gebhart/patrepeval huggingface dataset:
Cross Talk between Gibberellin and Cytokinin: The Arabidopsis GA Response Inhibitor SPINDLY Plays a Positive Role in Cytokinin Signaling (2004)

SPINDLY (SPY) is a negative regulator of gibberellin (GA) responses; however, spy mutants exhibit various phenotypic alterations not found in GA-treated plants. Assaying for additional roles for SPY revealed that spy mutants are resistant to exogenously applied cytokinin. GA also repressed the effects of cytokinin, suggesting that there is cross talk between the two hormone-response pathways, which may involve SPY function. Two spy alleles showing severe (spy-4) and mild (spy-3) GA-associated phenotypes exhibited similar resistance to cytokinin, suggesting that SPY enhances cytokinin responses and inhibits GA signaling through distinct mechanisms. GA and spy repressed numerous cytokinin responses, from seedling development to senescence, indicating that cross talk occurs early in the cytokinin-signaling pathway. Because GA3 and spy-4 inhibited induction of the cytokinin primary-response gene, type-A Arabidopsis response regulator 5, SPY may interact with and modify elements from the phosphorelay cascade of the cytokinin signal transduction pathway. Cytokinin, on the other hand, had no effect on GA biosynthesis or responses. Our results demonstrate that SPY acts as both a repressor of GA responses and a positive regulator of cytokinin signaling. Hence, SPY may play a central role in the regulation of GA/cytokinin cross talk during plant development.
Biochemical studies of phenylalanine ammonia-lyase encapsulated in erythrocytes (1990)

Conference Article| August 01 1990 Biochemical studies of phenylalanine ammonia-lyase encapsulated in erythrocytes ULRICH SPRANDEL; ULRICH SPRANDEL 1Medical Polyclinic, University of Munich, Pettenkoferstr. 8 a, 8000 Munich 2, F.R.G. Search for other works by this author on: This Site PubMed Google Scholar NEPOMUK ZÖLLNER NEPOMUK ZÖLLNER 1Medical Polyclinic, University of Munich, Pettenkoferstr. 8 a, 8000 Munich 2, F.R.G. Search for other works by this author on: This Site PubMed Google Scholar Biochem Soc Trans (1990) 18 (4): 654–655. https://doi.org/10.1042/bst0180654 Article history Received: November 21 1989 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Cite Icon Cite Get Permissions Citation ULRICH SPRANDEL, NEPOMUK ZÖLLNER; Biochemical studies of phenylalanine ammonia-lyase encapsulated in erythrocytes. Biochem Soc Trans 1 August 1990; 18 (4): 654–655. doi: https://doi.org/10.1042/bst0180654 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBiochemical Society Transactions Search Advanced Search Keywords: PAL, phenylalanine ammonia-lyase (EC 4.3.1.5) This content is only available as a PDF. © 1990 Biochemical Society1990 Article PDF first page preview Close Modal You do not currently have access to this content.
A Tetranuclear Gadolinium(III) Macrocyclic Complex: Towards High Relaxivity with the Rigid Linkers for Magnetic Resonance Imaging Contrast Agent (2014)

Abstract A tetranuclear neutral MRI contrast agent, (Gd‐DO3A) 4 ‐TPM, was designed and synthesized by appending four Gd‐DO3A moieties upon the tetraphenylmethane derivatives. The longitudinal relaxivity of (Gd‐DO3A) 4 ‐TPM measured at 20 MHz, 37 °C and pH 7.0 is 6.8 mM –1 ·s –1 per Gd atom, which is one‐fold higher than that of the mononuclear clinical agent [Gd(DOTA)(H 2 O)] – . In addition, the thermodynamic stability of (Gd‐DO3A) 4 ‐TPM was higher than that of [Gd(DTPA)(H 2 O)] 2– . The luminescence lifetime study on the (Eu‐DO3A) 4 ‐TPM analogue suggested that the complex contains one inner water molecule coordinated to each Ln 3+ ion. The cytotoxicity study of (Gd‐DO3A) 4 ‐TPM indicated quite low toxicity.
A genetic model of substrate deprivation therapy for a glycosphingolipid storage disorder (1999)

Inherited defects in the degradation of glycosphingolipids (GSLs) cause a group of severe diseases known as GSL storage disorders. There are currently no effective treatments for the majority of these disorders. We have explored a new treatment paradigm, substrate deprivation therapy, by constructing a genetic model in mice. Sandhoff's disease mice, which abnormally accumulate GSLs, were bred with mice that were blocked in their synthesis of GSLs. The mice with simultaneous defects in GSL synthesis and degradation no longer accumulated GSLs, had improved neurologic function, and had a much longer life span. However, these mice eventually developed a late-onset neurologic disease because of accumulation of another class of substrate, oligosaccharides. The results support the validity of the substrate deprivation therapy and also highlight some limitations.
Human neutrophil cytochrome b light chain (p22-phox). Gene structure, chromosomal location, and mutations in cytochrome-negative autosomal recessive chronic granulomatous disease. (1990)

A membrane-bound cytochrome b, a heterodimer formed by a 91-kD glycoprotein (heavy chain) and a 22-kD polypeptide (light chain), is an essential component of the phagocyte NADPH-oxidase responsible for superoxide generation. Cytochrome b is absent in two subgroups of chronic granulomatous disease (CGD), an inherited disorder characterized by the lack of oxidase activity. Mutations in the cytochrome heavy chain gene, encoded by the CYBB locus in Xp21.1, result in the X-linked form of CGD. A rare subgroup of autosomal recessive CGD also lacks cytochrome b (A- CGD), but the genetic defect has not previously been identified. In order to search for possible mutations in the cytochrome light chain locus, CYBA, the structure of this gene was characterized. The CYBA locus was localized to 16q24, and the approximately 600-bp open reading frame determined to be encoded by six exons that span approximately 8.5 kb. Three unrelated patients with A- CGD were studied for evidence of mutations in the light chain gene. One patient, whose parents were first cousins, was homozygous for a large deletion that removed all but the extreme 5' coding sequence of the gene. The other two patients had a grossly normal light chain transcript on Northern blot of mononuclear cell RNA. The light chain transcript was amplified by the polymerase chain reaction and sequenced. One patient was a compound heterozygote for two alleles containing point mutations in the open reading frame that predict a frame shift and a nonconservative amino acid replacement, respectively. The second patient, whose parents were second cousins, was homozygous for a different single-base substitution resulting in another nonconservative amino acid change. These results indicate that A- CGD can results from defects in the gene encoding the 22-kD light chain of the phagocyte cytochrome b.
Selective binding to DNA base pair mismatches by proteins from human cells (1989)

Using the technique of delayed oligonucleotide migration through polyacrylamide gels, we have demonstrated that cell-free extracts of the human Burkitt's lymphoma cell line Raji contain proteins which can recognize and bind to mismatched single base pairs in short fragments of DNA. One of these binding proteins resembles an activity previously reported in HeLa cells (Jiricny, J., Hughes, M., Corman, N., and Rudkin, B. B. (1988) Proc. Natl. Acad. Sci. U. S. A. 85, 8860-8864) and recognizes DNA containing G.T mismatches. Extracts of Raji cells contain an additional activity which recognizes A.C, T.C, or T.T mismatches in DNA. This second binding protein can be distinguished from the G.T binding activity by its size, substrate specificity, and its fractionation properties. In addition to Raji cells, the new mismatch binding protein is present in extracts of human lymphoblastoid cell lines from a normal individual and a xeroderma pigmentosum patient as well as the SV40-transformed human fibroblast cell line MRC5V1. It seems likely that this novel activity is involved in a broad specificity DNA repair pathway for the correction of single base mismatches in human cells.
Probing the Binding of Coumarins and Cyclothialidines to DNA Gyrase (1999)

DNA gyrase is the target of a number of antibacterial agents, including the coumarins and the cyclothialidines. To extend our understanding of the mechanism of action of these compounds, we have examined the previously published crystal structures of the complexes between the 24 kDa fragment of GyrB and coumarin and cyclothialidine drugs and made mutations by site-directed mutagenesis. We used proteolysis as a probe of drug binding to wild-type and mutant proteins. Limited proteolysis of gyrase revealed that binding of these antibiotics is associated with a characteristic proteolytic fingerprint, suggesting a drug-induced conformational change. The ability of the mutants to bind the drugs was studied by testing their ability to induce the coumarin-associated proteolytic signature and to bind to a novobiocin-affinity column. To analyze further the interaction of the drugs with gyrase, we studied the binding using surface plasmon resonance. Mutation of Asn46 to Asp has only a modest effect on the binding of coumarins, while an Asn46 to Leu mutation results in a 10-fold decrease in the affinity. Mutation of Asp73 to Asn completely abolishes binding to both coumarins and cyclothialidines. Mutations at these residues also abolish ATP hydrolysis, explaining the inability of such mutations to occur spontaneously.
Two distinct forms of active transcription factor CREB (cAMP response element binding protein). (1990)

Mammalian cells express two distinct forms of transcription factor CREB (cAMP response element binding protein) that are apparently the products of alternative splicing of the CREB gene transcript. The two proteins differ by a 14-amino acid serine-rich insertion present in one of the CREB isoforms. We show that both CREB isoforms are expressed in many cell types and mammalian species. Both encode proteins that bind specifically to a cAMP response element in vitro. As expected for proteins of this class, the CREB proteins bind DNA as dimers. Both proteins impart cAMP-regulated transcriptional activity to a heterologous DNA-binding domain, showing that cAMP directly modulates the transcriptional stimulatory activity of CREB. The presence of multiple CREB isoforms with identical DNA-binding specificities but differences in the presumed regulatory domain raises the possibility that CREB proteins may be able to integrate distinct regulatory signals at the level of gene transcription.
Influence of Chemical Structure and Solubility of Bisamide Additives on the Nucleation of Isotactic Polypropylene and the Improvement of Its Charge Storage Properties (2006)

A comparative study on the influence of chemical structure and solubility of a series of low-molecular-weight 1,4-phenylene−bisamides in isotactic polypropylene (i-PP) was conducted to explore their performance as nucleating agents and electret additives. The series consists of three isomers of dicyclohexyl-substituted 1,4-phenylene−bisamide and three asymmetrically substituted cyclohexyl/n-alkyl-1,4-phenylene−bisamides with different chain lengths. The symmetry of the molecules, the type of substitution and the length of the alkyl chain influence the solubility in the i-PP melt, the nucleation efficiency, the ratio of the α- to β-crystal modification and the charge storage properties. The best β-nucleating efficiency was observed for the symmetrically substituted compounds, whereas the nucleation efficiency was substantially reduced in the presence of n-alkyl-substituents. The charge storage behavior of i-PP was improved only for the three dicyclohexyl-substituted 1,4-phenylene bisamides at concentrations of 100 ppm and even below. For example, a film comprising 10 ppm additive displayed charge retention of 90% after an accelerated aging (annealing for 24 h at 90 °C).
The distributed compartment model for resource management and access control (1994)

Given the present trends regarding distributed computer systems, the standard model of security used on most distributed systems is outmoded. This older model dates back to simpler times and is based on the idea of a centrally managed system (usually a mainframe or minicomputer system). Even modern networked computer environments are usually centrally managed systems using this older model.
This older model is based on the idea that there is a central managing authority, called the system administration, that is ultimately responsible for the management of computer security. This management is usually done with some form of a discretionary access control method, where each user is granted (or denied) privileges and resources depending on the security policies enforced at that particular system. The system administration, among other things, manages the system resources, creates and destroys user accounts, and grants and revokes user privileges. This model is typified by an operating system such as UNIX.
This model introduces several difficulties when working in a distributed computing environment. The scope of this dissertation is in the problem areas of resource allocation and access control. The solution proposed herein is a Distributed Compartment model consisting of two major components. First, Distributed Handles are a method for user identification and access control. Second, Distributed Compartments are a method for allowing users to manage resources within a distributed system across computer system administrative boundaries without many of the restraints of the old model. A formal security model is presented that defines these concepts, and further refines them into a state transition model.
The formal axiomatic model presented consists of component sets and their members. There is a set of binary relations used to partially order the sets and specify operations on sets. The model defines a secure system state and rules of operation provide secure state transitions from one secure system state to another. There is a set of secure system state invariants that each rule must satisfy in order to maintain a secure system state. Each rule is proven secure within the model.
Effect of low level diode laser irradiation of human oral mucosa fibroblasts in vitro (1994)

The effects of low level laser (LLL) irradiation on the proliferation of human buccal fibroblasts were studied. A standardized LLL set-up was developed (812 nm, 4.5 +/- 0.5 mW/cm2). Cultures in petridishes were divided into eight groups (1 group served as control). On day 6 after seeding, routine growth medium was replaced with PBS for 1/2 hour. At the beginning of this period, LLL irradiation was performed for 0, 1, 3, 10, 32, 100, 316, or 1,000 seconds, respectively--corresponding to the radiant exposures 0, 4.5, 13.5, 45, 144, 450, 1,422, 4,500 mJ/cm2. Subsequently the cells received 3H-dT in fresh medium for 16 hours DNA-incorporation. Scintillations from tritium and total protein concentration per culture dish were determined. The individual 3H-cpm/protein-concentration ratios were calculated in % of control. Three experiments were performed (N = 151). Following LLL exposure the 3H-cpm/protein ratio was increased with maximum cpm/protein ratio (132.5% +/- 10.6% SEM) in the group receiving 450 mJ/cm2 (P < 0.03 nonparametric Kruskal Wallis one-way ANOVA-test). This study demonstrated an increased incorporation on tritiated thymidine in cultured human oral fibroblasts following LLL exposure and suggests that LLL irradiation can induce increased DNA synthesis.
The Physiology of Human Penile Erection (1972)

Human penile erection depends on integration of afferent signals in the thoracolumbar or sacral erection centers, intact autonomic nerves to the penis, normal erectile tissues, and an adequate blood supply to the penis. Cerebral influence is apparently not always necessary to facilitate erection and may even inhibit penile erection. Considering the tremendous importance of penile erection to nearly all of our patients, it is surprising to find how incomplete our knowledge is on many aspects of this fascinating neurophysiologic and hemodynamic process.
Two‐year interim results from a 5‐year study evaluating clinical recurrence of superficial basal cell carcinoma after treatment with imiquimod 5% cream daily for 6 weeks (2006)

Imiquimod 5% cream is approved in the USA, Europe and Australia to treat superficial basal cell carcinoma, using a regimen of once daily, 5 times per week for 6 weeks. Vehicle-controlled, phase III clinical trials show that imiquimod is safe and effective for treating superficial basal cell carcinoma with dosing 5 or 7 times per week for 6 weeks. This phase III, open-label study evaluates the long-term (5 years) clinical efficacy and safety of dosing once daily, for which this manuscript reports the 2-year time point in the follow-up period. For the 169 enrolled subjects, the tumour selected for treatment was assessed clinically to determine initial clearance at the 12-week post-treatment visit. If clinically clear of superficial basal cell carcinoma, subjects entered a 5-year, long-term follow-up period. Subjects were evaluated for recurrence at the 3-, 6-, 12- and 24-month follow-up visits. The initial clearance rate at 12 weeks post treatment was 94.1%. The proportion of subjects who were clinically clear at the 2-year follow-up visit was estimated to be 82.0%. Imiquimod was tolerated when applied daily, with erythema reported for all subjects participating in the study. The recurrence rate observed suggests that once daily dosing and 5x/week dosing yield similar clearance rates, but daily dosing increases local skin reactions.
Fine structure analysis and nucleotide sequence of the vaccinia virus thymidine kinase gene. (1983)

The thymidine kinase (ATP:thymidine 5'-phosphotransferase, EC 2.7.1.21) gene of vaccinia virus has previously been mapped near the middle of the viral DNA, within the 4.85-kilobase HindIII J fragment, and shown to encode a Mr 19,000 polypeptide [Hruby, D. E. & Ball, L. A. (1982) J. Virol. 43, 403-409]. To locate the gene more precisely and to determine the structure of the basic transcriptional unit, the positions of cleavage sites for several restriction endonucleases were mapped within the HindIII J DNA fragment. Four appropriate subfragments of HindIII J DNA were inserted into plasmid pBR322 derivatives and cloned in Escherichia coli. These recombinant plasmid DNAs were tested for their ability to inhibit the cell-free synthesis of active thymidine kinase and to retain the mRNA for this enzyme when immobilized on nitrocellulose filters. The data showed that the gene spanned an EcoRI cleavage site that lies 850 base pairs from the left-hand end of the HindIII J fragment (the HindIII L-J boundary). Because hybridization of vaccinia virus DNA to partially purified thymidine kinase mRNA detected only a single 670-nucleotide RNA species capable of hybridizing to this region of the genome, nuclease S1 mapping experiments were carried out with thymidine kinase mRNA to protect DNA fragments that were terminally labeled at this EcoRI site. The results indicated that the gene extended from about 550 to 1,150 base pairs from the left end of HindIII J, was transcribed in a rightward direction, and contained no intervening sequences. Hence, a 1.04-kilobase Ava II-Hpa II restriction fragment containing this region of DNA was isolated and subjected to nucleotide sequence analysis. An examination of this nucleotide sequence revealed the presence of an open reading frame of 531 nucleotides capable of encoding a protein of 177 amino acids with a Mr of 20,077.
Rational Design of an Unnatural Base Pair with Increased Kinetic Selectivity (2000)

ADVERTISEMENT RETURN TO ISSUEPREVCommunicationNEXTRational Design of an Unnatural Base Pair with Increased Kinetic SelectivityAnthony K. Ogawa, Yiqin Wu, Markus Berger, Peter G. Schultz, and Floyd E. RomesbergView Author Information Department of Chemistry, The Scripps Research Institute 10550 North Torrey Pines Road, La Jolla, California 92037 Cite this: J. Am. Chem. Soc. 2000, 122, 36, 8803–8804Publication Date (Web):August 26, 2000Publication History Received26 April 2000Published online26 August 2000Published inissue 1 September 2000https://pubs.acs.org/doi/10.1021/ja001450uhttps://doi.org/10.1021/ja001450urapid-communicationACS PublicationsCopyright © 2000 American Chemical SocietyRequest reuse permissionsArticle Views736Altmetric-Citations32LEARN 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-AlertscloseSupporting Info (1)»Supporting Information Supporting Information SUBJECTS:Genetics,Hydrophobicity,Peptides and proteins,Selectivity,Substituents Get e-Alerts
[Autoimmune mechanisms in the pathogenesis of neurologic paraneoplastic diseases]. (1997)

Neurologic paraneoplastic syndromes (NPS) are disorders of the nervous system that are associated with the presence of malignant tumors. They are also known as the remote effects of cancer. There is mounting circumstantial evidence supporting the autoimmune origin of NPS. In NPS patients, paraneoplastic autoantibodies have been identified which react with the same or similar antigenic epitopes in tumor cells and neurons. However, except for the Lambert-Eaton myasthenic syndrome (LEMS) it remains still unproven as to whether the autoantibodies are pathogenic or merely represent an epiphenomenon to the actual disease process, since the antigens identified by the paraneoplastic autoantibodies are primarily intracellular as to their location. Few data are available regarding the role of cell-mediated cytotoxicity and antigen dependent T-cell cytotoxicity. Further studies will be necessary to elucidate the role of autoimmunity in the production of paraneoplastic neurologic disorders. (Tab. 2, Ref. 6.)