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PubMed1996

Cloning, sequencing and functional analysis of a truncated cDNA encoding red deer prolactin receptor: an alternative tyrosine residue mediates beta-casein promoter activation.

This study reports the isolation and in vitro characterisation of a truncated cDNA encoding the red deer long form prolactin receptor. The cDNA sequence predicts a protein of 557 amino acids which differs from the rat sequence by a 3' truncation of the cytoplasmic domain located 34 residues before the stop codon. The deer sequence shares the regions of homology which are important for maintenance of structural and functional integrity, high affinity binding and signal transduction. However, the truncated deer receptor lacks the most C-terminal tyrosine residue in the intracellular domain which is believed to be essential for activation of the beta-casein promoter. Transfection studies of the cervine cDNA into human 293 fibroblast cells confirmed the expression of a receptor that has high affinity binding to ovine prolactin (Ka = 0.65 x 10(9)M(-1) and Bmax = 548.6 fmol/mg protein). Co-transfection of CHO cells with expression vector encoding the cervine prolactin receptor cDNA along with a fusion gene containing the promoter region of beta-casein followed by beta-luciferase coding sequence led to 8.13 +/- 0.13-fold induction of luciferase enzyme activity in the presence of 400 ng/ml ovine prolactin. This was comparable to fold induction observed with the wild type long form rat prolactin receptor (6.37 +/- 0.48); macaque growth hormone receptor was without effect. Western blot analysis demonstrated tyrosine phosphorylation of the cervine receptor and the associated kinase Jak2 following stimulation with prolactin. This confirms that the cervine cDNA although truncated is fully functional and that Jak2 and an alternative tyrosine residue in the intracellular domain are involved in the signalling pathway leading to activation of the beta-casein promoter. Northern blot analysis provides evidence that the prolactin receptor in the liver is encoded by transcripts of approximately 2.5 and 3.5 kb. Comparison of Northern blots of different deer species suggests that the receptor is conserved amongst the Cervidae. Northern blot analysis of red deer testis suggests that this species expresses a second form of the receptor, encoded by a transcript of 1.7 kb, which may correspond to a smaller receptor form or a binding protein.

Amino Acid Sequence↗
PubMed2006

A unique insertion/duplication in the VDR gene that truncates the VDR causing hereditary 1,25-dihydroxyvitamin D-resistant rickets without alopecia.

Hereditary vitamin D resistant rickets (HVDRR) is caused by mutations in the vitamin D receptor (VDR). Here we describe a patient with HVDRR who also exhibited some hypotrichosis of the scalp but otherwise had normal hair and skin. A 102 bp insertion/duplication was found in the VDR gene that introduced a premature stop (Y401X). The patient's fibroblasts expressed the truncated VDR, but were resistant to 1,25(OH)2D3. The truncated VDR weakly bound [3H]-1,25(OH)2D3 but was able to heterodimerize with RXR, bind to DNA and interact with the corepressor hairless (HR). However, the truncated VDR failed to bind coactivators and was transactivation defective. Since the patient did not have alopecia or papular lesions of the skin generally found in patients with premature stop mutations this suggests that this distally truncated VDR can still regulate the hair cycle and epidermal differentiation possibly through its interactions with RXR and HR to suppress gene transactivation.

Alopecia↗
PubMed2005

Truncation of the C-terminus of human MLH1 blocks intracellular stabilization of PMS2 and disrupts DNA mismatch repair.

The human DNA mismatch repair (MMR) protein MLH1 has essential roles in the correction of replication errors and the activation of cell cycle checkpoints and cytotoxic responses to DNA damage that contribute to suppression of cancer risk. MLH1 functions as a heterodimer with the PMS2 protein, and steady state levels of PMS2 are very low in MLH1-deficient cells. Unique to MLH1 among MutL-homolog proteins, and conserved in identified eukaryotic MLH1 proteins, is the so-called C-terminal homology domain (CTH). The function of these C-terminal 20-30 amino acids is not known. We investigated the effect of a C-terminal truncation of human MLH1 (MLH1-L749X) on mammalian MMR by testing its activity in MLH1-deficient cells. We found the CTH to be essential for suppression of spontaneous mutation, activation of a cytotoxic response to 6-thioguanine, and maintenance of normal steady state levels of PMS2. Co-expression in doubly mutant Mlh1-/-; Pms2-/- fibroblasts showed that MLH1-L749X was unable to stabilize PMS2. Over-expression of MLH1-L749X did not reduce stabilization of PMS2 mediated by wild-type MLH1, indicating that truncation of the CTH reduces the ability to compete with wild-type MLH1 for interaction with PMS2. Lack of PMS2 stabilization also was observed with a previously reported pathogenic truncation (MLH1-Y750X), but not with two different point mutations in the CTH. Biochemical assays demonstrated that truncation of the CTH reduced the stability of heterodimers, although MLH1-L749X retained significant capacity for interaction with PMS2. Thus, the CTH of human MLH1 is necessary for error correction, checkpoint signaling, and for promoting interaction with, and the stability of, PMS2. Analysis of the CTH role in stabilizing PMS2 was facilitated by a novel intracellular assay for MLH1-PMS2 interaction. This assay should prove useful for identifying additional amino acids in MLH1 and PMS2 necessary for interaction in cells, and for determining the functional consequences of MLH1 mutations identified in human cancers.

Adaptor Proteins, Signal Transducing↗
PubMed2006

Truncated tau from sporadic Alzheimer's disease suffices to drive neurofibrillary degeneration in vivo.

Truncated tau protein is the characteristic feature of human sporadic Alzheimer's disease. We have identified truncated tau proteins conformationally different from normal healthy tau. Subpopulations of these structurally different tau species promoted abnormal microtubule assembly in vitro suggesting toxic gain of function. To validate pathological activity in vivo we expressed active form of human truncated tau protein as transgene, in the rat brain. Its neuronal expression led to the development of the neurofibrillary degeneration of Alzheimer's type. Furthermore, biochemical analysis of neurofibrillary changes revealed that massive sarcosyl insoluble tau complexes consisted of human Alzheimer's tau and endogenous rat tau in ratio 1:1 including characteristic Alzheimer's disease (AD)-specific proteins (A68). This work represents first insight into the possible causative role of truncated tau in AD neurofibrillary degeneration in vivo.

Alzheimer Disease↗
PubMed2006

Truncations of gelonin lead to a reduction in its cytotoxicity.

Gelonin is a single chain ribosome-inactivating protein (RIP) with potential applications as a bullet of immunoconjugate for the treatment of cancer and AIDS. Using truncated forms of gelonin, we now report the relationship between its conformation and function. Circular dichroism (CD) and fluorescence spectra show that the N-terminus forms beta-sheets whereas the C-terminus contains alpha-helices of secondary structures. Biological experiments indicate that all gelonin truncation mutants lose partial toxicity compared to intact gelonin, an effect most strongly seen with C-terminally truncated gelonin. Similar evidence is also provided using a DNase-like activity assay. In addition, the intact gelonin exhibits the highest cytotoxicity to cancer cells. These results suggest that truncations of the terminal region of gelonin negatively regulate its function dominantly and that, due to its toxicity, intact gelonin is an important potential immunoconjugate.

Antineoplastic Agents, Phytogenic↗
PubMed2004

Characterization of human immunodeficiency virus type 1 Pr160 gag-pol mutants with truncations downstream of the protease domain.

We have constructed a series of HIV-1 Gag-pol mutants by progressive deletion of the pol sequence downstream of the viral protease (PR) domain. Effects of the truncation mutations on virus particle production and Gag particle processing were analyzed. Analysis indicated that removal of the integrase (IN) domain had no major effect on the efficiency of particle processing, but resulted in a marked reduction in virus particle budding. Deletion of both the IN and RNase H domains, however, restored the production of virus particles to wild-type level. The proteolytic processing of virus particle was significantly impaired when the p51RT domain was truncated. All of the truncated Gag-pol proteins could be incorporated into virus particles and demonstrated an immunofluorescence staining pattern similar to that of the wild type (wt). Our data are consistent with the proposal that signals for directing the Gag-pol transport and particle incorporation are determined by its N-terminal Gag domain. Truncated Gag-pol retaining an intact p51RT was able to complement a PR-defective mutant to produce infectious pseudotyped virions, with a virus titer 20-70% of that of wt. Pseudotyped virions produced by the Gag-pol lacking an intact p51RT were noninfectious or poorly infectious. This suggests that an intact p51RT domain is required for the Gag-pol to mediate production of mature infectious virus particles in trans.

Cell Line↗
PubMed2006

A truncated isoform of TMEFF2 encodes a secreted protein in prostate cancer cells.

The transmembrane protein TMEFF2, also known as tomoregulin or TENB2, has been proposed as a potential immunotherapeutic target for the treatment of prostate cancer. Much attention has focused on its limited tissue distribution, with strong expression seen only in the brain and the prostate. Here we describe the identification of a novel splice variant of TMEFF2 expressed both in the normal prostate and in prostate cancer. This variant encodes an isoform of TMEFF2 that is truncated after the first four coding exons, eliminating both the EGF-like and the transmembrane domains. Fusion of GFP to this isoform demonstrated that this variant transcript produces a truncated TMEFF2 protein (TMEFF2-S). In contrast to full-length TMEFF2-GFP, the truncated TMEFF2-S-GFP fusion protein was enriched in cytosolic granules, showed no staining at the plasma membrane, and was secreted into the medium of transfected cells grown in tissue culture. These results indicate that a truncated isoform of TMEFF2 is expressed from this locus. This secreted form of TMEFF2 may functionally interact with full-length TMEFF2, or its binding partners, and may also influence current immune-based treatment strategies.

Alternative Splicing↗
PubMed2004

Expression of a truncated form of the c-Kit tyrosine kinase receptor and activation of Src kinase in human prostatic cancer.

A truncated form of the c-Kit tyrosine kinase receptor, originally identified in mouse haploid germ cells, is aberrantly expressed in human cancer cell lines of various origin. This alternative transcript originates in the 15th intron of the human c-kit gene. We have previously demonstrated that sperm-carried mouse truncated c-Kit (tr-Kit) is a strong activator of the Src-family tyrosine kinases both in transfected cells and in mouse oocytes. In the present work, we report that human tr-Kit mRNA and protein are expressed in LNCaP prostatic cancer cells. We have identified two regions in the 15th and 16th introns of the human c-kit gene that show homology with sequences in the spermatid-specific tr-Kit promoter within the 16th intron of mouse c-kit. We also show that nuclear factors present in LNCaP cells bind to discrete sequences of the mouse tr-Kit promoter. Moreover, Western blot analysis of 23 primary prostate cancers indicated that tr-Kit was expressed in approximately 28% of the tumors at less advanced stages (Gleason grade 4 to 6) and in 66% of those at more advanced stages (Gleason grade 7 to 9), whereas it was not expressed in benign prostatic hypertrophies. Sequencing of the cDNA for the truncated c-Kit, amplified from both LNCaP cells and neoplastic tissues, confirmed the existence in prostate cancer cells of a transcript arising from the 15th intron of human c-kit. We also show that tr-Kit-expressing LNCaP cells and prostatic tumors have higher levels of phosphorylated/activated Src than tr-Kit-negative PC3 cells or prostatic tumors, and that transfection of tr-Kit in PC3 cells caused a dramatic increase in Src activity. Interestingly, we found that Sam68, a RNA-binding protein phosphorylated by Src in mitosis, is phosphorylated only in prostate tumors expressing tr-Kit. Indeed, both activation of Src and phosphorylation of Sam68 were observed in all of the three grade 7 to 9 tumors analyzed that expressed tr-Kit. Our data describe for the first time the existence of a truncated c-Kit protein in primary tumors and show a correlation between tr-Kit expression and activation of the Src pathway in the advanced stages of the disease. Thus, these results might pave the way for the elucidation of a novel pathway in neoplastic transformation of prostate cells.

Aged↗
PubMed2002

C-terminal lysine truncation increases thermostability and enhances chaperone-like function of porcine alphaB-crystallin.

The carboxyl-terminal segment of alpha-crystallin, a major lens protein of all vertebrates, has a short and flexible peptide extension of about 20 amino acid residues that are very susceptible to proteolytic truncation and modifications under physiological conditions. To investigate its role in crystallin aggregation and chaperone-like activity, we constructed a mutant of porcine alphaB-crystallin with C-terminal lysine truncated end, which unexpectedly showed better chaperone-like function than wild-type alphaB-crystallin. From circular dichroism (CD) spectra, we show that the mutant possesses similar secondary and tertiary structures to those of native purified and recombinant alphaB-crystallins. Analytical ultracentrifugation revealed that the truncated mutant was smaller than wild-type alphaB-crystallin in aggregation size and mass. The observed higher thermostability and anti-thermal aggregation propensity of the truncated alphaB-crystallin mutant than wild-type alphaB-crystallin are in contrast to the prevailing notion that mutations at the C-terminal lysines of alphaB-crystallin result in substantial loss of chaperone-like activity, despite the overall preservation of secondary structure. The detailed characterization of the C-terminal deletion mutants may provide some deeper insight into the chaperoning mechanism of the structurally related small heat-shock protein family.

Animals↗
PubMed2003

Molecular dynamics simulations of lipid bilayers: major artifacts due to truncating electrostatic interactions.

We study the influence of truncating the electrostatic interactions in a fully hydrated pure dipalmitoylphosphatidylcholine (DPPC) bilayer through 20 ns molecular dynamics simulations. The computations in which the electrostatic interactions were truncated are compared to similar simulations using the particle-mesh Ewald (PME) technique. All examined truncation distances (1.8-2.5 nm) lead to major effects on the bilayer properties, such as enhanced order of acyl chains together with decreased areas per lipid. The results obtained using PME, on the other hand, are consistent with experiments. These artifacts are interpreted in terms of radial distribution functions g(r) of molecules and molecular groups in the bilayer plane. Pronounced maxima or minima in g(r) appear exactly at the cutoff distance indicating that the truncation gives rise to artificial ordering between the polar phosphatidyl and choline groups of the DPPC molecules. In systems described using PME, such artificial ordering is not present.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed2000

Calpain-mediated truncation of rat brain AMPA receptors increases their Triton X-100 solubility.

Previous studies have indicated that calpain activation results in the truncation of the C-terminal domains of AMPA and NMDA receptor subunits. The present study determined the distribution of the truncated species of the subunits between Triton-soluble and -insoluble fractions. Western blots were performed with various antibodies to quantify the amounts of the various species of GluR1, GluR2, GluR3 and NR2B subunits. The results indicate that calpain activation decreased the amount of all the intact subunits in Triton-insoluble fractions. Calpain-generated truncated forms of GluR1 and GluR2, but not NR2B, were absent in these fractions, and were recovered in Triton-soluble fractions. These findings suggest that calpain-mediated truncation of AMPA but not NMDA receptor C-terminal domains results in modifications of the interactions between the receptors and postsynaptic densities, and that this mechanism could be involved in activity-dependent changes in the subcellular distribution of AMPA receptors.

Animals↗
PubMed1997

Extrapancreatic action of truncated glucagon-like peptide-I in Otsuka Long-Evans Tokushima Fatty rats, an animal model for non-insulin-dependent diabetes mellitus.

To clarify the mechanism(s) of the antidiabetic effects of truncated glucagon-like peptide-1 (GLP-1) in diabetics, we examined its insulinotropic and extrapancreatic effects in a newly established strain of spontaneously non-insulin-dependent diabetic (NIDDM) rats, Otsuka Long-Evans Tokushima Fatty (OLETF) rats, that received a continuous infusion of truncated GLP-1 620 pmol/d/kg (G group, n = 12) or of vehicle (V group, n = 12) for 4 weeks by Alzet pump. Nonfasting plasma glucose levels were significantly lower (P < .05) in the G group than in the V group (7.0 +/- 0.67 v 9.1 +/- 1.7 mmol/L), and fasting plasma immunoreactive insulin (IRI) levels were lower in the former than in the latter (0.63 +/- 0.31 v 0.78 +/- 0.25 nmol/L). At day 15 of infusion, the G group showed an attenuated plasma glucose response to an oral glucose load, but had plasma IRI levels comparable to those in the V group. A long-term infusion of truncated GLP-1 increased the glucose infusion rate (GIR) significantly (P < .05) during a euglycemic-hyperinsulinemic clamp test (59.0 +/- 14.8 mumol/kg/min for group G v 38.9 +/- 12.2 for group V), but hepatic glucose output (HGO) did not differ significantly for either group. Uptake of 2-deoxy-D-glucose (2DG) by peripheral muscles in the G group was as much as 2.4-fold higher than in the V group (5.52 +/- 2.04 v 2.29 +/- 0.97 mumol/100 g muscle weight/min). We conclude from these data that truncated GLP-1, in addition to its well-known incretin effect, is capable of augmenting insulin action in peripheral tissues of diabetics, which can contribute, in part, to improve glucose intolerance in OLETF rats.

Administration, Oral↗
PubMed2003

Truncated forms of human and simian immunodeficiency virus in infected individuals and rhesus macaques are unique or rare quasispecies.

Truncated proviruses of variable sizes are present in peripheral blood mononuclear cells (PBMC) of human immunodeficiency virus type 1 (HIV-1)-infected persons and simian immunodeficiency virus (SIV)-infected rhesus macaques. Here, we investigated whether the highly deleted HIV and SIV proviruses are present in infected organisms as multiple copies or whether each truncated provirus is unique. Using end-point dilution, multiple long-distance (LD) DNA PCR assays were run in parallel using DNA extracted from PBMC of seropositive, treatment-naive persons and from lymph nodes of a rhesus monkey inoculated with cloned, full-length SIVmac239 DNA. The PCR products were titrated and mapped. Most truncated proviruses were present in the DNA samples tested as single, nonintegrated molecules that differed from one another in size and/or nucleotide sequence. These results indicate that truncated primate lentiviral sequences found in infected tissues are unique or rare quasispecies that do not replicate significantly.

Animals↗
PubMed2001

Pepsin digestion of a mouse monoclonal antibody of IgG1 class formed F(ab')(2) fragments in which the light chains as well as the heavy chains were truncated.

In the preparation of F(ab')(2) fragments of monoclonal antibodies (mAbs) of IgG class, heavy (H) chains are truncated by pepsin and light (L) chains are remained intact. However, F(ab')(2) fragments formed by pepsin-digestion of a mouse mAb PM373, which was of the IgG1 class and raised against human prostate specific antigen (PSA), indicated that the L chains of 31 kDa were cleaved into 23-kDa fragments as well as the cleavage of H chains of 50 kDa into 28-kDa fragments. On the other hand, F(ab')(2) fragments formed by digesting the mAb by cathepsin D showed that the L chains were intact and the H chains were truncated. The immunoreactivities against PSA of the F(ab')(2) fragments containing the intact L chains and those containing the truncated L chains were almost the same as that of the parental mAb, suggesting that the truncation of the L chains does not affect the interaction of the mAb with its specific antigen.

Animals↗
PubMed2000

Two novel first exons in the prolactin receptor gene are transcribed in a tissue-specific and sexual maturation-dependent manner to encode multiple 5'-truncated transcripts in the testis of the chicken.

Cloning and sequencing of the chicken prolactin receptor (PRLR) gene segment from the transmembrane domain to the box 2 motif revealed the presence of the two testis-specific first exons, TSE-1 and TSE-2, encoding the unique 5'-end sequences of the reported and newly identified multiple 5'-truncated PRLR transcripts containing only the cytoplasmic domain in the testis. TSE-1 was located downstream of the exon encoding the transmembrane domain and TSE-2 presented downstream of the exon encoding the box 1 motif. These findings indicate that the box 1-containing 5'-truncated transcripts are generated by the utilization of TSE-1 as the first exon with distinct splicing donor sites to the box 1-containing exon, and that the utilization of TSE-2 as the first exon and its splicing to the box 2-containing exon results in the generation of the box 1-lacking transcript. Three transcription initiation sites for the box 1-containing 5'-truncated transcripts and two transcription initiation sites for the box 1-lacking transcript were detected by the RNase protection assays. Reverse transcription-polymerase chain reaction analysis showed that the expression levels of all these 5'-truncated PRLR transcripts are simultaneously increased during sexual maturation, accompanying the decrease of the amount of the canonical full-length transcript for PRLR.

Animals↗
PubMed2000

An alternatively spliced transcript of the rat nociceptin receptor ORL1 gene encodes a truncated receptor.

Opioid receptor-like protein ORL1, the receptor for the neuropeptide nociceptin (also named orphanin FQ), has two alternatively spliced isoforms in the rat. This alternative splicing event is generated by retaining of intron 3, 81 bases in length, in the mRNA region encoding the second extracellular loop of ORL1. A full-length rat ORL1 receptor has 367 amino acid residues. However, as revealed by sequencing of rat ORL1 genomic DNA and cDNA, the insertion of the unspliced intron 3 brings in an in-frame stop codon and, therefore, creates a truncated open-reading frame encoding only the N-terminal half of ORL1 (from the N-terminus to an alternate extracellular tail C-terminal to the fourth transmembrane domain). The two alternatively spliced transcripts are differentially expressed in tissues. In transfected mammalian cells, the full-length ORL1 displays high-affinity and selective binding for nociceptin, and inhibits the production of cyclic AMP. In contrast, the truncated ORL1 binds nociceptin and other opioid peptides very poorly and non-selectively (affinity in micromolar range), and it does not mediate any inhibitory effects on cyclic AMP production. Apparently, this truncated ORL1 does not function as a receptor for nociceptin or other ligands tested. Such alternative splicing to create a truncated ORL1 receptor might be an endogenous mechanism to negatively regulate nociceptin/ORL1 functions.

Alternative Splicing↗
PubMed1998

BDNF, and full length and truncated TrkB expression in the hippocampus of the rat following kainic acid excitotoxic damage. Evidence of complex time-dependent and cell-specific responses.

Systemic administration of kainic acid (KA) at convulsant doses results in irreversible cell damage and neuron loss in the hilus of the dentate gyrus and in the CA1 area of the hippocampus. This is followed by reactive astrocytosis in these regions, and sprouting of mossy fibers into the molecular layer of the dentate gyrus. Since trophic factors are probably implicated in the cellular responses to the excitotoxic insult, and early induction of BDNF and TrkB mRNAs has been observed following KA injection, the present study examines BDNF, full-length and truncated TrkB protein expression in the hippocampus, as revealed by immunohistochemistry, up to 30 days following KA administration to adult rats. Reduction in BDNF and full-length TrkB immunoreactivity preceding neuron loss is observed in the damaged areas. However, transient increase in BDNF immunoreactivity is observed in surviving CA1 neurons and in granule cells of the dentate gyrus. In contrast, full-length TrkB immunoreactivity progressively increases in the molecular layer of the dentate gyrus up to day 30 following KA administration. A second peak in BDNF immunoreactivity is observed in reactive astrocytes, as revealed with double-labeling immunohistochemistry to BDNF and GFAP, in the plexiform layers of CA1 and, to a lesser degree, in the molecular layer of the dentate gyrus. In addition, strong truncated TrkB immunoreactivity is found in reactive astrocytes, as revealed with double-labeling immunohistochemistry to truncated TrkB and GFAP, in the same regions. These results, in concert with previous observations in the same model of hippocampal damage, suggest that BDNF participates in the early response to excitotoxic damage, and that expression of full-length TrkB at strategic sites in the molecular layer of the dentate gyrus has a role in the regenerative response linked to mossy fiber sprouting. Interestingly, delayed expression of BDNF and truncated TrkB in reactive astrocytes may act as negative regulators of neurite growth in devastated regions, such as the CA1 area, which are impoverished of putative postsynaptic sites.

Animals↗
PubMed1994

Antibody-binding sites on truncated forms of varicella-zoster virus gpI(gE) glycoprotein.

Varicella-zoster virus (VZV)-seropositive human sera were shown to be reactive with the truncated VZV gpI(gE) candidate subunit vaccine (TgpI-511). To identify the location of antibody-binding sites (epitopes) on TgpI-511, three truncated forms of TgpI-511 glycoprotein (TgpI-124, TgpI-160, TgpI-316) DNA encoding the N-terminal region of this glycoprotein with amino acid residues of 124, 160 and 360, respectively, were inserted into the vaccinia virus genome. Infection of cells with recombinant vaccinia viruses resulted in the secretion of all three truncated gpI(gE) as well as TgpI-511 from the infected cells. Immunoprecipitation of these truncated glycoproteins with VZV-seropositive human sera and gpI(gE)-specific monoclonal antibodies identified the location of four new antibody-binding sites on the VZV TgpI-511 glycoprotein. In addition, tunicamycin treatment and O-glycanase digestion revealed the presence of both N-linked and O-linked oligosaccharides on TgpI-511. These results revealed the location of new epitopes on VZV TgpI-511 and demonstrated that the epitopes on TgpI-511 were recognized by human sera from VZV-seropositive individuals.

Aged↗