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PubMed1997

Co-localization of truncated tau and DNA fragmentation in Alzheimer's disease neurones.

Monoclonal antibody MN423 stains all hallmarks of tau neurofibrillary pathology in Alzheimer's disease (AD), without reacting with full-length tau. It recognizes tau molecules which are cleaved at Glu-391, suggesting that tau is endogenously truncated in AD brains. We investigated whether truncation of tau takes place in pre-tangle neurones. Our results showed that tau truncation occurs inside AD neurones in the absence of other signs of AD neurofibrillary pathology. Using in situ end labelling (ISEL) of DNA we found evidence for DNA fragmentation in a significant subpopulation of MN423-positive neurones. Our results therefore suggest that tau truncation is an early intracellular event preceding cell death in AD.

Aged↗
PubMed1999

BDNF and full-length and truncated TrkB expression in Alzheimer disease. Implications in therapeutic strategies.

Brain-derived neurotrophic factor (BDNF), and full-length and truncated tyrosin kinase B receptor (TrkB) protein expression were examined by Western blotting and immunohistochemistry in the frontal cortex and hippocampus of individuals affected by long-lasting severe Alzheimer disease (AD) and age-matched controls. Since preliminary processing studies in the brains of rats have shown loss of immunoreactivity depending on the postmortem delay in tissue processing and on the type, duration, and temperature of the fixative solution, only human samples obtained up to 6 hours (h) after death for biochemical and morphological studies and fixed by immersion in 4% paraformaldehyde for 24 h for morphological studies were included in the present series. Decreased BDNF and full-length TrkB expression accompanied by increased truncated TrkB expression, as revealed by Western blotting, was observed in the frontal cortex of patients with AD. Immunohistochemistry disclosed reduced BDNF and full-length TrkB immunoreactivity in neurons. BDNF decrease was equally observed in tangle-bearing and non-tangle-bearing neurons, as revealed with double-labeling immunohistochemistry to BDNF and phosphorylated tau or phosphorylated neurofilament epitopes. Full-length TrkB immunoreactivity was largely decreased in tangle-bearing neurons, whereas only moderate decreases occurred in neurons with granulovacuolar degeneration. Strong BDNF immunoreactivity was observed in dystrophic neurites surrounding senile plaques, whereas strong TrkB expression occurred in reactive glial cells, including those surrounding senile plaques. Finally, truncated TrkB immunoreactivity was observed in individual neurons and in reactive glial cells in the cerebral cortex and white matter in AD. These results show decay in the expression of BDNF and TrkB in AD neurons, accompanied by altered BDNF, and full-length and truncated TrkB expression in dystrophic neurites and reactive glial cells, respectively, in this disease. The present results demonstrate selective decline of the BDNF/TrkB neurotrophic signaling pathway in the frontal cortex and hippocampus in AD and provide supplemental data that may be relevant in discussing the suitability of the use of BDNF as a therapeutic agent in patients with AD.

Aged↗
PubMed1980

The effect of varying prism and truncation on the performance of soft contact lenses.

A group of 10 subjects were optimally fitted with soft senses by photoelectronic keratoscopic analysis of corneal form. Lenses with diameters of 12.8 and 13.5 mm were worn incorporating prism ballasting varying between 0 and 1.5 delta in 0.25 delta steps and truncation between 0 and 2.0 mm in 0.5-mm steps. The performance of each lens was evaluated according to eight commonly applied clinical criteria: visual stability, lens position, recentering ability, amount and direction of movement, subjective comfort, meridional location of the lens, and amount of blink-initiated rotation. No benefit in performance was obtained from incorporating larger amounts of prism and truncation in the lens design, the best combination being 0.75 delta with 0.5-mm truncation. As a single stabilizing feature, truncation appeared more effective in locating a lens in the correct meridian than prism ballasting. It was found that corneal-fitting soft lenses of differing diameters (between 12.8 and 13.5 mm) performed similarly with the same stabilizing features.

Astigmatism↗
PubMed1992

Synthesis and toxicity of full-length and truncated bacterial CryIVD mosquitocidal proteins expressed in lepidopteran cells using a baculovirus vector.

Full-length (72K) and truncated (61K) CryIVD mosquitocidal proteins of Bacillus thuringiensis (Bt) were expressed in Spodoptera frugiperda cells and larvae of Trichoplusia ni using a baculovirus vector to investigate the role of CryIVD peptides in toxicity as well as to evaluate further the baculovirus/lepidopteran system for expressing Bt proteins. The cryIVD genes were inserted into the Autographa californica multinucleocapsid nuclear polyhedrosis virus (AcMNPV) under control of the polyhedrin promoter by recombination in S. frugiperda cells between a transfer vector carrying the Bt genes and vDA26Z, a recombinant AcMNPV carrying the Escherichia coli beta-galactosidase gene under control of the DA26 promoter. Recombinant AcMNPVs carrying the genes were detected as blue occlusion body-negative plaques in monolayers of S. frugiperda cells grown in the presence of X-Gal. Infection of S. frugiperda cells and T. ni larvae with plaque-purified recombinant virus, expressing either the full-length or truncated CryIVD protein, resulted in the synthesis of proteins of the expected size, as confirmed by immunoblot analyses, and their crystallization into cuboidal inclusions in the cytoplasm. Infected cells and purified inclusions from the virus (AcCryIVD) expressing the full-length protein were highly toxic to mosquito larvae, but similar preparations from the virus (AcCryIVD-C) expressing the truncated protein with a 9.6K deletion at the N terminus were non-toxic. Proteolysis with trypsin of CryIVD proteins produced by Bt and the recombinant AcMNPVs yielded peptides corresponding in size, showing that synthesis of mosquitocidal Bt proteins in lepidopteran cells occurred. The lack of toxicity of the truncated CryIVD protein, which like the toxic full-length protein yielded a 34K protein on proteolysis that has been implicated in toxicity, indicates that by itself this protein is non-toxic. These results demonstrate the utility of the baculovirus system for expression of mosquitocidal Bt proteins and for investigation of their mode of action.

Animals↗
PubMed2004

The mouse homeobox gene Not is required for caudal notochord development and affected by the truncate mutation.

The floating head (flh) gene in zebrafish encodes a homeodomain protein, which is essential for notochord formation along the entire body axis. flh orthologs, termed Not genes, have been isolated from chick and Xenopus, but no mammalian ortholog has yet been identified. Truncate (tc) is an autosomal recessive mutation in mouse that specifically disrupts the development of the caudal notochord. Here, we demonstrate that truncate arose by a mutation in the mouse Not gene. The truncate allele (Nottc) contains a point mutation in the homeobox of Not that changes a conserved Phenylalanine residue in helix 1 to a Cysteine (F20C), and significantly destabilizes the homeodomain. Reversion of F20C in one allele of homozygous tc embryonic stem (ES) cells is sufficient to restore normal notochord formation in completely ES cell-derived embryos. We have generated a targeted mutation of Not by replacing most of the Not coding sequence, including the homeobox with the eGFP gene. The phenotype of NoteGFP/eGFP, NoteGFP/tc, and Nottc/tc embryos is very similar but slightly more severe in NoteGFP/eGFP than in Nottc/tc embryos. This confirms allelism of truncate and Not, and indicates that tc is not a complete null allele. Not expression is abolished in Foxa2 and T mutant embryos, suggesting that Not acts downstream of both genes during notochord development. This is in contrast to zebrafish embryos, in which flh interacts with ntl (zebrafish T) in a regulatory loop and is essential for development of the entire notochord, and suggests that different genetic control circuits act in different vertebrate species during notochord formation.

Amino Acid Sequence↗
PubMed2004

Reliable first-principles alloy thermodynamics via truncated cluster expansions.

In alloys cluster expansions (CE) are increasingly used to combine first-principles electronic-structure calculations and Monte Carlo methods to predict thermodynamic properties. As a basis-set expansion in terms of lattice geometrical clusters and effective cluster interactions, the CE is exact if infinite, but is tractable only if truncated. Yet until now a truncation procedure was not well defined and did not guarantee a reliable truncated CE. We present an optimal truncation procedure for CE basis sets that provides reliable thermodynamics. We then exemplify its importance in Ni3V, where the CE has failed unpredictably, and now show agreement to a range of measured values, predict new low-energy structures, and explain the cause of previous failures.

Journal Article↗
PubMed1993

Amino-terminal truncations of the ribulose-bisphosphate carboxylase small subunit influence catalysis and subunit interactions.

The first 20 residues at the amino terminus of the small subunit of spinach ribulose-1,5-bisphosphate carboxylase form an irregular arm that makes extensive contacts with the large subunit and also with another small subunit (S. Knight, I. Andersson, and C.-I. Brändén [1990] J Mol Biol 215: 113-160). The influence of these contacts on subunit binding and, indirectly, on catalysis was investigated by constructing truncations from the amino terminus of the small subunit of the highly homologous enzyme from Synechococcus PCC 6301 expressed in Escherichia coli. Removal of the first six residues (and thus the region of contact with a neighboring small subunit) affected neither the affinity with which the small subunits bound to the large subunits nor the catalytic properties of the assembled holoenzyme. Extending the truncation to include the first 12 residues (which encroaches into a highly conserved region that interacts with the large subunit) also did not weaken intersubunit binding appreciably, but it reduced the catalytic activity of the holoenzyme nearly 5-fold. Removal of an additional single residue (i.e. removal of a total of 13 residues) weakened intersubunit binding approximately 80-fold. Paradoxically, this partially restored catalytic activity to approximately 40% of that of the wild-type holoenzyme. None of these truncations materially affected the Km values for ribulose-1,5-bisphosphate or CO2. Removal of all 20 residues of the irregular arm (thereby deleting the conserved region of contact with large subunits) totally abolished the small subunit's ability to bind to large subunits to form a stable holoenzyme. However, this truncated small subunit was still synthesized by the E. coli cells. These data are interpreted in terms of the role of the amino-terminal arm of the small subunit in maintaining the structure of the holoenzyme.

Amino Acid Sequence↗
PubMed2003

Crystallization and preliminary analysis of native and N-terminal truncated isoforms of toluene-4-monooxygenase catalytic effector protein.

Single crystals have been obtained of the toluene 4-monooxygenase catalytic effector protein, the SeMet-enriched protein and a truncated isoform missing ten amino acids from the N-terminus. Complete X-ray diffraction data sets have been collected and analyzed to 2.0, 3.0 and 1.96 A resolution for the native, SeMet and truncated isoform crystals, respectively. The native and SeMet proteins crystallized in space group P6(1)22 (unit-cell parameters a = b = 86.41 +/- 0.15, c = 143.90 +/- 0.27 A), whereas the truncated isoform crystallized in space group P2(1)3 (a = b = c = 86.70 +/- 0.47 A). Matthews coefficient calculations suggest either two or three molecules per asymmetric unit in the P6(1)22 space group and two molecules per asymmetric unit in the P2(1)3 space group. Experimental phases from MAD analysis of the SeMet isoform and molecular replacement of the truncated isoform confirm the presence of two molecules per asymmetric unit in each case. These crystallographic results are the first available for the evolutionarily related but functionally diversified catalytic effector proteins from the multicomponent diiron monooxygenase family.

Crystallization↗
PubMed2001

E. coli methionine sulfoxide reductase with a truncated N terminus or C terminus, or both, retains the ability to reduce methionine sulfoxide.

The monomeric peptide methionine sulfoxide reductase (MsrA) catalyzes the irreversible thioredoxin-dependent reduction of methionine sulfoxide. The crystal structure of MsrAs from Escherichia coli and Bos taurus can be described as a central core of about 140 amino acids that contains the active site. The core is wrapped by two long N- and C-terminal extended chains. The catalytic mechanism of the E. coli enzyme has been recently postulated to take place through formation of a sulfenic acid intermediate, followed by reduction of the intermediate via intrathiol-disulfide exchanges and thioredoxin oxidation. In the present work, truncated MsrAs at the N- or C-terminal end or at both were produced as folded entities. All forms are able to reduce methionine sulfoxide in the presence of dithiothreitol. However, only the N-terminal truncated form, which possesses the two cysteines located at the C-terminus, reduces the sulfenic acid intermediate in a thioredoxin-dependent manner. The wild type displays a ping-pong mechanism with either thioredoxin or dithiothreitol as reductant. Kinetic saturation is only observed with thioredoxin with a low K(M) value of 10 microM. Thus, thioredoxin is likely the reductant in vivo. Truncations do not significantly modify the kinetic properties, except for the double truncated form, which displays a 17-fold decrease in k(cat)/K(MetSO). Alternative mechanisms for sulfenic acid reduction are also presented based on analysis of available MsrA sequences.

Amino Acid Sequence↗
PubMed1992

Mutants of human insulin-like growth factor II (IGF II). Expression and characterization of truncated IGF II and of two naturally occurring variants.

Insulin-like growth factor II (IGF II) and four structural analogs, constructed by site-directed mutagenesis, were expressed as protein A fusion proteins in Escherichia coli BL21pLysS cells, cleaved with cyanogen bromide and purified by affinity chromatography and HPLC. Two mutants (Ser29 substituted by Arg-Leu-Pro-Gly, and Ser33 substituted by Cys-Gly-Asp) represent two naturally occurring variants of IGF II. The other two mutants, (7-67)IGF II and (9-67)IGF II, are truncated at the amino-terminus in analogy to the naturally occurring des(1-3)IGF I ('truncated IGF I'). These mutants were tested for their binding affinities to type-1 and type-2 IGF receptors, to IGF binding protein-3 (IGFBP-3) and for their stimulation of thymidine incorporation into DNA. The affinities of the Ser29 and Ser33 mutants to the type-1 IGF receptor were 85% and 39%, respectively, compared to wild-type IGF II, those of (7-67)IGF II and (9-67)IGF II 96% and 15%, respectively. The potencies of the Ser33 and the (9-67) mutant to stimulate thymidine incorporation into DNA correlated closely with the affinities to the type-1 IGF receptor, whereas the bioavailability of the Ser29 mutant was lower and that of the (7-67) mutant higher than the type-1 receptor binding, possibly due to interferences with endogenously secreted IGFBPs. The affinities of the Ser29 and Ser33 mutants to the type-2 IGF receptor were 110% and 71%, respectively, those of the two truncated mutants 25% and 23%, respectively. The affinity of the Ser29 mutant to IGFBP-3 was increased to 171%, whereas those of the Ser33 mutant and the two truncated mutants were reduced (34%, 10% and 19%, respectively).

Amino Acid Sequence↗
PubMed1995

Structural organisation of human bile-salt-activated lipase probed by limited proteolysis and expression of a recombinant truncated variant.

Bile-salt-activated lipase belongs to the cholinesterase alpha/beta-hydrolase-fold family of proteins. Here, we have investigated the structural organisation of the human isoform by mapping tryptic cleavage sites using limited proteolysis and by expression studies using a recombinant truncated variant. Two accessible regions in the tertiary structure were identified. The first is defined by a tryptic cleavage at Lys429 and lies within the alpha/beta-hydrolase fold in bile-salt-activated lipase between a central beta-sheet and an active-site histidine residue, as deduced from sequence similarity across the cholinesterases and known structural properties. This region exhibits a proteolytic and topological similarity to the lid region in pancreatic lipase. The other accessible region in the tertiary structure is defined by a tryptic cleavage at Arg520 and occurs within a catalytically non-essential segment Leu519-Gln535, as identified by expression of a truncated variant which lacks the C-terminus starting from Leu519. This region is consistent with an interdomain region between the cholinesterase-related part of the protein structure and the unique proline-rich C-terminal repeats. Both protease-sensitive regions appear to occur at domain borders, and, therefore, are consistent with a multi-domain structure. The truncated variant was fully functional as a lipase and as a bile-salt-stimulated esterase. However, compared to the full-length enzyme, the truncated variant showed an increased susceptibility to limited proteolysis, suggesting that the C-terminal repeats may regulate proteolytic degradation of the protein.

Amino Acid Sequence↗
PubMed1995

Interactions of beta-thymosins, thymosin beta 4-sulfoxide, and N-terminally truncated thymosin beta 4 with actin studied by equilibrium centrifugation, chemical cross-linking and viscometry.

All beta-thymosins studied interact with G-actin in a bimolecular complex and inhibit the polymerization to F-actin under high salt conditions. The interactions between actin and beta-thymosins have been studied under polymerization conditions using actin labeled by a fluorescent reporter group at Cys374. Instead of labeling actin we employed equilibrium centrifugation of unlabeled G-actin, viscometry, and chemical cross-linking to investigate the interactions with several beta-thymosins, oxidized thymosin beta 4 and N-terminally truncated beta 4. The apparent dissociation constants for actin from bovine heart and beta-thymosins were 2.5, 0.1, and 2.7 microM for thymosin beta 4, [Ala1]beta 4(beta Ala4), and beta 10, respectively. Comparable apparent dissociation constants were obtained for the interaction of G-actin from rabbit skeletal muscle and thymosin beta 4 or beta Ala4. In rabbits thymosin beta Ala4 replaces beta 4 being different in amino acid residue 1 only. The apparent dissociation constant of thymosin beta 10 with actin from rabbit skeletal muscle, however, is about 10% of the value obtained with actin from bovine heart. Oxidation of thymosin beta 4 at Met6 (beta 4-sulfoxide) as well as truncation of 6 [beta 4-(7-43)] or 12 [beta 4-(13-43)] amino acid residues from the N-terminus increase apparent dissociation constants to 38-53 microM. Truncation of the first 23 amino acid residues [beta 4-(24-43)] abolishes interaction with G-actin completely. Therefore, amino acid residues between position 13 and 24 are necessary for 1-ethyl-3[3-(dimethyl-aminopropyl)-carbodiimide cross-linking of G-actin. In spite of comparable apparent dissociation constants between actin and thymosin beta 4-sulfoxide or beta 4-(7-43) or beta 4-(13-43), only beta 4-sulfoxide and not the truncated beta-thymosins inhibits actin polymerization, however, only at a 20-fold higher concentration than beta 4. Thus the first six amino acid residues are indispensable to inhibit salt-induced actin polymerization as analyzed by viscometry. While the apparent dissociation constant of the actin/thymosin beta 4 complex generated from a preformed actin/DNase-I complex is 160 microM, a fivefold excess of DNase I over the preformed actin/thymosin-beta 4 complex is necessary to observe a comparable dissociation constant.

Actins↗
PubMed1999

Plasmid-encoded tetracycline resistance in Salmonella enterica subsp. enterica serovars choleraesuis and typhimurium: identification of complete and truncated Tn1721 elements.

During routine screening of Salmonella enterica subsp., S. enterica isolates of animal origin for plasmid-encoded tetracycline resistance, two tetracycline resistance plasmids, the 50 kbp plasmid pGFT3 of Salmonella choleraesuis and the 9.5 kbp plasmid pGFT4 of Salmonella typhimurium var. Copenhagen DT002, were detected. The respective tetracycline resistance genes (tet) were identified by hybridization and PCR analysis to belong to hybridization class A. Conjugation experiments identified plasmid pGFT3 as a conjugative plasmid. Molecular analysis of the tet(A) gene area and the flanking regions identified a complete Tn1721-like transposon on plasmid pGFT3 and a truncated Tn1721-like element on plasmid pGFT4. The complete Tn1721-like element was integrated into a transposase reading frame of a truncated Tn3 transposon also located on plasmid pGFT3. The truncated Tn1721-like element of plasmid pGFT4 lacked the entire transposase part. This Tn1721-relic was integrated in an unknown reading frame which on amino acid level showed homology to the Rop protein of Escherichia coli. A model for the deletion of the transposase part was developed on the basis of the sequences present at the termini of the truncated Tn1721-like element.

Animals↗
PubMed1999

Truncated growth hormone receptor isoforms.

Truncated forms of the growth hormone receptor (GHR) that lack the majority of the cytoplasmic domain have been identified in a number of human tissues. In vitro, these truncated receptors act as dominant-negative inhibitors of the growth hormone (GH) signal and also generate large amounts of growth hormone binding protein (GHBP). Mutations that lead to high levels of expression of the truncated GHR are associated with short stature and GH insensitivity. Thus, truncated GHRs may be important as a physiological regulator of GH signalling in addition to providing a mechanism for the production of GHBP.

Animals↗
PubMed1993

Specific and effective T-cell recognition of cells transfected with a truncated human mucin cDNA.

Epithelial cell mucin has been characterized as a tumor-specific antigen in patients with pancreatic and breast cancer. Mucins are high molecular weight glycoproteins consisting of a heavily glycosylated tandemly repeating 20-amino acid sequence. Aberrant glycosylation of mucins on carcinomatous epithelial cells leads to the exposure of novel core epitopes that are recognized by cytotoxic T lymphocytes (CTLs). We previously reported the establishment of mucin-specific CTL clones that recognize mucin expressed on the surface of EBV-immortalized B cells transfected with the mucin cDNA (MUC1). This recognition was characterized as major histocompatibility complex (MHC)-unrestricted, because of the multivalent nature of mucin. The transfectants had to be incubated with an inhibitor of O-linked glycosylation, phenyl-N-acetyl-alpha-galactosaminide (phenyl-GalNAc) in order to unmask the tandem repeat core epitope recognized by CTLs. In the present study, we examined whether mucin molecules with fewer tandem repeats are capable of MHC-unrestricted recognition by mucin-specific CTL clones. A mucin cDNA expression vector expressing a "truncated" mucin molecule that contains only two tandem repeats was constructed. We found that mucin-specific CTL clones recognize the "truncated" mucin on allogeneic target cells, showing that recognition in this case was MHC-unrestricted as well. In addition, CTL clones lysed "truncated" mucin transfectants significantly better than full-length mucin transfectants treated with phenyl-GalNAc, and controls. The "truncated" construct may represent an effective means of immunizing patients with breast and pancreatic cancer, enabling them to mount a strong and efficient immune response against mucin-bearing tumor cells.

Amino Acid Sequence↗
PubMed2000

Intelligibility of bandpass speech: effects of truncation or removal of transition bands.

An intelligibility of over 90% was reported for keywords in "everyday" 1/3-octave sentences centered on 1500 Hz and having steep transition band slopes of 100 dB/octave [Warren et al., Percept. Psychophys. 57, 175-182 (1995)]. A subsequent study by Warren and Bashford [J. Acoust. Soc. Am. 106, L47-L52 (1999)] found that it was not the 1/3-octave passband, but the transition bands that were chiefly responsible for this high intelligibility: When the passband and transition bands were segregated using filter slopes of 1000 dB/octave, the isolated passband had an intelligibility score of only 24%, while the pair of transition bands had a score of over 80%. In the present study, experiment 1 examined the distribution of information along the transition bands' slopes by truncation at graded downpoints: Truncation at downpoints of 40 dB or more produced no significant change in intelligibility. Experiment 2 closed the gap separating the transition bands so that their slopes intersected at 1500 Hz. This triangular band had a negligible passband (as defined conventionally by 3-dB downpoints) and an intelligibility score of 60%; truncation at downpoints of 50 dB or more produced no significant change in intelligibility. Experiment 3 determined the intelligibilities of rectangular bands (1000-dB/octave slopes) centered on 1500 Hz. Their bandwidths ranged from 3 to 12 semitones in 1-semitone steps, resulting in intelligibility scores increasing monotonically from 14% to 94%. Calculations based upon experiments 2 and 3 showed that the triangular band truncated at 30-dB downpoints had half the intelligibility of a rectangular band having the same frequency range.

Humans↗
PubMed2006

Modulating the folding of P-glycoprotein and cystic fibrosis transmembrane conductance regulator truncation mutants with pharmacological chaperones.

Cystic fibrosis transmembrane conductance regulator (CFTR) and P-glycoprotein (P-gp) are ATP-binding cassette (ABC) transporters that have two transmembrane domains (TMDs) and two nucleotide-binding domains (NBDs). Defective folding of CFTR lacking phenylalanine 508 (DeltaPhe508) in NBD1 is the most common cause of cystic fibrosis. The Phe508 position seems to be universally important in ABC transporters because deletion of the equivalent residue (Tyr490) in P-gp also inhibits maturation of the protein. The pharmacological chaperone VRT-325 can repair the DeltaPhe508-type folding defects in P-gp or CFTR. VRT-325 may repair the folding defects by promoting dimerization of the two NBDs or by promoting folding of the TMDs. To distinguish between these two mechanisms, we tested the ability of VRT-325 to promote folding of truncation mutants lacking one or both NBDs. Sensitivity to glycosidases was used as an indirect indicator of folding. It was found that VRT-325 could promote maturation of truncation mutants lacking NBD2. Truncation mutants of CFTR or P-gp lacking both NBDs showed deficiencies in core-glycosylation that could be partially reversed by carrying out expression in the presence of VRT-325. The results show that dimerization of the two NBDs to form a "nucleotide-sandwich" structure or NBD interactions with the TMDs are not essential for VRT-325 enhancement of folding. Instead, VRT-325 can promote folding of the TMDs alone. The ability of VRT-325 to promote core-glycosylation of the NBD-less truncation mutants suggests that one mechanism whereby the compound enhances folding is by promoting proper insertion of TM segments attached to the glycosylated loops so that they adopt an orientation favorable for glycosylation.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2003

Recombinant truncated flagellin of Burkholderia pseudomallei as a molecular probe for diagnosis of melioidosis.

Current serological tests for melioidosis, using impure or uncharacterized cell antigens from Burkholderia pseudomallei, have problems in detection sensitivity and specificity. Therefore, we designed and expressed the recombinant flagellin (truncated at both the N- and C-terminal ends), and used the antigen to develop an indirect enzyme-linked immunosorbent assay (ELISA) to diagnose melioidosis. Comparison of the immunoreactivities of the full-length and truncated flagellins reveals that the truncated flagellin performed much better in detection specificity and sensitivity. Only the full-length flagellin was recognized by other bacterial causing septicemia and gave a false-positive result in Western analysis, indicating that the cross-reactive epitopes were located on the more highly conserved N- and C-terminal regions of flagellin. The indirect ELISA using recombinant truncated flagellin as the antigen achieved 93.8% sensitivity and 96.3% specificity and offered a more efficient serodiagnosis of melioidosis.

Antigens, Bacterial↗