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PubMed1996

Deletion of the carboxyl-terminal transactivation domain of MGF-Stat5 results in sustained DNA binding and a dominant negative phenotype.

The Stat (signal transducer and activator of transcription) factors transmit cytokine, growth factor, and hormone responses. Seven members of the Stat gene family are known. MGF-Stat5a has been discovered as a mediator of the prolactin response in mammary epithelial cells. Two closely related variants of Stat5, Stat5a and Stat5b, are encoded by distinct genes. We examined the functional properties of the carboxyl termini of these molecules. Wild-type Stat5a (794 amino acids) and the carboxyl-terminal deletion mutant Stat5a delta 772 supported prolactin-induced transcription of a beta-casein promoter-reporter construct in COS7 cells; Stat5a delta 750 did not. Upon prolactin activation, tyrosine phosphorylation and the specificity of DNA binding were indistinguishable among the three Stat5a variants. Tyrosine dephosphorylation and the downregulation of the DNA-binding activity were delayed in the Stat5a delta 750 mutant. The carboxyl-terminal transactivation domain of Stat5a, amino acids 722 to 794, can be conferred to the DNA-binding domain of the yeast transcription factor GAL4. Coexpression of Stat5a or Stat5b and of the carboxyl-terminal deletion mutants resulted in the suppression of transcriptional induction in COS or Ba/F3 cells. We propose that Stat5a delta 750 and Stat5b delta 754 are lacking functional transactivation domains and exert their dominant negative effects by blocking the DNA-binding site in Stat5-responsive gene promoters.

Amino Acid Sequence↗
PubMed2004

Tazobactam inactivation of SHV-1 and the inhibitor-resistant Ser130 -->Gly SHV-1 beta-lactamase: insights into the mechanism of inhibition.

The increasing number of bacteria resistant to combinations of beta-lactam and beta-lactamase inhibitors is creating great difficulties in the treatment of serious hospital-acquired infections. Understanding the mechanisms and structural basis for the inactivation of these inhibitor-resistant beta-lactamases provides a rationale for the design of novel compounds. In the present work, SHV-1 and the Ser(130) --> Gly inhibitor-resistant variant of SHV-1 beta-lactamase were inactivated with tazobactam, a potent class A beta-lactamase inhibitor. Apoenzymes and inhibited beta-lactamases were analyzed by liquid chromatography-electrospray ionization mass spectrometry (LC-ESI/MS), digested with trypsin, and the products resolved using LC-ESI/MS and matrix-assisted laser desorption ionization-time of flight mass spectrometry. The mass increases observed for SHV-1 and Ser(130) --> Gly (+ Delta 88 Da and + Delta 70 Da, respectively) suggest that fragmentation of tazobactam readily occurs in the inhibitor-resistant variant to yield an inactive beta-lactamase. These two mass increments are consistent with the formation of an aldehyde (+ Delta 70 Da) and a hydrated aldehyde (+ Delta 88 Da) as stable products of inhibition. Our results reveal that the Ser --> Gly substitution at amino acid position 130 is not essential for enzyme inactivation. By examining the inhibitor-resistant Ser(130) --> Gly beta-lactamase, our data are the first to show that tazobactam undergoes fragmentation while still attached to the active site Ser(70) in this enzyme. After acylation of tazobactam by Ser(130) --> Gly, inactivation proceeds independent of any additional covalent interactions.

Binding Sites↗
PubMed1986

[Variants of phage M13 DNA containing a fragment of the beta-galactosidase gene--a convenient mutation system for the study of oligonucleotide-directed mutagenesis].

A model system is developed to test oligonucleotide-directed mutations: T----C transition, T and C deletions (delta T and delta C), C insertion, double mutations (A----G, delta T), (T----C, A----G), and large oligonucleotide deletions (36 or 44 nucleotides). The system includes 9 variants of the phage M13 DNA carrying fragment of beta-galactosidase gene, and oligodeoxyribonucleotides partially noncomplementary to DNA sequence of this gene. Six variants are obtained by the site-localized mutagenesis, the other were described earlier. Induced mutations are easily tested by phenotype change of transformed bacteria (Lac+----Lac-); by formation or loss of the sites for BamHI and EcoRI restrictases; by DNA hybridization with 32P-labeled oligonucleotides; and by DNA sequencing by the Sanger method. The system is used to study the role of some factors, such as completeness of RF DNA synthesis, thermal stability of the oligonucleotide: DNA complex, quality of enzymes and substrates used in polymerase reaction, mutation type or the efficiency of mutagenesis. A number of unexpected mutations were observed in the course of oligonucleotide-directed mutagenesis. Lower yields of some mutants induced by oligonucleotides are shown to be due to the action of repair systems of bacteria.

Coliphages↗
PubMed1995

Variants of hepatitis B, C and D viruses: molecular biology and clinical significance.

Variants of hepatitis B virus (HBV), hepatitis C virus (HCV) and of the hepatitis Delta virus (HDV) have been identified in patients both with acute and chronic infections. In the HBV DNA genome, naturally occurring mutations have been found in all viral genes, most notably in the genes coding for the structural envelope and nucleocapsid proteins. In the HCV RNA genome, the regions coding for the structural envelope proteins 1 and 2 as well as the 3'-contiguous nonstructural region 1 were found to be hypervariable. Viral variants may be associated with a specific clinical course of the infection, e.g. acute-fulminant or chronic hepatitis. Specific mutations may reduce viral clearance by immune mechanisms ('immune escape') or response to antiviral therapy ('therapy escape'). Furthermore, mutations of envelope epitopes can lead to viral variants which are not recognized or neutralized by antibodies to wild-type virus, resulting in 'diagnosis escape' or 'vaccine escape'. The exact contribution, however, of specific mutations to the pathogenesis and natural course of HBV, HCV or HDV infection, including the development of hepatocellular carcinoma, remains to be established.

Genotype↗
PubMed1988

The T-cell antigen receptor: a complex signal-transducing molecule.

The T cell antigen-specific receptor (TCR) on most mature T cells is a multisubunit complex composed of 7 chains: alpha, beta, gamma, delta, epsilon, and either a zeta-zeta homodimer (zeta 2) or a zeta-eta heterodimer (zeta eta). We have derived a series of TCR variants and mutants from the antigen-specific murine T cell hybridoma, 2B4.11, permitting detailed analyses of the assembly and transport of the TCR. Loss of the zeta chain resulted in markedly reduced cell surface TCR expression. This was due to enhanced degradation of the other TCR chains in a post-Golgi, probably lysosomal, compartment. Loss of the beta chain, delta chain, or the combination of delta and zeta chains, also resulted in loss of cell surface TCR expression. Unlike the zeta loss variants, in these cases the other TCR chains were retained in the ER. Epsilon, gamma, and zeta could survive for prolonged periods in the ER, while the alpha, beta, and delta chains were rapidly and efficiently degraded. In another series of studies, variants that were deficient in the eta chain but that expressed normal levels of zeta 2-containing TCRs were analyzed for their functional properties. A positive relationship was found between the presence of zeta eta and the ability to respond to mitogenic stimuli with increases in phosphoinositide hydrolysis and, in one well characterized variant, increases in intracellular Ca2+. Despite this, late biological responses such as interleukin 2 (IL-2) production and inhibition of transformed growth were relatively normal. These results call into question the putative cause-and-effect relationship between some early biochemical events and these late biological responses. Further, they suggest a model in which zeta eta-containing TCR complexes are largely responsible for activation-induced phosphoinositide hydrolysis.

Animals↗
PubMed1981

Beta-thalassemia in Brazil.

1. Clinical, hematological, genetic and peripheral blood globin synthesis studies were carried out on 17 symptomatic Brazilian thalassemics and their parents who live in the northeast of São Paulo State. The group included 8 beta zero-thalassemia homozygotes, 7 carriers of at least one beta + gene, one delta beta zero/beta zero-thalassemia double heterozygote and one beta zero homozygote also carrying the alpha-chain variant Hb Hasharon (alpha 2(47) His beta 2). 2. The mean non-alpha/alpha ratio for globin biosynthesis of the patients lacking HbA (beta zero homozygotes and delta beta zero/beta zero double heterozygotes) was 0.26 +/- 0.11 (mean +/- SD), which is not statistically different from the value of 0.32 +/- 0.06 obtained for the carriers of at least one beta + gene. In contrast, the mean non-alpha/alpha ratio for the thalassemia major patients (0.22 +/- 0.07) was significantly lower than that obtained for the milder cases (0.34 +/- 0.06) although the beta/alpha ratios for the parents of the two groups were similar. 3. The heterogeneity within this group of Brazilian patients having two thalassemic genes, i.e. 60% who are beta zero homozygotes and 40% who are carriers of at least one beta + gene, is consistent with the Italian origin of most of these patients.

Adolescent↗
PubMed1996

A variation at position -30 of the beta-cell glucokinase gene promoter is associated with reduced beta-cell function in middle-aged Japanese-American men.

We sought to determine whether a G -> A variant at position -30 of the beta-cell promoter of the glucokinase (GCK) gene observed to be present more frequently in Japanese-American men with impaired glucose tolerance (IGT) than in Japanese-American men with normal glucose tolerance (NGT) is associated with impaired beta-cell function. We studied 125 unrelated Japanese-American men (aged 46-74 years; mean 61 +/- 0.5) who were nondiabetic by a 75-g oral glucose tolerance test (OGTT) (65 had NGT and 60 had IGT). The presence of the -30 beta-cell GCK gene promoter variant was determined by single-strand conformation polymorphism analysis. Beta-cell function was assessed using the ratio of the incremental response in immunoreactive insulin (IRI) to that of glucose during the first 30 min of the OGTT (delta IRI[30 min-0 min]/delta glucose[30 min-0 min]) performed at baseline and at 5 years of follow-up. Beta-cell function adjusted for basal IRI ([delta IRI[30 min-0 min]/delta glucose[30 min-0 min]]/basal IRI; the relative insulin response) was also evaluated. At baseline, the -30 beta-cell GCK gene promoter variant was present in 15.4% of subjects with NGT vs. 38.3% of subjects with IGT (P < 0.01). Fasting IRI did not differ between groups. At baseline, delta IRI[30 min-0 min]/delta glucose[30 min-0 min] was significantly lower in subjects with the promoter variant (57 x 10(-9) [35 x 10(-9) to 95 x 10(-9)] vs. 77 x 10(-9) [55 x 10(-9) to 128 x 10(-9)]; median [interquartile range]; P < 0.01) as was the relative insulin response (0.97 [0.70-1.24] vs. 1.37 [0.95-2.03]l/mmol; P < 0.0005). Similarly, at 5 years of follow-up, delta IRI[30 min-0 min]/delta glucose[30 min-0 min] and the relative insulin response were significantly reduced in the group with the variant. In the subgroups of subjects with IGT at baseline, IGT at 5 years, and NGT at 5 years, the relative insulin response was significantly lower in those with the variant. We conclude that the -30 beta-cell GCK gene promoter variant is associated with reduced beta-cell function in middle-aged Japanese-American men and may contribute to the high risk of abnormal glucose tolerance in this population.

Aged↗
PubMed1993

[Localization of an immunodominant site in the hepatitis delta viral antigen using synthetic peptides].

A set of 8 peptides from the immunodominant region (65-80 aa) of delta-antigen was prepared by solid-phase synthesis. Peptide 71-80 was synthesized in two variants--with different amino acid residues in positions 73, 74 and 76. Free peptides and their conjugates with bovine serum albumin were tested for antigenicity in ELISA. The correlation between the peptide chain's length and its antigenic activity was noted. Peptides 65-80 and 69-80 displayed a positive reaction with all individual sera and pools of sera from HDV chronic patients. Both variants of the peptide 71-80 reacted with 100% of sera pools but only with 83% of individual sera. Smaller peptides from the same 65-80 region (73-80, 69-78, 71-78, 71-76) did not bind to any anti-delta positive serum. All synthesized peptides reacted strongly with rabbit antisera raised to the conjugate of peptide 65-80 with bovine albumin. These findings suggest that delta-antigen contains multiple highly immunogenic epitopes associated with the single immunodominant site between 69 and 80 amino acid residues.

Amino Acid Sequence↗
PubMed1991

pUBEX/pUBSEX: a versatile expression vector system for production of fusion and nonfusion proteins in Escherichia coli.

Despite the large number of expression vectors now available, none provide the facility of allowing fusion and nonfusion protein production from the same vector system. In some situations it is preferable to obtain an insoluble fusion protein, in others a soluble nonfusion protein may be required. We have designed, constructed and tested a modification of the pEX vectors, in which it is possible to express the product of a suitably inserted cDNA either as part of a Cro-beta-galactosidase (Cro-beta Gal) fusion or as a delta Cro fusion which contains only nine noninsert-encoded amino acids at its N terminus. The conversion from Cro-beta Gal to delta Cro fusion protein production is achieved by a simple intramolecular deletion of lacZ sequence from the pUBEX vector, to create the pUBSEX variant. Plasmid pUBEX can be induced to produce large amounts of insoluble Cro-beta Gal fusion proteins, whereas pUBSEX will produce predominantly soluble delta Cro fusion proteins.

Animals↗
PubMed1992

Introduction of a disulfide bond into cytochrome c stabilizes a compact denatured state.

We introduced a novel disulfide bond, modeled on that of bullfrog cytochrome c, into yeast iso-1-cytochrome c. The disulfide spontaneously forms upon purification. A variety of techniques were used to examine the denaturation of this variant and several non-cross-linked controls. Denaturation is reversible and, with the exception of the protein in which the two cysteines are blocked, consistent with a two-state process. Comparison of the calorimetric and van't Hoff enthalpy changes indicates that denaturation is two-state at pH 4.6. Calorimetric and fluorescence-monitored guanidine hydrochloride (GdnHCl) denaturation data indicate that the free energy of denaturation for the cross-linked protein (delta Gd at 300 K) is decreased relative to non-cross-linked controls. The dependence of delta Gd on GdnHCl concentration, the GdnHCl concentration that denatures half the protein, as well as the enthalpy, entropy, and heat capacity changes (mGdnHCl, Cm, delta Hd, delta Sd, and delta Cp, respectively), all decrease in magnitude upon introduction of the cross-link. The decrease in delta Hd and delta Sd were confirmed by monitoring absorbance at several wavelengths as a function of temperature. The cross-link also decreases the pH dependence of these observables. Circular dichroism studies indicate the denatured state of the cross-linked protein possesses more structure than non-cross-linked proteins, and this structure is refractory to increases in temperature and chemical denaturant. We conclude that the diminished values of delta Gd, delta Hd, delta Sd, delta Cp, and mGdnHCl result from the denatured state of the cross-linked variant being more compact and possessing more structure than non-cross-linked controls.

Calorimetry, Differential Scanning↗
PubMed1983

Electron microscopy and single molecule averaging of subunit-deficient F1-ATPases from Escherichia coli and spinach chloroplasts.

The morphology of F1-ATPases lacking one or more small subunits has been investigated by minimal-beam electron microscopy of close-packed monolayers of molecules. Computer-based rotational analyses of single molecules were performed on reconstituted 3-subunit F1-ATPase (-delta epsilon) from Escherichia coli and both 3-subunit (-delta epsilon) and 4-subunit (-delta) F1-ATPase from chloroplasts. Optical diffraction measurements of close-packed arrays revealed maximal dimensions of 122 +/- 4 A and 129 +/- 9 A for 3-subunit ECF1 and 4-subunit CF1, respectively. Molecules which displayed either hollow or solid hexagonal morphologies were observed in all preparations. Averaged reconstructions were obtained from molecules with hollow morphologies in 3-subunit preparations and demonstrated strong hexagonal symmetry in projection with a central, stain-filled cavity. The average reconstruction obtained from molecules with the solid morphology in 4-subunit CF1 preparations, was also strongly hexagonal with six peripheral units ringed about a central subunit. Differences between hollow and solid morphologies cannot be attributed solely to the presence or absence of the delta and epsilon subunits; therefore, the two image types may represent staining variants of a common structure. Overall, the reconstructions are consistent with an alpha 3 beta 3 gamma stoichiometry for the coupling factors from both E. coli and chloroplasts.

Chloroplasts↗
PubMed1995

Drug-stimulated ATPase activity of a deletion mutant of the human multidrug-resistance protein (MDR1).

The baculovirus-insect cell system has been used for the functional expression of the human multidrug resistance protein (MDR1) and a mutant MDR1 variant lacking a twenty amino acid segment from the first extracellular loop (delta aa78-97 MDR1). Both MDR1 proteins were found to be correctly inserted into the insect cell membrane as indicated by their interaction with MRK 16 antibody. The removal of the 78-97 segment from the first extracellular loop dramatically altered drug-stimulated ATPase activity. Rhodamine 123 or vinblastine were not able to stimulate the mutant protein and Calcein AM had also little effect. In contrast, verapamil increased the ATPase activity of the mutant almost to the same maximal level as that of the wild type. However, the verapamil concentration needed for the half maximal stimulation of the ATPase activity was found to be about hundred times higher than that for the wild type MDR1. These results indicate that a partial deletion of an extracellular loop modulates the affinity of MDR1 for its transportable substrates in a variable fashion.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1993

GABAA/benzodiazepine receptor gamma 2 subunit gene expression in developing normal and mutant mouse cerebellum.

Recent studies have identified several subunits (alpha, beta, gamma and delta) of the gamma-aminobutyric acidA/benzodiazepine receptor; each consists of several variants. The gamma 2 subunit appears to mediate the interaction of the alpha and beta subunits making the receptor capable of modulation by benzodiazepines. In the present studies, the expression of mRNA encoding the gamma 2 subunit was examined in the cerebellum during development and in adult Purkinje cell degeneration, lurcher and reeler mutant mice. In the normal adult cerebellum, in situ hybridization with [35S]cRNA probes revealed a strong signal over the Purkinje cell layer and deep cerebellar nuclei, and a weaker signal over basket, stellate and granule cells. Labeling over Purkinje cells was detectable at birth, gradually becoming stronger and more punctate during postnatal weeks 1 and 2, as Purkinje cells formed a monolayer between the molecular and granule cell layers. Adult levels of grain density were reached by P20. The external germinal layer, which contained proliferating granule cells, was unlabeled throughout development; however, weak labeling was detected over the internal granular layer at the end of postnatal week 1, as granule cells began their migration across the molecular layer. During the second postnatal week, punctate labeling became visible over the molecular layer in a distribution indicative of basket and stellate cells. In adult Purkinje cell degeneration and lurcher mutants, in which Purkinje cells have degenerated, no punctate labeling characteristic of mature Purkinje cells was detected. In adult and developing reeler mutants, where all classes of cells are malpositioned throughout the cerebellum, the punctate hybridization signal was present and clearly associated with Purkinje cells in all cortical regions. Our results suggest that developing Purkinje cells express the gamma 2 gene at a time prior to receiving GABAergic inhibitory input, and that the continued expression in the adult is not affected by the absence of afferents.

Adult↗
PubMed1995

Site specific combinations of stabilizing and destabilizing amino acid replacements in yeast cytochrome c: in vivo and in vitro effects.

Oligonucleotide-directed mutagenesis in vivo was used to create destabilizing site specific changes at position 6 in iso-1-cytochrome c in Saccharomyces cerevisiae. These changes were made in combination with the stabilizing N52I substitution. The resulting proteins showed that a variety of forces and interactions are responsible for these destabilizations. Increasing side chain size was the strongest predictor of decreases in cytochrome c levels in vivo. With intermediate size replacements, increasing hydrophobicity correlated with the proteins' thermostability. Some differences in protein levels in vivo could not be explained by side chain size and hydrophobicity alone. Therefore, specific interactions of individual amino acids may also be involved. The N52I-stabilizing mutation tended to increase the protein levels to the same degree relative to the amino acid at position 6. These stabilized cytochromes had an increased specific activity when compared to the series with the original N52. Strains with these altered cytochromes c showed temperature sensitivities for protein levels and function. Thermodynamic measurements in vivo of the WT (C102A), N52I, G6A, G6A N52I, and G6S N52I correlated with the in vivo data. The variant G6A N52I showed additivity (Wells, 1990) of the Cm's and delta delta G's of unfolding for guanidine hydrochloride denaturation.

Amino Acid Sequence↗
PubMed1996

A low-barrier hydrogen bond in subtilisin: 1H and 15N NMR studies with peptidyl trifluoromethyl ketones.

The N delta 1 proton of His 64 forms a hydrogen bond with Asp 32, as part of the catalytic triad in serine proteases of the subtilisin family. His 64 in subtilisin has been studied by 1H and 15N NMR spectroscopy in the presence and absence of peptidyl trifluoromethyl ketones (TFMKs) that are transition state analog inhibitors. For subtilisin Carlsberg, the downfield resonance of the imidazolium N delta 1 proton is approximately 18.3 ppm and the D/H fractionation factor is 0.55 +/- 0.04 at pH 5.5 (11 degrees C), and 0.63 +/- 0.04 (5 degrees C) and 0.68 +/- 0.04 at pH 6 (11 degrees C). In the complex between subtilisin Carlsberg and Z-L-leucyl-L-leucyl-L-phenylalanyltrifluoromethyl ketone (Z-LLF-CF3) at pH values between 6.5 and 10.6, His 64 remains positively charged, and the D/H fractionation factor of its N delta 1 proton is 0.85 +/- 0.05. In the complex between a subtilisin variant from Bacillus lentus and Z-LLF-CF3, the proton resonance at 18.8 ppm is correlated with a 15N resonance at 197.6 ppm downfield from liquid NH3 with a 1JNH of 81 Hz. The chemical shifts of subtilisin complexes with peptidyl TFMKs are among the most downfield shifts reported for any protein. At pH 9.5, His 64 is neutral and the D/H fractionation factor increases to 1.2 with a chemical shift of 15.0. His 64 is positively charged in the free enzyme at low pH, the inhibitor hemiketal complex at neutral pH, and the transition state for amide bond hydrolysis. These data thus provide indirect evidence for the presence of a low-barrier hydrogen bond in the catalytic mechanism of subtilisin proteases.

Bacterial Proteins↗
PubMed1997

Role of transmembrane pH gradient and membrane binding in nisin pore formation.

Nisin is a cationic antimicrobial peptide that belongs to the group of lantibiotics. It is thought to form oligomeric pores in the target membrane by a mechanism that requires the transmembrane electrical potential delta psi and that involves local pertubation of the lipid bilayer structure. Here we show that nisin does not form exclusively voltage-dependent pores: even in the absence of a delta psi, nisin is able to dissipate the transmembrane pH gradient (delta pH) in sensitive Lactococcus lactis cells and proteoliposomes. The rate of dissipation increases with the magnitude of the delta pH. Nisin forms pores only when the delta pH is inside alkaline. The efficiency of delta psi-induced pore formation is strongly affected by the external pH, whereas delta pH-induced pore formation is rather insensitive to the external pH. Nisin(1-12), an amino-terminal fragment of nisin, and (des-deltaAla5)-(nisin(1-32) amide have a strongly reduced capacity to dissipate the delta psi and delta pH in cytochrome c oxidase proteoliposomes and L. lactis cells. Both variants bind with reduced efficiency to liposomes containing negatively charged phospholipids, suggesting that both ring A and rings C to E play a role in membrane binding. Nisin(1-12) competes with nisin for membrane binding and antagonizes pore formation. These findings are consistent with the wedge model of nisin-induced pore formation.

Animals↗
PubMed1993

Temperature-induced conformational transition in xanthans with partially hydrolyzed side chains.

The conformational properties of xanthans with partially hydrolyzed side chains were investigated by optical rotation, CD, and differential scanning calorimetry (DSC). All variants displayed the well-known temperature-driven, cooperative order-disorder transition, and both optical rotation and DSC showed that the transition temperature was essentially independent of the content of terminal beta-mannose. It was found that up to 80% of the changes in the specific optical rotation accompanying the transition reflects conformational changes linked to the terminal beta-mannose in the side chains. Modification of the side chains also affected the CD when xanthan was in the ordered state, but in this case the data suggest that the glucuronic acid is the major component determining the magnitude of the CD signal. DSC measurements showed that the transition enthalpy (delta Hcal) increased linearly with the fraction of beta-mannose, again indicating that a significant part (up to 80%) of delta Hcal reflects conformational changes in the side chains. The conformational transition of the xanthan variants generally showed a higher degree of cooperativity (sharper transition) than unmodified, pyruvated xanthan. Calculation of the cooperativity parameter sigma by means of the Zimm-Bragg theory (OR data) or from the ratio between delta Hcal and the van't Hoff enthalpy (delta HvH) using DSC data showed a correlation between sigma and the content of beta-mannose, but the two methods gave different results when the content of beta-mannose approached 100%. The ionic strength dependence of the transition temperature, expressed as d (log I)/d(T-1m), was nearly identical for intact xanthan and a sample containing only 6% of the terminal beta-mannose. Application of the Manning polyelectrolyte theory does not readily account for the observed delta Hcal values, neither does it provide new information on the nature of the ordered and disordered conformations in xanthan.

Calorimetry, Differential Scanning↗
PubMed1998

Access to a syllabus of human hemoglobin variants (1996) via the World Wide Web.

Information on mutations in human hemoglobin is important in many efforts, including understanding the pathophysiology of hemoglobin diseases, developing therapies, elucidating the dynamics of sequence alterations inhuman populations, and dissecting the details of protein structure/function relationships. Currently, information is available on a large number of mutations and variants, but is distributed among thousands of papers. In an effort to organize this voluminous data set, two Syllabi have been prepared compiling succinct information on human hemoglobin abnormalities. In both of these, each entry provides amino acid and/or DNA sequence alterations, hematological and clinical data, methodology used for characterization, ethnic distribution, and functional properties and stability of the hemoglobin, together with appropriate literature references. A Syllabus of Human Hemoglobin Variants (1996) describes 693 abnormal hemoglobins resulting from alterations in the alpha-, beta-, gamma-, and delta-globin chains, including special abnormalities such as double mutations, hybrid chains, elongated chains, deletions, and insertions. We have converted this resource to an electronic form that is accessible via the World Wide Web at the Globin Gene Server (http://globin.cse.psu.edu). Hyperlinks are provided from each entry in the tables of variants to the corresponding full description. In addition, a simple query interface allows the user to find all entries containing a designated word or phrase. We are in the process of converting A Syllabus of Thalassemia Mutations (1997) to a similar electronic format.

Computer Communication Networks↗