gebhart/patrepeval huggingface dataset:
Two Pathways for Removal of Nonhomologous DNA Ends during Double-Strand Break Repair in Saccharomyces cerevisiae (1997)

During repair of a double-strand break (DSB) by gene conversion, one or both 3' ends of the DSB invade a homologous donor sequence and initiate new DNA synthesis. The use of the invading DNA strand as a primer for new DNA synthesis requires that any nonhomologous bases at the 3' end be removed. We have previously shown that removal of a 3' nonhomologous tail in Saccharomyces cerevisiae depends on the nucleotide excision repair endonuclease Rad1/Rad10, and also on the mismatch repair proteins Msh2 and Msh3. We now report that these four proteins are needed only when the nonhomologous ends of recombining DNA are 30 nucleotides (nt) long or longer. An additional protein, the helicase Srs2, is required for the RAD1-dependent removal of long 3' tails. We suggest that Srs2 acts to extend and stabilize the initial nascent joint between the invading single strand and its homolog. 3' tails shorter than 30 nt are removed by another mechanism that depends at least in part on the 3'-to-5' proofreading activity of DNA polymerase delta.
Construction of a Bacillus subtilis double mutant deficient in extracellular alkaline and neutral proteases (1984)

A mutant strain of Bacillus subtilis carrying lesions in the structural genes for extracellular neutral (nprE) and serine (aprA) proteases was constructed by the gene conversion technique. This mutant had less than 4% of the extracellular protease activity of the wild type and sporulated normally, indicating that neither of these sporulation-associated proteases is essential for development.
Optical communications for small satellites (2015)

Thesis: Ph. D., Massachusetts Institute of Technology, Department of Aeronautics and Astronautics, 2015.
Synthesis of oligodeoxynucleoside phosphorodithioates via thioamidites (1989)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTSynthesis of oligodeoxynucleoside phosphorodithioates via thioamiditesWolfgang K. D. Brill, Jin Yan Tang, Yun Xi Ma, and Marvin H. CaruthersCite this: J. Am. Chem. Soc. 1989, 111, 6, 2321–2322Publication Date (Print):March 1, 1989Publication History Published online1 May 2002Published inissue 1 March 1989https://pubs.acs.org/doi/10.1021/ja00188a066https://doi.org/10.1021/ja00188a066research-articleACS PublicationsRequest reuse permissionsArticle Views300Altmetric-Citations56LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-Alertsclose Get e-Alerts
Cellular Eukaryotic Initiation Factor 5A Content as a Mediator of Polyamine Effects on Growth and Apoptosis (1997)

The polyamines are essential for eukaryotic cell growth. One of the most critical effects of polyamines on cell growth is the availability of spermidine for the post-translational modification of eIF-5A. Because hypusine-containing eIF-5A is necessary for cell proliferation, depletion of cellular polyamines suppresses growth by depleting cellular modified eIF-5A content. Excess putrescine accumulations in DH23A/b cells induces apoptosis and suppresses the formation of hypusine-containing eIF-5A. Treatment of DH23A/b cells with diaminoheptane also suppresses modified eIF-5A formation and induces apoptosis. These data suggest that suppression of modified eIF-5A formation may play a role in putrescine-induced apoptosis as well.
H+/peptide transporter (PEPT2) is expressed in human epidermal keratinocytes and is involved in skin oligopeptide transport (2016)

Peptide transporter 2 (PEPT2) is a member of the proton-coupled oligopeptide transporter family, which mediates the cellular uptake of oligopeptides and peptide-like drugs. Although PEPT2 is expressed in many tissues, its expression in epidermal keratinocytes remains unclear. We investigated PEPT2 expression profile and functional activity in keratinocytes. We confirmed PEPT2 mRNA expression in three keratinocyte lines (normal human epidermal keratinocytes (NHEKs), immortalized keratinocytes, and malignant keratinocytes) by reverse transcription-polymerase chain reaction (RT-PCR) and quantitative real-time RT-PCR. In contrast to PEPT1, PEPT2 expression in the three keratinocytes was similar or higher than that in HepG2 cells, used as PEPT2-positive cells. Immunolocalization analysis using human skin showed epidermal PEPT2 localization. We studied keratinocyte transport function by measuring the oligopeptide content using liquid chromatography/tandem mass spectrometry. Glycylsarcosine uptake in NHEKs was pH-dependent, suggesting that keratinocytes could absorb small peptides in the presence of an inward H(+) gradient. We also performed a skin-permeability test of several oligopeptides using skin substitute, suggesting that di- and tripeptides pass actively through the epidermis. In conclusion, PEPT2 is expressed in keratinocytes and involved in skin oligopeptide uptake.
Grey matter changes associated with medication-overuse headache: Correlations with disease related disability and anxiety (2012)

These findings are consistent with dysfunction of antinociceptive systems in MOH, which is influenced by anxiety. Dysfunction of the reward system may be a neurobiological basis for dependence in a subgroup of MOH patients.
Bootstrap decoding of low-density parity-check codes (2002)

An initial bootstrap step for the decoding of low-density parity-check (LDPC) codes is proposed. Decoding is initiated by first erasing a number of less reliable bits. New values and reliabilities are then assigned to erasure bits by passing messages from nonerasure bits through the reliable check equations. The bootstrap step is applied to the weighted bit-flipping algorithm to decode a number of LDPC codes. Large improvements in both performance and complexity are observed.
Calorimetric Study of the Glassy State. IV. Heat Capacities of Glassy Water and Cubic Ice (1968)

Abstract By making use of the vapor-condensation type calorimeter, the heat capacity measurements of amorphous, cubic and hexagonal ices were made between 20°K and 250°K. The glass transition phenomenon was found near 135°K with the sudden change of the heat capacity amounting to 35 J/(mol°K). The drastic crystallization with the exothermic effect which amounts to 1.64 kJ/mol was then followed at this temperature. The transformation of the cubic crystal to the hexagonal one was confirmed to occur in the temperature region from 160 to 210°K and to proceed in two steps with the activation energies of 21.3 and 44.7 kJ/mol, respectively. The amount of the exothermic effect accompanying this transformation was found to be about 160 J/mol.
Body water compartments with human aging using fat-free mass as the reference standard (1979)

Forty-five healthy men and women aged 16-39 and 59-89 yr were studied for total body water (TBW) and extracellular water (ECW); intracellular water (ICW) was calculated as the difference (ICW = TBW - ECW). An independent measurement of total body fat by inert gas uptake provided a value (+/- 2%) for fat-free mass (FFB is wt minus body fat). Results agreed with observations by others that TBW and ICW are lower in the aged and lower in women, whether expressed as absolute volumes or per unit of weight, surface area, or height. However, with FFB as the reference standard very different aging trends appeared. TBW/FFB remained constant to our oldest measured subjects (704 +/- 7 ml/kg). ICW/FFB was slightly lower at advanced age, but the 4-5% decrease for each sex was within statistical variability. With age ECW increased slightly and its proportion within the fat-free body (ECW/FFB) was significantly higher. Based upon FFB, the distribution, proportions, and aging trends of body water compartments were similar for men, women, and male rats. Although its potential limitations must be appreciated, the FFB appears widely useful as a reference standard. The stability of ICW volume and of fat-free mass in aging man does not support the hypothesis that cellular mass is lost by healthy mammals with age.
Vascular endothelial growth factor-toxin conjugate specifically inhibits KDR/flk-1-positive endothelial cell proliferation in vitro and angiogenesis in vivo. (1996)

Inhibition of tumor neovascularization has profound effects on the growth of solid tumors. An endothelial cell-specific cytotoxic conjugate was prepared by chemically linking recombinant vascular endothelial growth factor (VEGF165) and a truncated diphtheria toxin molecule (DT385). The treatment of subconfluent cultures of human umbilical vein endothelial cells and human microvascular endothelial cells with the VEGF165-DT385 conjugate resulted in a selective, dose-dependent inhibition of growth. Parallel experiments with either the free toxin or a mixture of VEGF and the toxin polypeptide did not affect proliferation (DNA synthesis) of these cells. The selective cytotoxicity correlated with the appropriate receptor expression (KDR/flk-1 positive) on the target cells. VEGF-toxin conjugate inhibited the growth of a murine hemangioma-derived endothelial cell line (Py-4-1), which was positive for flk-1 expression. Under similar conditions, the conjugate did not affect the proliferation of a receptor-negative ovarian cancer cell line in vitro. In an in vivo model of angiogenesis, the VEGF165-DT385 conjugate blocked basic fibroblast growth factor-induced neovascularization of the chick chorioallantoic membrane. These studies demonstrate the successful targeting of a cytotoxic polypeptide to proliferating vascular endothelial cells (normal and tumorigenic) and the potential utility of such conjugates in blocking tumor neovascularization.
pH-induced Conformational Transitions of the Propeptide of Human Cathepsin L (1998)

Synthesis of proteases as inactive zymogens is a very important mechanism for the regulation of their activity. For lysosomal proteases proteolytic cleavage of the propeptide is triggered by the acidic pH. By using fluorescence, circular dichroism, and NMR spectroscopy, we show that upon decreasing the pH from 6.5 to 3 the propeptide of cathepsin L loses most of the tertiary structure, but almost none of the secondary structure is lost. Another partially structured intermediate, prone to aggregation, was identified between pH 6.5 and 4. The conformation, populated below pH 4, where the activation of cathepsin L occurs, is not completely unfolded and has the properties of molten globule, including characteristic binding of the 1-anilinonaphthalene-8-sulfonic acid. This pH unfolding of the propeptide parallels a decrease of its affinity for cathepsin L and suggests the mechanism for the acidic zymogen activation. Addition of anionic polysaccharides that activate cathepsin L already at pH 5.5 unfolds the tertiary structure of the propeptide at this pH. Propeptide of human cathepsin L which is able to fold independently represents an evolutionary intermediate in the emergence of novel inhibitors originating from the enzyme proregions.
Implications for RNase L in Prostate Cancer Biology (2003)

Recently, the interferon (IFN) antiviral pathways and prostate cancer genetics and have surprisingly converged on a single-strand specific, regulated endoribonuclease. Genetics studies from several laboratories in the U.S., Finland, and Israel, support the recent identification of the RNase L gene, RNASEL, as a strong candidate for the long sought after hereditary prostate cancer 1 (HPC1) allele. Results from these studies suggest that mutations in RNASEL predispose men to an increased incidence of prostate cancer, which in some cases reflect more aggressive disease and/or decreased age of onset compared with non-RNASEL linked cases. RNase L is a uniquely regulated endoribonuclease that requires 5'-triphosphorylated, 2',5'-linked oligoadenylates (2-5A) for its activity. The presence of both germline mutations in RNASEL segregating with disease within HPC-affected families and loss of heterozygosity (LOH) in tumor tissues suggest a novel role for the regulated endoribonuclease in the pathogenesis of prostate cancer. The association of mutations in RNASEL with prostate cancer cases further suggests a relationship between innate immunity and tumor suppression. It is proposed here that RNase L functions in counteracting prostate cancer by virtue of its ability to degrade RNA, thus initiating a cellular stress response that leads to apoptosis. This monograph reviews the biochemistry and genetics of RNase L as it relates to the pathobiology of prostate cancer and considers implications for future screening and therapy of this disease.
Pain control by ionizing radiation of bone metastasis (2004)

Pain treatment due to cancer is a large fraction of the care in a radiotherapy department. While radiation treatment is very effective in reducing pain, the pathophysiology of bone metastases remains very complex. Reducing the number of tumour cells by radiation will reduce the pressure in bone marrow, but the very rapid response to radiation treatment seen in some patients is probably related to the presence of highly radiosensitive inflammatory cells. In this review we give an overview of the pathophysiological mechanisms which lead to pain associated with bone metastasis and the impact of radiation treatment and other treatments on this mechanism.
Mobilized Peripheral Blood Cells Administered Intravenously Produce Functional Recovery in Stroke (2003)

Filgratism (granulocyte colony stimulating factor, G-CSF)-mobilized peripheral blood progenitor cells (PBPCs) have replaced bone marrow (BM) as a preferred source of autologous stem cells, in light of the faster hematologic recovery and lesser supportive care requirement exhibited by PBPC transplants. Other hematopoietic stem cells, like the human umbilical cord blood-derived stem cells (hUCBs), and nonhematopoietic stem cells have been shown to improve motor function in rodent models of injury and degenerative disease. In the present study we transplanted either G-CSF-mobilized PBPCs or hUCBs in rats 24 h after permanent middle cerebral artery occlusion (MCAO), and assessed their behavioral abnormalities in spontaneous activity and spontaneous motor asymmetry. In both transplanted groups of rats we observed a significant reduction of the stroke-induced hyperactivity compared with nontransplanted, stroked animals. In addition, transplantation of G-CSF PBPC and hUCB cells prevented the development of extensive motor asymmetry. Our findings raise the possibility that PBPCs could provide a novel transplantation therapy to treat stroke.
Abstract 4240: Targeting Galectin-3 to reverse tumor stemness and drug resistance (2014)

Abstract We have recently linked integrin αvβ3 expression to metastatic potential, stemness, and therapy resistance due to its capacity to couple to KRAS. This leads to the induction of RalB/TBK-1 and the activation of NFκB to shift tumor cells to a stem-like phenotype. To understand how integrin αvβ3 couples to KRAS, we generated β3 domain swap mutants containing either the intracellular or extracellular domains of β1 integrin. Each chimera partially reduced KRAS association with αvβ3, suggesting interactions on each side of the plasma membrane may contribute. Since the short β3 cytoplasmic tail has no putative KRAS binding regions, we considered Galectin-3 as a putative scaffolding partner to facilitate the αvβ3/KRAS association due to its reported binding to both KRAS and integrins. Indeed, treating cells with GCS-100, a complex polysaccharide that has the ability to bind to and block the effects of Galectin-3, decreased Galectin-3 surface expression, αvβ3 clustering, and αvβ3/KRAS association. Exposing cells to this drug also decreased tumor stem properties. Our observations provide a molecular basis for the αvβ3/KRAS/Galectin-3 complex and highlight the potential for Galectin-3 blockade as a therapeutic approach to reverse the aggressive behavior of αvβ3-expressing tumors. Citation Format: Shumei Kato, Laetitia Seguin, Aleksandra Franovic, Hisashi Kato, Maria Camargo, Jay Desgrosellier, Sudarshan Anand, Sara Weis, Sanford Shattil, David A. Cheresh. Targeting Galectin-3 to reverse tumor stemness and drug resistance. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4240. doi:10.1158/1538-7445.AM2014-4240
Visualization of Tau–Tubulin Interaction in a Living Cell Using Bifluorescence Complementation Technique (2018)

Tau is a neuron-specific microtubule-binding protein that stabilizes microtubules. It is generally thought that highly phosphorylated tau dissociates from microtubules and becomes insoluble aggregates, leading to neuronal degeneration. Due to the implication of tau aggregation in neurodegenerative disorders, including Alzheimer's disease, great efforts have been made to identify the tau aggregation process. However, tau interaction with tubulin during the aggregation process remains largely unknown. To scrutinize the tau-tubulin interaction, we generated a cell model that enables visualization of the tau-tubulin interaction in a living cell using the Bifluorescence Complementation (BiFC) Technique. Upon diverse chemical stimulation that induced tau pathology, tau-tubulin BiFC cells showed significantly increased levels of BiFC fluorescence, indicating that tau aggregates together with tubulin. Our results suggest that tubulin should be considered as a key component in the tau aggregation process.
Increased microtubule stability and alpha tubulin acetylation in cells transfected with microtubule-associated proteins MAP1B, MAP2 or tau (1992)

We previously transfected MAP2, tau and MAP1B cDNA into fibroblasts and have studied the effect of expression of these microtubule-associated proteins on microtubule organization. In this study, we examined some additional characteristics of microtubule bundles and arrays formed in fibroblasts transfected with these microtubule-associated proteins. It was found that microtubule bundles formed in MAP2c- or tau-transfected cells were stabilized against microtubule depolymerizing reagents and were enriched in acetylated alpha tubulin. When mouse MAP1B cDNA was expressed following transfection into COS cells, MAP1B was localized along microtubule arrays, but no extensive reorganization of microtubules such as bundle formation was observed, in agreement with our previous finding using HeLa and 3T3 cells. However, stabilization of microtubules was indicated: (a) microtubules in MAP1B-transfected cells were stabilized against a microtubule depolymerizing reagent, although stabilization was less efficient than that seen in MAP2c- or tau-transfected cells, and (b) microtubules in MAP1B-transfected cells were enriched in acetylated alpha tubulin. These results suggest that neuronal microtubule-associated proteins introduced into fibroblasts by cDNA transfection stabilize microtubules and affect the state of post-translational modification of tubulin.
Analytical evaluation of three enzymatic assays for measuring total bile acids in plasma using a fully-automated clinical chemistry platform (2017)

This study suggests that the analytical performance of the three commercial enzymatic assays is excellent, thus confirming that automation of this important test by means of enzymatic assessment may be feasible, practical, reliable and supposedly cheap. Nevertheless, the underestimation of values compared to the reference LC-MS also suggests that the local definition and validation of reference ranges according to the combination between the specific enzymatic assay and the different clinical chemistry platforms may be advisable.
Complete nucleotide sequence of a putative G protein coupled receptor: RDC7 (1990)

Journal Article Complete nucleotide sequence of a putative G protein coupled receptor: RDC7 Get access F. Libert, F. Libert 1IRIBHNBelgium Search for other works by this author on: Oxford Academic PubMed Google Scholar M. Parmentier, M. Parmentier 1IRIBHNBelgium Search for other works by this author on: Oxford Academic PubMed Google Scholar A. Lefort, A. Lefort 1IRIBHNBelgium Search for other works by this author on: Oxford Academic PubMed Google Scholar J.E. Dumont, J.E. Dumont 1IRIBHNBelgium Search for other works by this author on: Oxford Academic PubMed Google Scholar G. Vassart G. Vassart 1IRIBHNBelgium2Department of Genetics, Université Libre de BruxellesCampus Erasme, 808 Route de Lennik, 1070 Brussels, Belgium Search for other works by this author on: Oxford Academic PubMed Google Scholar Nucleic Acids Research, Volume 18, Issue 7, 11 April 1990, Page 1915, https://doi.org/10.1093/nar/18.7.1915 Published: 11 April 1990 Article history Published: 11 April 1990 Accepted: 01 December 1990
Staphylococcus aureus Panton-Valentine Leukocidin Is a Very Potent Cytotoxic Factor for Human Neutrophils (2010)

The role of the pore-forming Staphylococcus aureus toxin Panton-Valentine leukocidin (PVL) in severe necrotizing diseases is debated due to conflicting data from epidemiological studies of community-associated methicillin-resistant S. aureus (CA-MRSA) infections and various murine disease-models. In this study, we used neutrophils isolated from different species to evaluate the cytotoxic effect of PVL in comparison to other staphylococcal cytolytic components. Furthermore, to study the impact of PVL we expressed it heterologously in a non-virulent staphylococcal species and examined pvl-positive and pvl-negative clinical isolates as well as the strain USA300 and its pvl-negative mutant. We demonstrate that PVL induces rapid activation and cell death in human and rabbit neutrophils, but not in murine or simian cells. By contrast, the phenol-soluble modulins (PSMs), a newly identified group of cytolytic staphylococcal components, lack species-specificity. In general, after phagocytosis of bacteria different pvl-positive and pvl-negative staphylococcal strains, expressing a variety of other virulence factors (such as surface proteins), induced cell death in neutrophils, which is most likely associated with the physiological clearing function of these cells. However, the release of PVL by staphylococcal strains caused rapid and premature cell death, which is different from the physiological (and programmed) cell death of neutrophils following phagocytosis and degradation of virulent bacteria. Taken together, our results question the value of infection-models in mice and non-human primates to elucidate the impact of PVL. Our data clearly demonstrate that PVL acts differentially on neutrophils of various species and suggests that PVL has an important cytotoxic role in human neutrophils, which has major implications for the pathogenesis of CA-MRSA infections.