (By similarity).
p>The checksum is a form of redundancy check that is calculated from the sequence. It is useful for tracking sequence updates.,/p> ,p>It should be noted that while, in theory, two different sequences could have the same checksum value, the likelihood that this would happen is extremely low.,/p> ,p>However UniProtKB may contain entries with identical sequences in case of multiple genes (paralogs).,/p> ,p>The checksum is computed as the sequence 64-bit Cyclic Redundancy Check value (CRC64) using the generator polynomial: x,sup>64,/sup> + x,sup>4,/sup> + x,sup>3,/sup> + x + 1. The algorithm is described in the ISO 3309 standard. ,/p> ,p class="publication">Press W.H., Flannery B.P., Teukolsky S.A. and Vetterling W.T.,br /> ,strong>Cyclic redundancy and other checksums,/strong>,br /> ,a href="http://www.nrbook.com/b/bookcpdf.php">Numerical recipes in C 2nd ed., pp896-902, Cambridge University Press (1993),/a>),/p> Checksum:i ...
... is a rare genetic condition that causes accelerated aging. Affected individuals usually display normal growth and development during childhood but then lack a normal growth spurt at puberty. As a result, they are typically short in height. Those with the condition also typically have unique facial features that include a beaked nose and prominent eyes. Individuals with Werner syndrome usually notice the first signs of rapid aging during their twenties. These first symptoms may include graying or loss of hair, a hoarse voice, and the development of thinner, rougher skin. In the individuals thirties, more advanced signs of aging will likely begin. These include cloudy eye lenses (cataracts), sores or open wounds on the skin (ulcers), type II diabetes, thinning of bones (osteoporosis), various types of cancer, and a decrease or loss of fertility and other genital functioning (hypogonadism). Most affected individuals pass away in their late forties to early fifties from conditions ...
Complete information for BLM gene (Protein Coding), Bloom Syndrome RecQ Like Helicase, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Michael Fry The author is in the Department of Biochemistry, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Post Office Box 9649, Bat Galim Haifa 31096, Israel. E-mail: [email protected] http://sageke.sciencemag.org/cgi/content/full/sageke;2002/13/re2 Key Words: Werner helicase exonuclease progeroid progeria DNA replication DNA repair. Abstract: Werner syndrome (WS) is an autosomal recessive condition characterized by an early onset of age-related symptoms that include ocular cataracts, premature graying and loss of hair, arteriosclerosis and atherosclerosis, diabetes mellitus, osteoporosis, and a high incidence of some types of cancers. A major motivation for the study of WS is the expectation that elucidation of its underlying mechanisms will illuminate the basis for "normal" aging. In 1996, the gene responsible for the syndrome was positionally cloned. This advance launched an explosion of experiments aimed at unraveling the molecular mechanisms that lead to ...
causes a rapid bone marrow failure in mice that involves cells from across the myeloid, lymphoid, and, most profoundly, erythroid lineages. Apoptosis was markedly elevated in multipotent progenitors lacking RECQL4 compared with WT cells. While the stem cell compartment was relatively spared in RECQL4-deficent mice, HSCs from these animals were not transplantable and even selected against. The requirement for RECQL4 was intrinsic in hematopoietic cells, and loss of RECQL4 in these cells was associated with increased replicative DNA damage and failed cell-cycle progression. Concurrent deletion of p53, which rescues loss of function in animals lacking the related helicase BLM, did not rescue BM phenotypes in RECQL4-deficient animals. In contrast, hematopoietic defects in cells from ...
Loss of WRN causes the genomic instability progeroid syndrome, Werner syndrome. WRN encodes a multifunctional nuclear protein with 3--|5 exonuclease and 3--|5 helicase activities. Linear plasmids with noncompatible ends introduced to Werner syndrome cells underwent extensive deletions at n …
Clinical Synopsis- Short stature - Stocky trunk - Scleroderma - like skin, especially of face and distal extremities - Subcutaneous calcification - Ulceration - [Hair] - Thin, sparse, ... Premature balding ... - Prematurely aged face - Beaked nose ... - Cataracts - Retinal degeneration ... Premature arteriosclerosis ... Diabetes mellitus - Hypogonadism ... - Osteoporosis ... Malignancy in approximately 10 % - Osteosarcoma and meningioma especially ... - Variegated translocation mosaicism in cultured fibroblasts - Poor mitogenic response to growth factors ... Autosomal recessive ... The features of Werner syndrome are scleroderma - like skin changes, especially in the extremities, cataract, subcutaneous calcification, premature arteriosclerosis, diabetes mellitus, and a wizened and prematurely aged facies ... habitus is characteristic, with short stature, slender limbs, and stocky trunk. The nose is beaked ... Malignancy was frequent in the patients and in the families generally ... osteosarcoma ...
C16orf57 Full-Length MS Protein Standard (NP_078874), Labeled with [U- 13C6, 15N4]-L-Arginine and [U- 13C6, 15N2]-L-Lysine, was produced in human 293 cells (HEK293) with fully chemically defined cell culture medium to obtain incorporation efficiency at Creative-Proteomics. This gene encodes a protein with several conserved domains, however, its exact function is not known. Mutations in this gene are associated with poikiloderma with neutropenia (PN), which shows phenotypic overlap with Rothmund-Thomson syndrome (RTS) caused by mutations in the RECQL4 gene. It is believed that this gene product interacts with RECQL4 protein via SMAD4 proteins, explaining the partial clinical overlap between PN and RTS. Alternatively spliced transcript variants encoding different isoforms have been noted for this gene.
Blooms syndrome (BS) is an autosomal recessive disease, caused by mutations in the BLM gene. This gene codes for BLM protein, which is a helicase involved in DNA repair. DNA repair is especially impo
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Our group studies the process of homologous recombination. We focus on the DNA motor protein complexes or DNA nano-machines responsible for driving this process. These machines are frequently coupled to, or powered by, DNA helicases. DNA helicases are ubiquitous enzymes whose primary function is to unwind DNA duplexes into their component single strands, a process that is coupled to the hydrolysis of nucleoside 5-triposphates. Our work is aimed at understanding the biochemical mechanism of DNA helicases and how these mechanisms contribute to and are adapted to the processes of recombination and DNA repair.. To see how DNA nano-machines put it all together, we use state-of-the-art single molecule techniques to visualize in real time, the dynamic properties of DNA nan-machines that are lost in the averaging process using conventional ensemble assays. Single molecule manipulation and observation techniques provide an unparalleled and dramatic means to study biological reactions. The two techniques ...
... : Werner are one of my favorite Bands from Italy. Before them, Ka Mate Ka Ora, which Stefano Venturini, - vocals and guitars there and now here -, ...
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The Blooms syndrome (BS) gene, BLM, plays an important role in the maintenance of genomic stability in somatic cells. The BLM protein is a 1417 amino…
The Blooms syndrome (BS) gene, BLM, plays an important role in the maintenance of genomic stability in somatic cells. The BLM protein is a 1417 amino…
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Like all truly great films, Werner Herzog's hallucinatory Amazonian adventure announces itself as something special in its first shots.
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Werner syndrome is a progeroid disorder characterized by premature age-related phenotypes. Although it is well established that autosomal recessive mutations in the WRN gene is responsible for Werner syndrome, the molecular alterations that lead to disease phenotype remain still unidentified. To address whether epigenetic changes can be associated with Werner syndrome phenotype, we analysed genome-wide DNA methylation profile using the Infinium MethylationEPIC BeadChip in the whole blood from three patients affected by Werner syndrome compared with three age- and sex-matched healthy controls. Hypermethylated probes were enriched in glycosphingolipid biosynthesis, FoxO signalling and insulin signalling pathways, while hypomethylated probes were enriched in PI3K-Akt signalling and focal adhesion pathways. Twenty-two out of 47 of the differentially methylated genes belonging to the enriched pathways resulted differentially expressed in a publicly available dataset on Werner syndrome fibroblasts.
Laure Crabbe, Ramiro E. Verdun, Candy I. Haggblom, and Jan Karlseder http://sageke.sciencemag.org/cgi/content/abstract/2004/50/or22 Abstract: Science 306, 1951-1953 (2004).. Cells from Werner syndrome patients are characterized by slow growth rates, premature senescence, accelerated telomere shortening rates, and genome instability. The syndrome is caused by the loss of the RecQ helicase WRN, but the underlying molecular mechanism is unclear. Here we report that cells lacking WRN exhibit deletion of telomeres from single sister chromatids. Only telomeres replicated by lagging strand synthesis were affected, and prevention of loss of individual telomeres was dependent on the helicase activity of WRN. Telomere loss could be counteracted by telomerase activity. We propose that WRN is necessary for efficient replication of G-rich telomeric DNA, preventing telomere dysfunction and consequent genomic instability.. [Abstract/Full Text]. ...
The Werner protein (WRN) is encoded by the WRN gene. Mutations in this gene are the causal factor for the outset of an autosomal recessive progerid disorder known as Werner Syndrome. WRN has been proposed to function in ALT, a pathway that maintains telomere length independent of telomerase and involves high level of recombination processes observed in about 15% of cancer cells. These functions are probably accomplished by the interactions between WRN and many other proteins. Thus I studied the WRN complex formation in ALT cells to further investigate the potential role of WRN in ALT pathway. In this study, I used CCL75.1 cell as a representative for ALT cell lines and synchronized CCL75.1 cells to S phase using optimized double thymidine block. I found out that the optimal condition for harvesting S phase CCL75.1 cells was as follows: cells were blocked with media containing 4 mM thymidine for 18 hours, released in regular media for 9 hours, blocked again in 4 mM thymidine media for 19 hours ...
RAPADILINO syndrome is a rare condition that involves many parts of the body. Bone development is especially affected, causing many of the characteristic features of the condition.. Most affected individuals have underdevelopment or absence of the bones in the forearms and the thumbs, which are known as radial ray malformations. The kneecaps (patellae) can also be underdeveloped or absent. Other features include an opening in the roof of the mouth (cleft palate) or a high arched palate; a long, slender nose; and dislocated joints.. Many infants with RAPADILINO syndrome have difficulty feeding and experience diarrhea and vomiting. The combination of impaired bone development and feeding problems leads to slow growth and short stature in affected individuals.. Some individuals with RAPADILINO syndrome have harmless light brown patches of skin that resemble a skin finding known as café-au-lait spots. In addition, people with RAPADILINO syndrome have a slightly increased risk of developing a type ...
Werner syndrome (WS) is a premature aging disorder caused by WRN protein deficiency. Here, we report on the generation of a human WS model in human embryonic stem cells (ESCs). Differentiation of WRN-null ESCs to mesenchymal stem cells (MSCs) recapitulates features of premature cellular aging, a global loss of H3K9me3, and changes in heterochromatin architecture. We show that WRN associates with heterochromatin proteins SUV39H1 and HP1α and nuclear lamina-heterochromatin anchoring protein LAP2β. Targeted knock-in of catalytically inactive SUV39H1 in wild-type MSCs recapitulates accelerated cellular senescence, resembling WRN-deficient MSCs. Moreover, decrease in WRN and heterochromatin marks are detected in MSCs from older individuals. Our observations uncover a role for WRN in maintaining heterochromatin stability and highlight heterochromatin disorganization as a potential determinant of human aging. ...
The protein encoded by this gene is a DNA helicase that belongs to the RecQ helicase family. DNA helicases unwind double-stranded DNA into single-stranded DNAs and may modulate chromosome segregation. This gene is predominantly expressed in thymus and testis. Mutations in this gene are associated with Rothmund-Thomson, RAPADILINO and Baller-Gerold syndromes. [provided by RefSeq, Jan 2010 ...
Blooms syndrome (BS) is a recessive human genetic disorder characterized by short stature, immunodeficiency and elevated risk of malignancy. BS cells have genomic instability and an increased frequency of sister chromatid exchange. The gene mutated in BS, BLM, encodes a 3′-5′ helicase (BLM) with homology to bacterial recombination factor, RecQ. Human males homozygous for BLM mutations are infertile and heterozygous individuals display increased frequencies of structural chromosome abnormalities in their spermatozoa. Also, mutations in the Saccharomyces cerevisiae homolog of BLM, Sgs1, cause a delay in meiotic nuclear division and a reduction in spore viability. These observations suggest that BLM may play a role during meiosis. Our antibodies raised against the C terminus of the human protein specifically recognize both mouse and human BLM in western blots of cell lines and in successive developmental stages of spermatocytes, but fail to detect BLM protein in a cell line with a C-terminally ...
RECQL4 is located on the q arm of chromosome 8 and is 6,562 bases long ranging from 144,511,284 to 144,517,845 base pairs pter. It contains 21 exons and translates into a 1208aa long protein with a molecular weight of 133,077Da. 4 paralogs of this gene exist. The protein exhibits a unique Sld-2 like N-terminal domain thought to be essential for initiating DNA replication, as well as helicase domains with 7 nucleic acid binding consensus motifs. RECQL4 is variably expressed in the nucleus in most tissues. The gene is most expressed in the testis, thymus, skin, and bone marrow. Protein expression is most abundant in dividing cells and in the lung. Over 40 loss of function homozygous and compound heterozygous RECQL4 mutations are associated with 60% of Rothmund-Thomson Syndrome (RTS) cases; RTS cases are at a high risk of developing osteosarcoma. RECQL4 is the only gene linked to RTS; cytogenetic abnormalities in chromosome 8 including partial duplication, trisomy, and tetrasomy were reported in ...
We studied a new cellular model for Blooms syndrome consisting of HeLa cells constitutively expressing a shRNA specific for BLM and transiently transfected with a pool of siRNAs directed against sequences other than that targeted by shBLM. These cells display the growth defect, cytogenetic features (high levels of SCE), and mitotic abnormalities (anaphase bridges and lagging chromosomes) typical of Blooms syndrome cells.. We found that SCE formation in response to BLM depletion was strictly dependent on RAD51, showing an epistatic interaction between the two genes. In mammalian cells, RAD51 involvement has been reported in the formation of induced, but not spontaneous, SCEs (32), suggesting that the SCEs in Blooms syndrome cells are induced. Thus, the constitutively high levels of RAD51-mediated SCEs in Blooms syndrome cells are probably induced by the decrease in fork velocity in these cells, which may render them susceptible to DNA breaks (33, 34). RAD51 would then be recruited to the ...
Rabbit monoclonal antibody raised against a human RECQL5 peptide using ARM Technology. A synthetic peptide of human RECQL5 is used for rabbit immunization.Customer or Abnova will decide on the preferred peptide sequence. (H00009400-K) - Products - Abnova
Progeria is a type of genetic disorder where aging is rapid and premature. There are different genetic disorders with this condition. All of them reflect rapid premature aging in victims. Collectively, they are called progeroid syndromes. But they...
It was December of 2013 when Werner and his wife Barb flew from Edmonton to Kelowna . Their purpose was to put a face to the real person, Donna Roth , who they heard had a totally different approach to cancer. Werner was diagnosed with prostate cancer. His doctor stated, "This is a dense and very aggressive cancer." Werner was devastated. He was horrified. The world came crashing down on him. He was not prepared for this! At this point Werner decided that an alternative would be the way to go and if that did not work he would do the hormone treatment. That approach did not really appeal to Werner as the side effects were nasty. Even Dr. John, diagnosed with prostate cancer , whose story is written in Donnas book ,Practical Solution to the Cancer Injury, refused hormone treatment. Werner and Barb listened to Donna Roth share the many testimonials she had witnessed in the past." I liked the success stories. Donna had worked with a number of people who had cancer very successfully and she had a ...
Frye, Stephan Alfons; Balasingham, Seetha; Beyene, Getachew Tesfaye; Homberset, Håvard; Namouchi, Amine & Tonjum, Tone (2016). Meningococcal DNA binding and unwinding proteins. Show summary Background: DNA helicases are a ubiquitous group of enzymes that use the energy of nucleoside triphosphate (dNTP) hydrolysis to catalyze the separation of double-stranded DNA (dsDNA). Helicases are involved in essentially every step in DNA metabolism, including replication, DNA repair, recombination, transcription, Holliday junction movement, and displacement of proteins from DNA. We investigated the DNA helicases RecG and DinG from Neisseria meningitidis (NmRecG and NmDinG) and their roles during genotoxic stress, including DNA damage. These helicases belong to superfamily 2, are ATP dependent and exert 5′to 3′ directionality. Our aim was to define the potential roles of NmRecG and NmDinG in DNA repair, recombination and replication (3R). Methods and results: Cell lysates from Nm wildtype and recG and ...