bluuebunny/crossref_metadata_2025_split huggingface dataset:
The AppA and PpsR Proteins from
Rhodobacter sphaeroides
Can Establish a Redox-Dependent Signal Chain but Fail To Transmit Blue-Light Signals in Other Bacteria
Authors: Jäger Andreas , Braatsch Stephan , Haberzettl Kerstin , Metz Sebastian , Osterloh Lisa , Han Yuchen , Klug Gabriele 
Published: January 2007

ABSTRACT

The AppA protein of
Rhodobacter sphaeroides
has the unique ability to sense and transmit redox and light signals. In response to decreasing oxygen tension, AppA antagonizes the transcriptional regulator PpsR, which represses the expression of photosynthesis genes, including the
puc
operon. This mechanism, which is based on direct protein-protein interaction, is prevented by blue-light absorption of the BLUF domain located in the N-terminal part of AppA. In order to test whether AppA and PpsR are sufficient to transmit redox and light signals, we expressed these proteins in three different bacterial species and monitored oxygen- and blue-light-dependent
puc
expression either directly or by using a luciferase-based reporter construct. The AppA/PpsR system could mediate redox-dependent gene expression in the alphaproteobacteria
Rhodobacter capsulatus
and
Paracoccus denitrificans
but not in the gammaproteobacterium
Escherichia coli
. Analysis of a
prrA
mutant strain of
R. sphaeroides
strongly suggests that light-dependent gene expression requires a balanced interplay of the AppA/PpsR system with the PrrA response regulator. Therefore, the AppA/PpsR system was unable to establish light signaling in other bacteria. Based on our data, we present a model for the interdependence of AppA/PpsR signaling and the PrrA transcriptional activator.
Amplification of
lac
Cannot Account for Adaptive Mutation to Lac
+
in
Escherichia coli
Authors: Stumpf Jeffrey D. , Poteete Anthony R. , Foster Patricia L. 
Published: January 2007

ABSTRACT

When the Lac
−
strain of
Escherichia coli
, FC40, is incubated with lactose as its sole carbon and energy source, Lac
+
revertants arise at a constant rate, a phenomenon known as adaptive mutation. Two alternative models for adaptive mutation have been proposed: (i) recombination-dependent mutation, which specifies that recombination occurring in nongrowing cells stimulates error-prone DNA synthesis, and (ii) amplification-dependent mutation, which specifies that amplification of the
lac
region and growth of the amplifying cells creates enough DNA replication to produce mutations at the normal rate. Here, we examined several of the predictions of the amplification-dependent mutation model and found that they are not fulfilled. First, inhibition of adaptive mutation by a gene that is toxic when overexpressed does not depend on the proximity of the gene to
lac
. Second, mutation at a second locus during selection for Lac
+
revertants is also independent of the proximity of the locus to
lac
. Third, mutation at a second locus on the episome occurs even when the
lac
allele under selection is on the chromosome. Our results support the hypothesis that most Lac
+
mutants that appear during lactose selection are true revertants that arise in a single step from Lac
−
cells, not from a population of growing or amplifying precursor cells.
Infiltrating giant cellular blue naevus
Authors: Bittencourt A L , Monteiro D A , De Pretto O J 
Published: January 2007

Introduction:Cellular blue naevi (CBN) measure 1–2 cm in diameter and affect the dermis, occasionally extending into the subcutaneous fat. The case of a 14-year-old boy with a giant CBN (GCBN) involving the right half of the face, the jugal mucosa and the lower eyelid with a tumour that had infiltrated the bone and the maxillary and ethmoidal sinuses is reported.Methods:Biopsies were taken from the skin, jugal mucosa and maxillary sinus. The following markers were used in the immunohistochemical evaluation: CD34, CD56, HMB-45, anti-S100, A-103, Melan A and MIB-1.Results:The biopsy specimens showed a biphasic pattern affecting the lower dermis, subcutaneous fat, skeletal muscle, bone, jugal mucosa and maxillary sinus, but there was no histological evidence of malignancy. The tumour cells were CD34−, CD56−, HMB45+, anti-S100+ and A-103+. Melan A was focally expressed. No positive MIB-1 cells were identified.Discussion:The present case shows that GCBN may infiltrate deeply, with no evidence of malignancy.
Sand, Fish and Sea: A Legal Reflection on Islands—From Orkney to Vanuatu
Authors: Farran Sue 
Published: January 2007

AbstractIt might be thought that the Orkney and Shetland Islands to the north of Scotland have little in common with the tropical islands in the South Pacific region. This article demonstrates that islands across time and space can share many similar concerns by reflecting on a number of legal issues which either have been or are pertinent to islands in both hemispheres, taking into account the role and relevance of customary or traditional law, the influence of introduced or colonial law, and the legal consequences of political domination of one group by another. In particular the article looks at the challenges presented where there is more than one system of law or set of rules applicable to questions of ownership of the sea, the seashore and fishing, and the consequences this can have for management and control of marine resources.
X-linked gray platelet syndrome due to a GATA1 Arg216Gln mutation
Authors: Tubman Venée N. , Levine Jason E. , Campagna Dean R. , Monahan-Earley Rita , Dvorak Ann M. , Neufeld Ellis J. , Fleming Mark D. 
Published: January 2007

AbstractWe identified a family with gray platelet syndrome (GPS) segregating as a sex-linked trait. Affected males had a mild bleeding disorder, thrombocytopenia, and large agranular platelets characteristic of GPS, while obligate carrier females were asymptomatic but had dimorphic platelets on peripheral smear. Associated findings included mild erythrocyte abnormalities in affected males. Linkage analysis revealed a 63 cM region on the X chromosome between markers G10578 and DXS6797, which segregated with the platelet phenotype and included the GATA1 gene. Sequencing of GATA1 revealed a G-to-A mutation at position 759 corresponding to amino acid change Arg216Gln. This mutation was previously described as a cause of X-linked thrombocytopenia with thalassemia (XLTT) but not of gray platelet syndrome. Our findings suggest that XLTT is within a spectrum of disorders constituting the gray platelet syndrome, and we propose that GATA1 is an upstream regulator of the genes required for platelet α-granule biogenesis.
A sequence variation scan of the coagulation factor VIII (FVIII) structural gene and associations with plasma FVIII activity levels
Authors: Viel Kevin R. , Machiah Deepa K. , Warren Diane M. , Khachidze Manana , Buil Alfonso , Fernstrom Karl , Souto Juan C. , Peralta Juan M. , Smith Todd , Blangero John , Porter Sandra , Warren Stephen T. , Fontcuberta Jordi , Soria Jose M. , Dana Flanders W. , Almasy Laura , Howard Tom E. 
Published: January 2007

AbstractPlasma factor VIII coagulant activity (FVIII:C) level is a highly heritable quantitative trait that is strongly correlated with thrombosis risk. Polymorphisms within only 1 gene, the ABO blood-group locus, have been unequivocally demonstrated to contribute to the broad population variability observed for this trait. Because less than 2.5% of the structural FVIII gene (F8) has been examined previously, we resequenced all known functional regions in 222 potentially distinct alleles from 137 unrelated nonhemophilic individuals representing 7 racial groups. Eighteen of the 47 variants identified, including 17 single-nucleotide polymorphisms (SNPs), were previously unknown. As the degree of linkage disequilibrium across F8 was weak overall, we used measured-genotype association analysis to evaluate the influence of each polymorphism on the FVIII:C levels in 398 subjects from 21 pedigrees known as the Genetic Analysis of Idiopathic Thrombophilia project (GAIT). Our results suggested that 92714C>G, a nonsynonymous SNP encoding the B-domain substitution D1241E, was significantly associated with FVIII:C level. After accounting for important covariates, including age and ABO genotype, the association persisted with each C-allele additively increasing the FVIII:C level by 14.3 IU dL−1 (P = .016). Nevertheless, because the alleles of 56010G>A, a SNP within the 3′ splice junction of intron 7, are strongly associated with 92714C>G in GAIT, additional studies are required to determine whether D1241E is itself a functional variant.
ABT-869, a multitargeted receptor tyrosine kinase inhibitor: inhibition of FLT3 phosphorylation and signaling in acute myeloid leukemia
Authors: Shankar Deepa B. , Li Junling , Tapang Paul , Owen McCall J. , Pease Lori J. , Dai Yujia , Wei Ru-Qi , Albert Daniel H. , Bouska Jennifer J. , Osterling Donald J. , Guo Jun , Marcotte Patrick A. , Johnson Eric F. , Soni Niru , Hartandi Kresna , Michaelides Michael R. , Davidsen Steven K. , Priceman Saul J. , Chang Jenny C. , Rhodes Katrin , Shah Neil , Moore Theodore B. , Sakamoto Kathleen M. , Glaser Keith B. 
Published: January 2007

Abstract
In 15% to 30% of patients with acute myeloid leukemia (AML), aberrant proliferation is a consequence of a juxtamembrane mutation in the FLT3 gene (FMS-like tyrosine kinase 3–internal tandem duplication [FLT3-ITD]), causing constitutive kinase activity. ABT-869 (a multitargeted receptor tyrosine kinase inhibitor) inhibited the phosphorylation of FLT3, STAT5, and ERK, as well as Pim-1 expression in MV-4-11 and MOLM-13 cells (IC50 approximately 1-10 nM) harboring the FLT3-ITD. ABT-869 inhibited the proliferation of these cells (IC50 = 4 and 6 nM, respectively) through the induction of apoptosis (increased sub-G0/G1 phase, caspase activation, and PARP cleavage), whereas cells harboring wild-type (wt)–FLT3 were less sensitive. In normal human blood spiked with AML cells, ABT-869 inhibited phosphorylation of FLT3 (IC50 approximately 100 nM), STAT5, and ERK, and decreased Pim-1 expression. In methylcellulose-based colony-forming assays, ABT-869 had no significant effect up to 1000 nM on normal hematopoietic progenitor cells, whereas in AML patient samples harboring both FLT3-ITD and wt-FLT3, ABT-869 inhibited colony formation (IC50 = 100 and 1000 nM, respectively). ABT-869 dose-dependently inhibited MV-4-11 and MOLM-13 flank tumor growth, prevented tumor formation, regressed established MV-4-11 xenografts, and increased survival by 20 weeks in an MV-4-11 engraftment model. In tumors, ABT-869 inhibited FLT3 phosphorylation, induced apoptosis (transferase-mediated dUTP nick-end labeling [TUNEL]) and decreased proliferation (Ki67). ABT-869 is under clinical development for AML.
Inhibition of HIV-1 infection by viral chemokine U83A via high-affinity CCR5 interactions that block human chemokine-induced leukocyte chemotaxis and receptor internalization
Authors: Catusse Julie , Parry Chris M. , Dewin David R. , Gompels Ursula A. 
Published: January 2007

AbstractHIV-1 strains use C-C-chemokine receptor 5, CCR5, as a coreceptor for host transmission. Human CCR5 chemokine ligands inhibit binding and infection, whereas CCR5 mutations also inhibit infection by preventing surface expression, resulting in delayed progression to AIDS. Here, we describe a human herpesvirus 6 (HHV-6A) chemokine, U83A, which binds CCR5 with higher affinity than human chemokines, displacing their binding and leading to inhibition of chemotaxis of human leukocytes. Similarly, U83A inhibits infection by HIV-1 strains which use CCR5, but not the CXCR4, coreceptor. Unlike human CCR5 chemokine ligands which induce rapid CCR5 internalization mediated via clathrin, treatment with U83A prevents internalization. A spliced truncated U83A isoform, U83A-N, also binds CCR5 albeit with lower affinity, and this correlates with lower HIV-1 infection inhibition, whereas further truncation abolishes binding and any inhibition. Confocal microscopy confirms CCR5 internalization inhibition by U83A treatment, whereas labeled transferrin uptake shows that endocytosis via clathrin is unaltered. Previous results show that, although U83A-N is an antagonist, U83A is an agonist for CCR1, CCR4, CCR6, and CCR8 present on immune effector and antigen-presenting cells and here also shown for CCR5. Thus, U83A could act as a novel inhibitor of HIV-1 infection while also stimulating local immunity to the virus.
Cladribine in a weekly versus daily schedule for untreated active hairy cell leukemia: final report from the Polish Adult Leukemia Group (PALG) of a prospective, randomized, multicenter trial
Authors: Robak Tadeusz , Jamroziak Krzysztof , Gora-Tybor Joanna , Blonski Jerzy Z. , Kasznicki Marek , Dwilewicz-Trojaczek Jadwiga , Wiater Elzbieta , Zdunczyk Andrzej , Dybowicz Jacek , Dmoszynska Anna , Wojtaszko Maria , Zdziarska Barbara , Calbecka Malgorzata , Kostyra Aleksandra , Hellmann Andrzej , Lewandowski Krzysztof , Stella-Holowiecka Beata , Sulek Kazimierz , Gawronski Krzysztof , Skotnicki Aleksander B. , Nowak Wieslaw , Zawilska Krystyna , Molendowicz-Portala Lucyna , Kloczko Janusz , Sokolowski Jarosław , Warzocha Krzysztof , Seferyńska Ilona , Ceglarek Bernardeta , Konopka Lech ,   for the Polish Adult Leukemia Group
Published: January 2007

Abstract
Cladribine (2-chlorodeoxyadenosine, 2-CdA) treatment-associated infections may shorten potentially long-term survival in hairy cell leukemia (HCL). In search of the optimal mode of 2-CdA administration, 132 patients with untreated HCL were randomized to receive either standard 5-day 2-CdA protocol or a novel schedule of 6 weekly 2-CdA infusions suggested to be less toxic. Analysis of treatment response confirmed similar complete remission rates, overall response rates, progression-free survival, and overall survival in both 2-CdA protocols. However, we did not observe lower toxicity in the weekly schedule. Of special interest, no significant differences were found in the rate of grade 3/4 infections (18% for daily and 26% for weekly protocol, difference −8.2%; 95% confidence interval [CI] −23.2% to 6.9%; P = .28) and the rate of septic deaths (3% for daily and 2% for weekly protocol, difference 1.4%; 95% CI −4.3% to 7.0%; P = .64). In conclusion, HCL treatment with weekly 2-CdA infusions is equally effective but no safer than the standard 5-day 2-CdA protocol.
Vitamin A potentiates CpG-mediated memory B-cell proliferation and differentiation: involvement of early activation of p38MAPK
Authors: Ertesvag Aase , Aasheim Hans-Christian , Naderi Soheil , Blomhoff Heidi Kiil 
Published: January 2007

AbstractForeign CpG-DNA from viruses and bacteria can activate memory B cells through binding to toll-like receptor 9, and this pathway has been hypothesized to be involved in the continuous activation of memory B cells ensuring life-long humoral immunity. In this study, we demonstrate that retinoic acid (RA) is a potent coactivator of this pathway in human B cells. RA enhanced the CpG-mediated proliferation of CD27+ memory B cells, and the proliferative response was accompanied by increased immunoglobulin (Ig) secretion indicative of plasma-cell formation. The RA-induced proliferation was preceded by enhanced expression of cyclin D3, and both the expression of cyclin D3 and the induced Ig secretion were found to be dependent on IL-10. Of importance, RA increased the CpG-induced phosphorylation of ERK1/2, p38MAPK, and IκB as early as 30 minutes after stimulation. By using specific inhibitors, all the RA-mediated events, including proliferation, cyclin D3 expression, IL-10 secretion, and Ig secretion, were shown to be dependent on p38MAPK. Hence, we propose that RA can strengthen humoral immunity by promoting CpG-mediated stimulation of CD27+ B cells via activation of p38MAPK resulting in increased proliferation and differentiation to Ig-secreting plasma cells.
Mapping early conformational changes in αIIb and β3 during biogenesis reveals a potential mechanism for αIIbβ3 adopting its bent conformation
Authors: Beau Mitchell W. , Li Jihong , Murcia Marta , Valentin Nathalie , Newman Peter J. , Coller Barry S. 
Published: January 2007

AbstractCurrent evidence supports a model in which the low-affinity state of the platelet integrin αIIbβ3 results from αIIbβ3 adopting a bent conformation. To assess αIIbβ3 biogenesis and how αIIbβ3 initially adopts the bent conformation, we mapped the conformational states occupied by αIIb and β3 during biogenesis using conformation-specific monoclonal antibodies (mAbs). We found that αIIbβ3 complex formation was not limited by the availability of either free pro-αIIb or free β3, suggesting that other molecules, perhaps chaperones, control complex formation. Five β3-specific, ligand-induced binding site (LIBS) mAbs reacted with much or all free β3 but not with β3 when in complex with mature αIIb, suggesting that β3 adopts its mature conformation only after complex formation. Conversely, 2 αIIb-specific LIBS mAbs directed against the αIIb Calf-2 region adjacent to the membrane reacted with only minor fractions of free pro-αIIb, raising the possibility that pro-αIIb adopts a bent conformation early in biogenesis. Our data suggest a working model in which pro-αIIb adopts a bent conformation soon after synthesis, and then β3 assumes its bent conformation by virtue of its interaction with the bent pro-αIIb.
A sequence based synteny map between soybean and Arabidopsis thaliana
Authors: Shultz Jeffry L , Ray Jeffery D , Lightfoot David A 
Published: January 2007

Abstract

Background
Soybean (Glycine max, L. Merr.) is one of the world's most important crops, however, its complete genomic sequence has yet to be determined. Nonetheless, a large body of sequence information exists, particularly in the form of expressed sequence tags (ESTs). Herein, we report the use of the model organism Arabidopsis thaliana (thale cress) for which the entire genomic sequence is available as a framework to align thousands of short soybean sequences.

Results
A series of JAVA-based programs were created that processed and compared 341,619 soybean DNA sequences against A. thaliana chromosomal DNA. A. thaliana DNA was probed for short, exact matches (15 bp) to each soybean sequence, and then checked for the number of additional 7 bp matches in the adjacent 400 bp region. The position of these matches was used to order soybean sequences in relation to the A. thaliana genome.

Conclusion
Reported associations between soybean sequences and A. thaliana were within a 95% confidence interval of e-30 – e-100. In addition, the clustering of soybean expressed sequence tags (ESTs) based on A. thaliana sequence was accurate enough to identify potential single nucleotide polymorphisms (SNPs) within the soybean sequence clusters. An EST, bacterial artificial chromosome (BAC) end sequence and marker amplicon sequence synteny map of soybean and A. thaliana is presented. In addition, all JAVA programs used to create this map are available upon request and on the WEB.
Ashbya Genome Database 3.0: a cross-species genome and transcriptome browser for yeast biologists
Authors: Gattiker Alexandre , Rischatsch Riccarda , Demougin Philippe , Voegeli Sylvia , Dietrich Fred S , Philippsen Peter , Primig Michael 
Published: January 2007

Abstract

Background
The Ashbya Genome Database (AGD) 3.0 is an innovative cross-species genome and transcriptome browser based on release 40 of the Ensembl developer environment.

Description
AGD 3.0 provides information on 4726 protein-encoding loci and 293 non-coding RNA genes present in the genome of the filamentous fungus Ashbya gossypii. A synteny viewer depicts the chromosomal location and orientation of orthologous genes in the budding yeast Saccharomyces cerevisiae. Genome-wide expression profiling data obtained with high-density oligonucleotide microarrays (GeneChips) are available for nearly all currently annotated protein-coding loci in A. gossypii and S. cerevisiae.

Conclusion
AGD 3.0 hence provides yeast- and genome biologists with comprehensive report pages including reliable DNA annotation, Gene Ontology terms associated with S. cerevisiae orthologues and RNA expression data as well as numerous links to external sources of information. The database is accessible at http://agd.vital-it.ch/.
Analysis of the thiol status of peripheral blood leukocytes in rheumatoid arthritis patients
Authors: Pedersen-Lane Joan H , Zurier Robert B , Lawrence David A 
Published: January 2007

AbstractAlthough the exact etiology of rheumatoid arthritis (RA) remains unknown, there is increasing evidence that reactive oxygen species and a pro-oxidant/antioxidant imbalance are an important part of the pathogenesis of joint tissue injury. Flow cytometry was used to evaluate the thiol status [surface-thiols and intracellular glutathione (iGSH)] of leukocytes from RA patients and controls. Levels of surface-thiols and iGSH of leukocytes from RA patients were significantly lower than of leukocytes from controls. CD53, a glycoprotein of the tetraspanin superfamily, which coprecipitates with the GSH recycling enzyme γ-glutamyl transpeptidase, was elevated significantly on leukocytes from RA patients compared with leukocytes from controls. Surface-thiols and GSH play important roles in redox buffering of cells, providing protection from oxidative stress. The chronic inflammation of RA has been associated with oxidative stress, which is shown to cause a decline in the levels of cellular antioxidant sulfhydryls (R-SH). As antioxidant-protective levels also decline with age, the problem is compounded in older RA patients, who did have fewer R-SH. Chronic stress can also have an effect on telomere lengths, determining cell senescence and longevity. Although telomeres shorten with increasing age, our flow cytometry studies indicate that accelerated shortening in telomere lengths occurs with increasing age of RA patients, suggesting premature cellular aging. The paradox is that lymphocytes from RA patients are believed to resist apoptosis, and we suggest that the elevated expression of CD53, which results from the increased oxidative stress, may protect against apoptosis.
Interaction analysis of theCBLBandCTLA4genes in type 1 diabetes
Authors: Payne Felicity , Cooper Jason D , Walker Neil M , Lam Alex C , Smink Luc J , Nutland Sarah , Stevens Helen E , Hutchings Jayne , Todd John A 
Published: January 2007

AbstractGene-gene interaction analyses have been suggested as a potential strategy to help identify common disease susceptibility genes. Recently, evidence of a statistical interaction between polymorphisms in two negative immunoregulatory genes, CBLB and CTLA4, has been reported in type 1 diabetes (T1D). This study, in 480 Danish families, reported an association between T1D and a synonymous coding SNP in exon 12 of the CBLB gene (rs3772534 G&gt;A; minor allele frequency, MAF=0.24; derived relative risk, RR for G allele=1.78; P=0.046). Furthermore, evidence of a statistical interaction with the known T1D susceptibility-associated CTLA4 polymorphism rs3087243 (laboratory name CT60, G&gt;A) was reported (P&lt;0.0001), such that the CBLB SNP rs3772534 G allele was overtransmitted to offspring with the CTLA4 rs3087243 G/G genotype. We have, therefore, attempted to obtain additional support for this finding in both large family and case-control collections. In a primary analysis, no evidence for an association of the CBLB SNP rs3772534 with disease was found in either sample set (2162 parent-child trios, P=0.33; 3453 cases and 3655 controls, P=0.69). In the case-only statistical interaction analysis between rs3772534 and rs3087243, there was also no support for an effect (1994 T1D affected offspring, and 3215 cases, P=0.92). These data highlight the need for large, well-characterized populations, offering the possibility of obtaining additional support for initial observations owing to the low prior probability of identifying reproducible evidence of gene-gene interactions in the analysis of common disease-associated variants in human populations.