Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “DNA sensing”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 613 records · Page 34Linked to original sources
PubMed1997

A bacterial group II intron encoding reverse transcriptase, maturase, and DNA endonuclease activities: biochemical demonstration of maturase activity and insertion of new genetic information within the intron.

The Lactococcus lactis group II intron Ll.ltrB is similar to mobile yeast mtDNA group II introns, which encode reverse transcriptase, RNA maturase, and DNA endonuclease activities for site-specific DNA insertion. Here, we show that the Lactococcal intron can be expressed and spliced efficiently in Escherichia coli. The intron-encoded protein LtrA has reverse transcriptase and RNA maturase activities, with the latter activity shown both in vivo and in vitro, a first for any group II intron-encoded protein. As for the yeast mtDNA introns, the DNA endonuclease activity of the Lactococcal intron is associated with RNP particles containing both the intron-encoded protein and the excised intron RNA. Also, the intron RNA cleaves the sense-strand of the recipient DNA by a reverse splicing reaction, whereas the intron-encoded protein cleaves the antisense strand. The Lactococcal intron endonuclease can be obtained in large quantities by coexpression of the LtrA protein with the intron RNA in E. coli or reconstituted in vitro by incubating the expressed LtrA protein with in vitro-synthesized intron RNA. Furthermore, the specificity of the endonuclease and reverse splicing reactions can be changed predictably by modifying the RNA component. Expression in E. coli facilitates the use of group II introns for the targeting of specific foreign sequences to a desired site in DNA.

Bacterial Proteins↗
PubMed2005

The ataxia telangiectasia-mutated and Rad3-related protein is dispensable for retroviral integration.

Integration into the host cell DNA is an essential part of the retroviral life cycle and is required for the productive replication of a retrovirus. Retroviral integration involves cleavage of the host DNA and insertion of the viral DNA, forming an integration intermediate that contains two gaps, each with a viral 5' flap. The flaps are then removed, and the gap is filled by as yet unidentified nuclease and polymerase activities. It is thought that repair of these gaps flanking the site of retroviral integration is achieved by host DNA repair machinery. The ATM and Rad3-related protein (ATR) is a member of the phosphatidylinositol 3 kinase-related family of protein kinases that play a major role in sensing and triggering repair of DNA lesions in mammalian cells. In an effort to examine the role of ATR in retroviral integration, we used RNA interference to selectively downregulate ATR and measured integration efficiency. In addition, we examined the possible role that Vpr may play in enhancing integration and, in particular, whether activation of ATR by Vpr (Roshal et al., J. Biol. Chem. 278:25879-25886, 2003) will favor human immunodeficiency virus type 1 integration. We conclude that cells in which ATR has been depleted are competent for retroviral integration. We also conclude that the presence of Vpr as a virion-bound protein does not enhance integration of a lentivirus vector in dividing cells.

Animals↗
PubMed2004

Association between up-regulation of stress-responsive genes and hypomethylation of genomic DNA in tobacco plants.

Transcripts that specifically accumulate in transgenic tobacco plants expressing an anti-sense construct for a tobacco type I DNA methyltransferase, NtMET1, were screened by the differential display method. Of the 31 genes identified, 16 encoded proteins with known functions; ten of these were related to biotic and abiotic stress responses, and the other six to cellular functions. In order to examine whether expression of these genes is correlated with DNA methylation status under natural stress conditions, a pathogen-responsive gene (NtAlix1) was selected as representative, and assayed for transcript induction and genomic methylation in tobacco plants infected with tobacco mosaic virus (TMV). In inoculated leaves of wild-type plants, NtAlix1 transcripts began to accumulate 12 h after the onset of the hypersensitive response (HR), and levels remained high for up to 24 h. Changes in the methylation status at the locus became obvious 24 h later, as detected by digestion of genomic DNA with a methylation-sensitive restriction enzyme. The results suggest that the level of DNA methylation may change in response to external stresses, and that this is closely related to the activation of stress-responsive genes.

Amino Acid Sequence↗
PubMedDate not supplied

[Fanconi anemia: genes and function(s) revisited].

Fanconi anemia (FA), a rare inherited disorder, exhibits a complex phenotype including progressive bone marrow failure, congenital malformations and increased risk of cancers, mainly acute myeloid leukaemia. At the cellular level, FA is characterized by hypersensitivity to DNA cross-linking agents and by high frequencies of induced chromosomal aberrations, a property used for diagnosis. FA results from mutations in one of the eleven FANC (FANCA to FANCJ) genes. Nine of them have been identified. In addition, FANCD1 gene has been shown to be identical to BRCA2, one of the two breast cancer susceptibility genes. Seven of the FANC proteins form a complex, which exists in four different forms depending of its subcellular localisation. Four FANC proteins (D1(BRCA2), D2, I and J) are not associated to the complex. The presence of the nuclear form of the FA core complex is necessary for the mono-ubiquitinylation of FANCD2 protein, a modification required for its re-localization to nuclear foci, likely to be sites of DNA repair. A clue towards understanding the molecular function of the FANC genes comes from the recently identified connection of FANC to the BRCA1, ATM, NBS1 and ATR genes. Two of the FANC proteins (A and D2) directly interact with BRCA1, which in turn interacts with the MRE11/RAD50/NBS1 complex, which is one of the key components in the mechanisms involved in the cellular response to DNA double strand breaks (DSB). Moreover, ATM, a protein kinase that plays a central role in the network of DSB signalling, phosphorylates in vitro and in vivo FANCD2 in response to ionising radiations. Moreover, the NBS1 protein and the monoubiquitinated form of FANCD2 seem to act together in response to DNA crosslinking agents. Taken together with the previously reported impaired DSB and DNA interstrand crosslinks repair in FA cells, the connection of FANC genes to the ATM, ATR, NBS1 and BRCA1 links the FANC genes function to the finely orchestrated network involved in the sensing, signalling and repair of DNA replication-blocking lesions.

Chromosome Aberrations↗
PubMed1983

The consequences of base-pair substitution mutations in AT- and GC-rich bacteria.

The likely consequences, in terms of premature stop codons, detectable missense mutants, silent missense mutants, and degenerate codon changes, have been determined for all 12 individual base substitution changes. This has been done for the full, 61 sense codon, genetic code and also for the much more limited codon availabilities of AT- or GC-rich DNA. The specificities and outcomes of individual base substitutions are likely to be rather different at AT- or GC-rich extremes, and also from the situation at an intermediate DNA base-ratio where all 61 sense codons are available. In particular, at DNA base-ratio extremes many mutations will be to non-utilized codons, which may well act as nonsense mutants. These in turn will give novel classes of suppressor-containing revertants. Even in bacteria with intermediate DNA base-ratios, particular codons for a given amino acid may be favoured, over alternatives, because their use maximizes, or minimizes, the mutational consequences of one, or more, base substitution changes.

Adenine↗
PubMed1992

Making sense from antisense: a review of experimental data and developing ideas on sense--antisense peptide recognition.

Peptides encoded in the antisense strand of DNA have been predicted and found experimentally to bind to sense peptides and proteins with significant selectivity and affinity. Such sense--antisense peptide recognition has been observed in many systems, most often by detecting binding between immobilized and soluble interaction partners. Data obtained so far on sequence and solvent dependence of interaction support a hydrophobic-hydrophilic (amphipathic) model of peptide recognition. Nonetheless, the mechanistic understanding of this type of molecular recognition remains incomplete. Improving this understanding likely will require expanding the types of characteristics measured for sense--antisense peptide complexes and hence the types of analytical methods applied to such interactions. Understanding the mechanism of sense--antisense peptide recognition also may provide insights into mechanisms of native (sense) peptide and protein interactions and protein folding. Such insight may be helpful to learn how to design macromolecular recognition agents in technology for separation, diagnostics and therapeutics.

Amino Acid Sequence↗
PubMed1996

Zn2+-sensing by the cyanobacterial metallothionein repressor SmtB: different motifs mediate metal-induced protein-DNA dissociation.

SmtB is a member of a family of repressors which dissociate from DNA in the presence of metals; Zn2+ being the most potent inducer of metallothionein gene (smtA) transcription in vivo. In Synechococcus PCC 7942 cells devoid of chromosomal smtB, four plasmid-encoded mutants of SmtB (C61S, T11S/C14S, C121S and H105R/H106R) repressed lacZ expression driven by the smtA operator-promoter. Gel retardation assays with extracts from the complemented cells detected multiple SmtB-dependent complexes similar to those obtained with extracts from wild-type cells or with recombinant-SmtB. Elevated [Zn2+] alleviated repression in vivo by all of the mutants except H105R/H106R. These His residues (one or both) are therefore essential for Zn2+-sensing while, contrary to expectations, Cys residues are not. Hence different motifs facilitate metal-induced DNA-dissociation by SmtB and ArsR (the related oxyanion-sensing repressor), presumably generating variety in the spectra of metals sensed. Nucleotides and amino acids involved in DNA-SmtB interaction have been further defined/inferred and we also confirm that additional unknown factors form specific associations with the smt operator-promoter in elevated [Zn2+].

Amino Acid Sequence↗
PubMed2003

Potentiation of chemotherapeutic agents following antagonism of nuclear factor kappa B in human gliomas.

Future success using chemotherapy against human gliomas may result from exploiting unique molecular vulnerabilities of these tumors. Chemotherapy frequently results in DNA damage. When such damage is sensed by the cell, programmed cell death, or apoptosis, may be initiated. However, chemotherapy-induced DNA damage may activate nuclear factor kappa B (NF-kappaB) and block apoptosis. We inhibited NF-kappaB using a gene therapy approach to determine whether this would render human glioma cells more susceptible to chemotherapy. U87 and U251 glioma cell lines were infected with either treatment adenovirus containing the gene for a mutant non-degradable form of IkappaBalpha, which is an inhibitor of NF-kappaB nuclear translocation, or empty control virus. Following viral infection, cells were treated either with BCNU, carboplatin, tumor necrosis factor alpha (TNF-alpha), or SN-38. Chemotherapy resulted in a marked increase in active intranuclear NF-kappaB. This response was greatly decreased by insertion of the mutant repressor gene. Similarly, a significant increase in cell killing by all chemotherapy age was demonstrated following infection with treatment virus. Expression of the mutant repressor gene also resulted in increased apoptosis by TUNEL assay following chemotherapy. Numerous genes are responsible for glioma chemoresistance. DNA damage by chemotherapy may induce the antiapoptotic factor NF-kappaB and prevent programmed cell death. Insertion of a mutant inhibitor of NF-kappaB strips cells of this antiapoptotic defense and renders them more susceptible to killing by chemotherapy via increased apoptosis.

Adenoviridae↗
PubMed2002

Natural transformation of Pseudomonas stutzeri by single-stranded DNA requires type IV pili, competence state and comA.

Pseudomonas stutzeri, in addition to being transformed by duplex DNA, is also transformed by the sense or antisense strand of the genetic marker employed (hisX(+)) or by heat-denatured chromosomal DNA. Transformation was absent in non-competent cells and in mutants defective for pilus biogenesis (pilA, pilC) and function (pilT) or DNA translocation into the cytoplasm (comA). Uptake of (3)H-thymidine-labeled single-stranded DNA was hardly detectable reflecting the 20- to 60-fold lower transformation compared to duplex DNA. The results suggest that the steps in natural transformation also accommodate single-stranded DNA and that DNA translocation from the periplasm into the cytoplasm is not necessarily coupled to the degradation of a complementary strand. Small DNA single-stranded fragments are thus not excluded from horizontal gene transfer by transformation.

Bacterial Proteins↗
PubMed2003

UV radiation-induced enterobacterial responses, other processes that influence UV tolerance and likely environmental significance.

The ability of enterobacteria to become UV-tolerant is important because such tolerance may enable organisms to resist irradiation in the environment, in water treatment, in shell-fish, in stages of food processing, and at locations in the domestic, commercial and hospital environment The mechanism for regulation of tolerance induction and SOS response induction has been studied for many years, and is well understood, except for the early stages of induction. Such early stages, namely sensing of the stimulus (UV irradiation) and the way in which such sensing leads to signal production, have until now been poorly understood. The claim has been made that DNA is the sensor and that either damage to DNA or production of SS regions in DNA (following interaction of UV with DNA) triggers the signal that sets in train RecA activation and other stages of tolerance induction. This claimed induction mechanism is a "classical" one in the sense that it involves intracellular sensing (by DNA) of the stressing stimulus (UV), and production of an intracellular signalling molecule. It is not, however, firmly established as the mechanism for initiation of UV tolerance induction and SOS response induction. The results reviewed here give firm evidence for a different and unique mechanism for sensing of UV and production of the signal. These results establish without doubt that, for UV tolerance induction, the UV sensor is an extracellular protein, which is a UV tolerance-specific extracellular sensing component (ESC). This component is formed by unstressed cells and on interacting with the stimulus (UV) in the medium, is converted to the tolerance induction signalling molecule, which is a UV tolerance-specific extracellular induction component (EIC). It is this extracellular signal which interacts with the sensitive organisms and triggers tolerance induction. This pair of extracellular components (ECs) may offer the only means of switching-on such tolerance induction; certainly they offer the only known way for early warning to be given of impending UV challenge. Thus, the EIC can diffuse from a region of UV stress to a stress-free region and there warn organisms of impending stress and prepare them to resist it. As indicated here, UV irradiation not only induces UV tolerance, but also switches-on acid tolerance, alkali tolerance and thermotolerance responses. The fact that all three responses involve ESC/EIC pairs strongly supports the view that functioning of such EC pairs form the major, if not the only, means for UV tolerance induction. The UV tolerance-specific ESC can detect other stresses and becomes activated, leading to cross-tolerance responses. Of particular interest, this ESC acts as a biological thermometer, detecting increases in temperature, such increases leading to gradually increasing formation of the EIC and, accordingly, gradual increases in UV tolerance. This UV tolerance-specific ESC can also detect other stresses e.g. acting as a pH sensor. In all cases, on activation, the EIC formed (from this specific ESC) only induces UV tolerance. It is proposed that the interaction of EICs with stress-sensitive organisms should be examined, and it is suggested that such EICs may, directly or indirectly, interact with and activate the same stress response regulators as are used to detect internal stressors and which, on activation, also trigger the switching-on of stress responses. For example, EICs either a in a protonated or oxidised state (formed by activation of ESCs by H+ or H2O2) or b produced by irradiation, may lead to protonation or oxidation or other forms of activation of the appropriate regulator (e.g. Fur or OxyR or RecA etc), leading to response induction.

DNA Damage↗
PubMed2003

Sensing phenothiazine drugs at a gold electrode co-modified with DNA and gold nanoparticles.

DNA and gold nanoparticles are co-immobilized at a gold electrode through elaborate self-assembly processes. This configuration has proven to be useful as a sensor for phenothiazine drugs, taking advantage of the well-known, relatively large surface area of gold nanoparticles and the strong intercalation between dsDNA and phenothiazine drugs. This modified electrode has demonstrated good sensitivity and stability towards the oxidation of two model phenothiazine drugs: promethazine and chlorpromazine. A linear dependence between the concentration of phenothiazine drugs and the peak current is observed, with a concentration range of 2.0 x 10(-5)-1.6 x 10(-4) M and 1.0 x 10(-5)-1.2 x 10(-4) M, and a detection limit of 1.0 x 10(-5) M and 7.0 x 10(-6) M, for promethazine and chlorpromazine, respectively.

Animals↗
PubMed1984

Unusual regulation of simian virus 40 early-region transcription in genomes containing two origins of DNA replication.

As part of our efforts to create multifunctional vectors for the transduction of animal cells, a set of simian virus 40 recombinants were constructed which contain an inverted duplication of the region including the origin of viral DNA replication (ori) and the early-region promoter. The unusual aspects of the structure of these recombinant genomes revealed several unexpected features of their function. In particular, transcription from the early-region promoters on these recombinants occurred primarily after the start of DNA replication, and, in that sense, these promoters behaved as if they were late-region promoters. This behavior results from the fact that these genomes contain multiple ori segments, and, therefore, they replicate earlier and faster than wild-type virus DNA, thereby causing a precocious shift in the initiation of early-region transcription from sites downstream of ori to sites located upstream of ori. The abnormal expression from multiple ori genomes is consistent with our present notions regarding the replication-dependent shift in early-region transcriptional start sites (Buchman et al., Mol. Cell. Biol. 4:1900-1914). Since our experiments demonstrate that RNAs initiated upstream of ori contribute to T-antigen formation late in infection, we suggest that the shift in early-region transcription starts modulates large T-antigen production in concert with viral DNA replication.

Animals↗
PubMed1993

Altered expression of nerve growth factor in the skin of transgenic mice leads to changes in response to mechanical stimuli.

It has recently become clear that the neurotrophic factor, nerve growth factor, interacts specifically with nociceptive sensory neurons during development and maturity. Indeed, it may serve as a critical link between inflammation and the hyperalgesia that ensues in adult animals. Nerve growth factor is normally expressed in limiting amounts in target tissues of sensory and postganglionic sympathetic neurons. In the present study we have altered the basal level of nerve growth factor expression in the skin by producing transgenic mice that express a fusion gene construct containing either a sense or antisense nerve growth factor complementary DNA linked to the K14 keratin promoter. The K14-nerve growth factor transgene (sense or antisense) is abundantly expressed in skin from approximately embryonic day 15 and is then constitutively expressed throughout the life of the animal. In light of the fact that systemic administration of nerve growth factor to neonatal or adult rats leads to hyperalgesia, we have asked whether mice expressing the sense K14-nerve growth factor transgene exhibit similar sensory abnormalities and whether mice expressing the antisense nerve growth factor complementary DNA were hypoalgesic. Here we show that mice over-expressing nerve growth factor in skin display a profound hyperalgesia to noxious mechanical stimulation. Additionally, K14-nerve growth factor antisense mice displayed a profound hypoalgesia to the same stimuli.

Animals↗
PubMed1949

Quantitative cytochemical determination of desoxyribonucleic acid with the Feulgen nucleal reaction.

The possibility of using the Feulgen nucleal reaction for a quantitative cytochemical estimation of desoxyribonucleic acid (DNA) was investigated. The intensity of the reaction in nuclei was determined by absorption measurements with the microscope. The accuracy of such measurements was tested by comparison with measurements on the same material with a Beckman spectrophotometer. The values obtained with the microscope agreed within a few per cent with those obtained with the Beckman spectrophotometer. Furthermore, the errors introduced by uneven distribution of absorbing material, by variations in the numerical aperture of the system, and by variation in the area used on the phototube were investigated empirically. The following variables were studied with regard to their effect on the intensity of the Feulgen reaction: type of fixation, time of hydrolysis after acetic acid-alcohol and formalin fixation, time of staining in leucobasic fuchsin, method of preparation of leucobasic fuchsin. The intensity of the Feulgen reaction in liver and erythrocyte nuclei of various vertebrates, fixed in acetic acid-alcohol, was then compared with the DNA content of these nuclei as determined by chemical analysis on a known number of nuclei. The intensity of the reaction was found to be proportional to the DNA content of the nuclei, if nuclei of similar structure and DNA concentration were compared. In nuclei of different structure and DNA concentration (i.e. liver and erythrocyte nuclei), fixed in acetic acid-alcohol, the intensity of the Feulgen reaction was, however, not proportional to the DNA content. This difficulty was overcome by isolating nuclei in sucrose and by fixing them in formalin. Uniform distribution of DNA and therefore uniform coloring after the Feulgen reaction were thus obtained. In such nuclei with uniform distribution of absorbing material the Feulgen reaction was found to be proportional to the DNA content of nuclei, even if they differed greatly in their DNA concentration. The Feulgen nucleal reaction is not quantitative in an absolute sense. For absolute determinations nuclei of known DNA content must be treated together with the unknown material to serve as standard. From these data it therefore appears possible to determine cytochemically relative amounts of DNA in cellular structures by measuring their absorption after treatment with the Feulgen nucleal reaction.

Animals↗
PubMed1993

UV irradiation of Escherichia coli modulates mutagenesis at a site-specific ethenocytosine residue on M13 DNA. Evidence for an inducible recA-independent effect.

Mutagenic action of chemical and physical mutagens is mediated through DNA damage and subsequent misreplication at sites of unrepaired damage. Most DNA damage is noninstructive in the sense that the causative chemical modification either destroys the template information or renders it inaccessible to the DNA polymerase. Noninstructive adducts possess high genotoxicity because they stop DNA replication. Replication past noninstructive adducts is thought to depend on induced functions in addition to the regular replication machinery. In Escherichia coli, noninstructive DNA damage leads to induction of the SOS regulon, which in turn is thought to provide the inducible functions required for replicative bypass of the lesion. Because of the absence of accessible template instruction, base incorporation opposite noninstructive lesions is inherently error-prone and results in mutagenesis. Ethenocytosine (epsilon C), an exocyclic DNA lesion induced by carcinogens such as vinyl chloride and urethane, is a highly mutagenic, noninstructive lesion on the basis of its template characteristics in vivo and in vitro. However, mutagenesis at epsilon C does not require SOS functions, as evidenced by efficient mutagenesis in recA-deleted E. coli. Even though efficient mutagenesis in recA-deleted cells shows a lack of SOS dependence, the question remains whether SOS induction can modulate mutagenesis opposite epsilon C. To examine the possible contribution of SOS functions to mutagenesis at epsilon C, we constructed an M13 duplex circular DNA molecule containing an epsilon C residue at a unique site. The construct was transfected into nonirradiated or UV-irradiated E. coli.(ABSTRACT TRUNCATED AT 250 WORDS)

Bacteriophage M13↗
PubMed2003

A cell surface receptor mediates extracellular Ca(2+) sensing in guard cells.

Extracellular Ca(2+) (Ca(2+)(o)) is required for various physiological and developmental processes in animals and plants. In response to varied Ca(2+)(o) levels, plants maintain relatively constant internal Ca(2+) content, suggesting a precise regulatory mechanism for Ca(2+) homeostasis. However, little is known about how plants monitor Ca(2+)(o) status and whether Ca(2+)(o)-sensing receptors exist. The effects of Ca(2+)(o) on guard cells in promoting stomatal closure by inducing increases in the concentration of cytosolic Ca(2+) ([Ca(2+)](i)) provide a clue to Ca(2+)(o) sensing. Here we have used a functional screening assay in mammalian cells to isolate an Arabidopsis complementary DNA clone encoding a Ca(2+)-sensing receptor, CAS. CAS is localized to the plasma membrane, exhibits low-affinity/high-capacity Ca(2+) binding, and mediates Ca(2+)(o)-induced [Ca(2+)](i) increases. CAS is expressed predominantly in the shoot, including guard cells. Repression of CAS disrupts Ca(2+)(o) signalling in guard cells, and impairs bolting (swift upward growth at the transition to seed production) in response to Ca(2+) deficiency, so we conclude that CAS may be a primary transducer of Ca(2+)(o) in plants.

Amino Acid Sequence↗
PubMed1993

Molecular, biochemical, and functional characteristics of tumor necrosis factor-alpha produced by human placental cytotrophoblastic cells.

Previous studies have shown that the TNF-alpha gene is transcribed and translated in fully differentiated human placental syncytiotrophoblast. In this study, TNF transcripts were identified by in situ hybridization in cytotrophoblastic cells, a progenitor subpopulation that proliferates rapidly in early gestation tissues. To establish molecular and biochemical characteristics of cytotrophoblastic TNF and to evaluate potential utilization, experiments were conducted on two cytotrophoblastic cell lines, Jar and JEG-3. Northern blot hybridization and immunocytochemical tests showed that Jar and JEG-3 cells contained TNF mRNA and specific protein. Enzyme immunoassays demonstrated production of TNF, and immunoprecipitation experiments showed that Jar cell TNF protein was the same molecular mass as macrophage TNF. DNA synthesis in both lines was promoted by rTNF, and experiments employing 17-mer TNF antisense and sense oligonucleotides showed specific inhibition of DNA synthesis by antisense sequences. Both p60 and p80 TNF-R mRNA were present in the choriocarcinoma cell lines, and DNA synthesis was inhibited by antibody to the p60 TNF-R. Although the two lines were similar in many respects, Jar cells produced more TNF and demonstrated a greater reliance on TNF for their growth. Collectively, the results indicate that: 1) the TNF gene is expressed in both normal and malignant cytotrophoblast; 2) certain molecular, immunologic, and biochemical characteristics of trophoblast-derived TNF are similar to macrophage TNF; and 3) the p60 TNF-R facilitates utilization of TNF as an autocrine growth factor by choriocarcinoma cells. Although TNF apparently serves important functions in cytotrophoblast during the course of placental development that might include promotion of proliferation and invasion, constitutive expression of this gene in neoplastic cells could account in part for the remarkable ability of trophoblastic tumors to overcome host defenses.

Base Sequence↗
PubMed1997

Quartz balance DNA sensor.

Single-strand DNA-containing thin films were deposited onto quartz oscillators by the Langmuir-Blodgett technique towards the realization of a device capable of sensing the presence of the complementary DNA sequences which hybridize with the immobilized ones. DNA, once complexed with aliphatic amines, appears as a monolayer in a single-stranded form by X-ray small angle scattering. A quartz nanobalance is then utilized to monitor mass increment related to specific hybridization with a complementary DNA probe. The crystal quartz nanobalance, capable of high sensitivity, indeed appears capable of obtaining a prototype of a device capable of sensing the occurrence of particular genes or sequences in the sample under investigation. The validity of the nanogravimetric assay was confirmed by independent fluorescence measurements utilizing DAPI and a CCD camera.

Biosensing Techniques↗