gebhart/patrepeval huggingface dataset:
FXYD Proteins Stabilize Na,K-ATPase (2011)

FXYD proteins are a family of seven small regulatory proteins, expressed in a tissue-specific manner, that associate with Na,K-ATPase as subsidiary subunits and modulate kinetic properties. This study describes an additional property of FXYD proteins as stabilizers of Na,K-ATPase. FXYD1 (phospholemman), FXYD2 (γ subunit), and FXYD4 (CHIF) have been expressed in Escherichia coli and purified. These FXYD proteins associate spontaneously in vitro with detergent-soluble purified recombinant human Na,K-ATPase (α1β1) to form α1β1FXYD complexes. Compared with the control (α1β1), all three FXYD proteins strongly protect Na,K-ATPase activity against inactivation by heating or excess detergent (C(12)E(8)), with effectiveness FXYD1 > FXYD2 ≥ FXYD4. Heating also inactivates E(1) ↔ E(2) conformational changes and cation occlusion, and FXYD1 protects strongly. Incubation of α1β1 or α1β1FXYD complexes with guanidinium chloride (up to 6 m) causes protein unfolding, detected by changes in protein fluorescence, but FXYD proteins do not protect. Thus, general protein denaturation is not the cause of thermally mediated or detergent-mediated inactivation. By contrast, the experiments show that displacement of specifically bound phosphatidylserine is the primary cause of thermally mediated or detergent-mediated inactivation, and FXYD proteins stabilize phosphatidylserine-Na,K-ATPase interactions. Phosphatidylserine probably binds near trans-membrane segments M9 of the α subunit and the FXYD protein, which are in proximity. FXYD1, FXYD2, and FXYD4 co-expressed in HeLa cells with rat α1 protect strongly against thermal inactivation. Stabilization of Na,K-ATPase by three FXYD proteins in a mammalian cell membrane, as well the purified recombinant Na,K-ATPase, suggests that stabilization is a general property of FXYD proteins, consistent with a significant biological function.
Structure, biosynthesis, and function of teichoic acids (1970)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTStructure, biosynthesis, and function of teichoic acidsJames BaddileyCite this: Acc. Chem. Res. 1970, 3, 3, 98–105Publication Date (Print):March 1, 1970Publication History Published online1 May 2002Published inissue 1 March 1970https://pubs.acs.org/doi/10.1021/ar50027a003https://doi.org/10.1021/ar50027a003research-articleACS PublicationsRequest reuse permissionsArticle Views424Altmetric-Citations54LEARN 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
Inhibition of cell death by lens-specific overexpression of bcl-2 in transgenic mice (1997)

Previous studies on cell cycle regulation in the ocular lens using transgenic mice have shown that inactivation of the retinoblastoma tumor suppressor protein (pRb) can cause postmitotic lens fiber cells to enter the cell cycle. However, when the p53 gene and protein are intact, inactivation of pRb in this terminally differentiated cell type results in cell death, rather than continued proliferation. Since bcl-2 has been shown to act as a cell death repressor, the ability of this gene to block p53-dependent apoptosis in lenses was examined. Transgenic mice were generated that overexpress bcl-2 in a lens-specific fashion. Surprisingly, overexpression of bcl-2 was sufficient to interfere with normal fiber cell differentiation, inducing cataracts, microphakia, vacuolization, fiber cell disorganization, and inhibition of fiber cell denucleation. The bcl-2 mice were mated to mice exhibiting lens-specific expression of the N-terminal region of simian virus 40 large T antigen (termed truncT). The resulting double transgenic mice showed a marked reduction in the truncT-induced fiber cell death. Apoptosis in the truncT mice could also be suppressed by crossing these mice into a p53-deficient background. Either overexpression of bcl-2 or loss of p53 in truncT mice resulted in proliferation of fiber cells around the cortex of the lens. These proliferating fiber cells continue to express beta- and gamma-crystallin proteins, which are normally only expressed following withdrawal from the cell cycle. The p53 protein is known to upregulate expression of certain target genes, including p21, a protein that can block cell cycle progression by inhibition of cyclin-dependent kinases. In order to assess whether bcl-2 interferes with the transcriptional activation activity of p53, transgenic lenses were assayed by in situ hybridization for levels of p21 expression. Lenses that expressed both truncT and bcl-2 showed elevated p21, implying that bcl-2 does not inhibit apoptosis by directly inhibiting p53, but instead may block a later step in the apoptosis pathway. In addition, overexpression of p21 is not sufficient to cause apoptosis. These experiments show that the lenses of transgenic mice represent a valuable in vivo setting for studies of both induction and inhibition of programmed cell death.
In vitro assessment of bioactive coatings for neural implant applications (2003)

Recent efforts in our laboratory have focused on developing methods for immobilizing bioactive peptides to low cell-adhesive dextran monolayer coatings and promoting biospecific cell adhesion for biomaterial implant applications. In the current study, this dextran-based bioactive coating technology was developed for silicon, polyimide, and gold, the base materials utilized to fabricate our prototype neural implants. Chemical composition of all modified surfaces was verified by X-ray photoelectron spectroscopy (XPS). We observed that surface-immobilized dextran supported very little cell adhesion in vitro (24-h incubation with serum-supplemented medium) on all base materials. Inactive nonadhesion-promoting Gly-Arg-Ala-Asp-Ser-Pro peptides immobilized on dextran-coated materials promoted adhesion and spreading at low levels not significantly different from dextran-coated substrates. Arg-Gly-Asp (RGD) peptide-grafted surfaces were observed to promote substantial fibroblast and glial cell adhesion with minimal PC12 (neuronal cell) adhesion. In contrast, dextran-coated materials with surface-grafted laminin-based, neurite-promoting Ile-Lys-Val-Ala-Val (IKVAV) peptide promoted substantial neuron cell adhesion and minimal fibroblast and glial cell adhesion. It was concluded that neuron-selective substrates are feasible using dextran-based surface chemistry strategies. The chemical surface modifications could be utilized to establish a stable neural tissue-implant interface for long-term performance of neural prosthetic devices.
Chronic Hypoxia and Tubulointerstitial Injury (2005)

Recent studies emphasize the role of chronic hypoxia in the tubulointerstitium as a final common pathway to end-stage renal failure. When advanced, tubulointerstitial damage is associated with the loss of peritubular capillaries. Associated interstitial fibrosis impairs oxygen diffusion and supply to tubular and interstitial cells. Hypoxia of tubular cells leads to apoptosis or epithelial-mesenchymal transdifferentiation. This in turn exacerbates fibrosis of the kidney and subsequent chronic hypoxia, setting in train a vicious cycle whose end point is ESRD. A number of mechanisms that induce tubulointerstitial hypoxia at an early stage have been identified. Glomerular injury and vasoconstriction of efferent arterioles as a result of imbalances in vasoactive substances decrease postglomerular peritubular capillary blood flow. Angiotensin II not only constricts efferent arterioles but, via its induction of oxidative stress, also hampers the efficient utilization of oxygen in tubular cells. Relative hypoxia in the kidney also results from increased metabolic demand in tubular cells. Furthermore, renal anemia hinders oxygen delivery. These factors can affect the kidney before the appearance of significant pathologic changes in the vasculature and predispose the kidney to tubulointerstitial injury. Therapeutic approaches that target the chronic hypoxia should prove effective against a broad range of renal diseases. Current modalities include the improvement of anemia with erythropoietin, the preservation of peritubular capillary blood flow by blockade of the renin-angiotensin system, and the use of antioxidants. Recent studies have elucidated the mechanism of hypoxia-induced transcription, namely that prolyl hydroxylase regulates hypoxia-inducible factor. This has given hope for the development of novel therapeutic approaches against this final common pathway.
Pathophysiological Roles of ASK1-MAP Kinase Signaling Pathways (2007)

Apoptosis signal-regulating kinase 1 (ASK1) is a mitogenactivated protein kinase (MAPK) kinase kinase that activates JNK and p38 kinases. ASK1 is activated by various stresses, such as reactive oxygen species (ROS), endoplasmic reticulum (ER) stress, lipopolysaccharide (LPS) and calcium influx which are thought to be responsible for the pathogenesis or exacerbations of various human diseases. Recent studies revealed the involvement of ASK1 in ROS- or ER stressrelated diseases, suggesting that ASK1 may be a potential therapeutic target of various human diseases. In this review, we focus on the current findings for the relationship between pathogenesis and ASK1-MAPK pathways.
Shape Deposition Manufacturing (2018)

One challenge for solid freeform fabrication has been to develop the capability to directly&#13;\ncreate functional metal shapes which are dense, metallurgically bonded, geometrically accurate&#13;\nand with good surface appearance. Shape Deposition is a manufacturing paradigm which attempts&#13;\nto address these issues. It incorporates the advantages of several processes including solid freeform&#13;\nfabrication (complex geometries, rapidly planned), 5-axis CNC machining (accuracy,&#13;\nsmooth surfaces), shot-peening (for stress relief) and 'microcasting' (a high-performance, weldbased&#13;\nmaterial deposition process). These processes are integrated within a CAD/CAM system&#13;\nusing robotic automation. This paper will present the current research in this effort.
Ethnic and Racial Differences in the Smoking-Related Risk of Lung Cancer (2006)

Among cigarette smokers, African Americans and Native Hawaiians are more susceptible to lung cancer than whites, Japanese Americans, and Latinos.
Optical Rotatory Dispersion of Cobrotoxin* (1967)

Journal Article Optical Rotatory Dispersion of Cobrotoxin Get access CHEN-CHUNG YANG, CHEN-CHUNG YANG Department of Biochemistry, Kaohsiung Medical CollegeKaohsiung, Taiwan, Republic of China Search for other works by this author on: Oxford Academic PubMed Google Scholar CHUN-CHANG CHANG, CHUN-CHANG CHANG Department of Biochemistry, Kaohsiung Medical CollegeKaohsiung, Taiwan, Republic of China Search for other works by this author on: Oxford Academic PubMed Google Scholar KOZO HAMAGUCHI, KOZO HAMAGUCHI Faculty of Science, Kwansei Gakuin UniversityNishinomiya Search for other works by this author on: Oxford Academic PubMed Google Scholar KIYOSHI IKEDA, KIYOSHI IKEDA Faculty of Science, Kwansei Gakuin UniversityNishinomiya Search for other works by this author on: Oxford Academic PubMed Google Scholar KYOZO HAYASHI, KYOZO HAYASHI Institute for Protein Research, Osaka UniversityOsaka Search for other works by this author on: Oxford Academic PubMed Google Scholar TOMOJI SUZUKI TOMOJI SUZUKI Institute for Protein Research, Osaka UniversityOsaka Search for other works by this author on: Oxford Academic PubMed Google Scholar The Journal of Biochemistry, Volume 61, Issue 2, February 1967, Pages 272–274, https://doi.org/10.1093/oxfordjournals.jbchem.a128543 Published: 01 February 1967 Article history Received: 13 October 1966 Published: 01 February 1967
A shRNA library constructed through the generation of loop‐stem‐loop DNA (2010)

We constructed a shRNA library through four reaction steps, including the generation of loop-stem-loop DNA, without the polymerase chain reaction. A shRNA generated by this method retained its specificity of RNAi; however, the shRNA contained a target-irrelevant 7 nt sequence adjacent to the loop. This method could be valuable in the area of functional genomics.
Variable rate speech coding for asynchronous transfer mode (1990)

A new speech coding and multiplexing scheme matched to the asynchronous transfer mode is described. A block coding technique that is based on a variable-rate coding algorithm that makes the most of the burstiness of voice information is employed. The main feature of the scheme is considerable bit reduction, which is attained by a fairly simple algorithm. It is demonstrated that the proposed algorithm exhibits better quality than that of a 32 kb/s ADPCM at a mean bit rate of less than 13 kb/s. The effect of statistical multiplexing is verified by means of simulation employing long conversational speech samples. Methods for constructing variable- and fixed-length frames (units of information multiplexed and transferred in the network) are proposed. The proposed coding algorithm is shown to be applicable to both variable- and fixed-length frame strategies.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
DNA Probe for Lactobacillus delbrueckii (1990)

From a genomic DNA library of Lactobacillus delbrueckii subsp. bulgaricus, a clone was isolated which complements a leucine auxotrophy of an Escherichia coli strain (GE891). Subsequent analysis of the clone indicated that it could serve as a specific DNA probe. Dot-blot hybridizations with over 40 different Lactobacillus strains showed that this clone specifically recognizes L. delbrueckii subsp. delbrueckii, bulgaricus, and lactis. The sensitivity of the method was tested by using an alpha-P-labeled DNA probe.
An efficient algorithm for optimizing DCT quantization (2000)

We describe the RD-OPT algorithm for DCT quantization optimization, which can be used as an efficient tool for near-optimal rate control in DCT-based compression techniques, such as JPEG and MPEG. RD-OPT measures DCT coefficient statistics for the given image data to construct rate/distortion-specific quantization tables with nearly optimal tradeoffs.
Lab-on-Paper with Dual Electrochemical/Colorimetric Detection for Simultaneous Determination of Gold and Iron (2010)

A novel lab-on-paper device combining electrochemical and colorimetric detection for the rapid screening of Au(III) in the presence of a common interference, Fe(III), in industrial waste solutions is presented here. With dilute aqua regia (0.1 M HCl + 0.05 M HNO(3)) as the supporting electrolyte, square wave voltammetry on paper provided a well-defined reduction peak for Au(III) at approximately 287 +/- 12 mV vs Ag/AgCl. Under the optimized working conditions, the calibration curve showed good linearity in the concentration range of 1-200 ppm of Au(III) with a correlation coefficient of 0.997. The limit of detection (LOD) of the proposed method is 1 ppm. Interferences from various cations were also studied. Fe(III) is the only metal that affects the electrochemical determination of Au(III) when present above a 2.5-fold excess concentration of that of the Au(III). To overcome this limitation, a colorimetric method was used to simultaneously detect Fe(III) as a screening tool. The procedure was then successfully applied to determine Au(III) in gold-refining waste solutions. The results are in agreement with those obtained from inductively coupled plasma-atomic emission spectrometry (ICP-AES).
Severe deficiency of cystic fibrosis transmembrane conductance regulator messenger RNA carrying nonsense mutations R553X and W1316X in respiratory epithelial cells of patients with cystic fibrosis. (1991)

Cystic fibrosis (CF) is the most common, lethal inherited disorder in the Caucasian population. We have recently reported two African-American patients with nonsense mutations in each CF gene and severe pancreatic disease, but mild pulmonary disease. In order to examine the effect of these nonsense mutations on CF gene expression, bronchial and nasal epithelial cells were obtained from one of these patients (no. 246), a compound heterozygote for nonsense mutations R553X and W1316X; a healthy normal individual; a patient (no. 528) homozygous for the common CF mutation (delta F508); and a CF patient (no. 272) who carries the R553X mutation and a missense mutation, S549N. When mRNA from bronchial cells of the normal individual, the delta F508 homozygote, and the S549N/R553X compound heterozygote was reverse transcribed and amplified by polymerase chain reaction using primers derived from the CF gene, DNA fragments of the predicted size were observed. However, patient no. 246 with nonsense mutations in each CF gene has no detectable cystic fibrosis transmembrane conductance regulator (CFTR) messenger RNA, and therefore should have severely diminished, and possibly absent, CFTR protein. Furthermore, less than 2% of the CFTR transcripts in nasal epithelial cells from patient no. 272 (S549N/R553X) were derived from the gene with the nonsense mutation. We conclude that severe reduction in CFTR mRNA causes CF, but can have different consequences in the lung and pancreas.
Administration of highly purified eicosapentaenoic acid to statin-treated diabetic patients further improves vascular function (2012)

We prospectively examined the additional effects of highly purified eicosapentaenoic acid (EPA) particularly on the vascular function of diabetic patients with hypercholesterolemia receiving statin therapy. We enrolled 28 patients with type 2 diabetes complicated by dyslipidemia who had been treated with statins for at least one year. The patients were randomly assigned to 2 groups: administration of statin alone (group S: n = 13) and addition of EPA to the current statin therapy (group SE: n = 15). The highly purified EPA was administered at a dose of 1,800 mg/day for 6 months. To evaluate vascular function, the duration of reactive hyperemia (DRH), which is the time required for forearm blood flow to return to the basal level after inducing reactive hyperemia, was measured using strain gauge plethysmography. There were no significant differences in the clinical background factors between the 2 groups. Low-density lipoprotein cholesterol (LDL-C), and non-high-density lipoprotein cholesterol levels significantly decreased after 6 months only in group SE. Compared with the baseline data, no significant change in DRH was observed after 6 months in group S. By contrast, DRH was significantly prolonged after 6 months in group SE, indicating that the addition of highly purified EPA improved vascular function. Our results showed that in patients with type 2 diabetes and receiving statin therapy whose LDL-C level was less than 100 mg/dL, the addition of highly purified EPA for 6 months significantly improved vascular function.
Chicken major histocompatibility complex class II B genes: analysis of interallelic and inter‐locus sequence variance (1993)

Five different chicken B-LB genes were cloned and sequenced. The comparison of these sequences shows that they can be classified as members of two different families, the B-LBII family (containing the B-LBI and B-LBII genes) and the B-LBIII family (containing the B-LBIII, B-LBIV, and B-LBV genes). The extent of polymorphism within each of these families was assessed by in vitro amplification of DNA fragments encompassing exon 2 in several haplotypes. The nucleotide sequences were determined, and pairwise relationships were evaluated. In the course of this work, a sixth gene termed B-LBVI was identified, defining a third family (B-LBVI family). Polymorphism of the B-LBIII or B-LBVI families is far less extensive than that of the B-LBII family. In this latter, the distribution of conserved and polymorphic residues is similar to what has been described in mammals. These families seem to have been generated by gene duplication events giving rise to several isotypes, as observed in mammals. However, phylogenetic analyses indicate that these families are not homologous to their mammalian counterparts. Evaluation of the level of transcription of these different genes showed that genes from the B-LBII family are predominantly transcribed over those of the other families.
Sec-independent Protein Translocation in Escherichia coli (1999)

In Escherichia coli, transmembrane translocation of proteins can proceed by a number of routes. A subset of periplasmic proteins are exported via the Tat pathway to which proteins are directed by N-terminal "transfer peptides" bearing the consensus (S/T)RRXFLK "twin-arginine" motif. The Tat system involves the integral membrane proteins TatA, TatB, TatC, and TatE. Of these, TatA, TatB, and TatE are homologues of the Hcf106 component of the DeltapH-dependent protein import system of plant thylakoids. Deletion of the tatB gene alone is sufficient to block the export of seven endogenous Tat substrates, including hydrogenase-2. Complementation analysis indicates that while TatA and TatE are functionally interchangeable, the TatB protein is functionally distinct. This conclusion is supported by the observation that Helicobacter pylori tatA will complement an E. coli tatA mutant, but not a tatB mutant. Analysis of Tat component stability in various tat deletion backgrounds shows that TatC is rapidly degraded in the absence of TatB suggesting that TatC complexes, and is stabilized by, TatB.