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At least 1,675 records · Page 93Linked to original sources
PubMed1988

Effects of the parathyroid hormone antagonist [Tyr34]bPTH-(7-34)amide on avian renal phosphate transport.

The in vivo parathyroid hormone antagonist, [Tyr34]bPTH-(7-34)amide, was tested for its ability to block endogenous parathyroid hormone (PTH) activity in parathyroid-intact European starlings. The inhibitor was infused at two dose levels, 0.005 and 0.05 mg/hr. A third group received a vehicle/control infusion. High-dose infusion led to rapid and significant decreases in plasma calcium and in both absolute and relative phosphate (Pi) excretion. Low-dose infusion significantly reduced plasma calcium, but had no effect on Pi excretion. Plasma Pi tended to increase with time in all three groups. Removal of the antagonist after 140 min of high-dose infusion led to a rapid recovery of relative Pi excretion, and a subsequent overshoot to more than twice the original control level. To further test the ability of the antagonist to block endogenous PTH activity, an EGTA challenge was used to induce hypocalcemia and subsequent elevation of circulating PTH levels. In vehicle-infused birds, EGTA challenge led to a doubling of relative Pi excretion, but in birds receiving the high-dose infusion, no effect of EGTA was observed. These results demonstrate that [Tyr34]bPTH-(7-34)amide can completely block endogenous PTH activity in birds at the receptor level, including the hormone response of the renal Pi secretory transport mechanism.

Animals↗
PubMed1992

A mosquito neuropeptide in a moth larva (Helicoverpa zea): relation to FMRF-amide immunoreactivity.

The cerebral nervous and midgut endocrine systems of the larval corn earworm, Helicoverpa zea, were examined using light microscopy and immunocytochemistry for RF-amide family peptides. Immunoreactivity for a mosquito neuropeptide, Aedes Head Peptide-I (Aea-HP-I,pERPhPSLKTRFa), is widely distributed in this lepidopteran. Immunostaining for Aea-HP-I is localized (1a) in perikarya and axons of the brain, the subesophageal ganglion, and the first thoracic ganglion, (b) in peripheral axons innervating muscles of the midgut, and (2) in numerous midgut endocrine cells. Aea-HP-I-associated activity generally occurs as a subset of FMRF-amide (FMRFa; a molluscan cardioactive peptide) immunoreactivity. Cross-reactivity studies indicate that Aea-HP-I and FMRFa immunoreactivities are heterogeneous in the cerebral nervous system and in axons innervating the muscles of the midgut, but may be homogeneous in midgut endocrine cells. Radioimmunoassay for Aea-HP-I reveals immunoreactivity in hemolymph, as well as in extracts of midguts and heads.

Amino Acid Sequence↗
PubMed1992

Autoradiographic localization of receptors for glucagon-like peptide-1 (7-36) amide in rat brain.

Glucagon-like peptide-1 (GLP-1) has a sparse but well defined distribution in the rat brain where it is co-localized with glucagon-like immunoreactivity due to other fragments of the glucagon precursor. We have investigated the localization of GLP-1 receptors in rat brain using mono-125I-iodinated GLP-1(7-36) amide, the biologically active form of the peptide that occurs in brain, as the tracer for binding and autoradiographic studies of tissue sections. Displaceable binding of the label was sharply localized to discrete areas, being high in mamillary nuclei, the arcuate nucleus, nucleus of the solitary tract and the pretectal area, intermediate in the lateral septal nuclei, olfactory bulb, dorsal tegmental nuclei and the interpenduncular nucleus, and low in other regions. These results indicate areas where GLP-1(7-36) amide may have a role as a neurotransmitter or neuromodulator.

Animals↗
PubMed1994

Evidence showing that the 1105 and 1106 isotypic residues of the fourth component of human complement, C4A, are not involved in amide bond formation.

Human C4A and C4B have different functions that may stem from their ability to bind hydroxyl or free amino groups on complement activating surfaces. Previous studies suggest that C4B binds to hydroxyl or amino groups whereas C4A binds to free amino groups on acceptor molecules. Comparison of the derived amino acid sequences of C4A and C4B has shown that differences exist between them at positions 1101, 1102, 1105 and 1106. These residues appear to be involved in the binding specificity of C4B. Less is known about the corresponding residues of C4A. It has been suggested that the aspartic acid of C4A at position 1106 is involved in amide bond formation by serving as a catalytic residue for the reaction or by promoting an increased interaction with amino nucleophilic groups. To examine the functional role of residues 1101-1106, we studied the effects of the C4A site-specific antipeptide mAb, AII-1 in assays dependent on the covalent binding properties of C4A; the C4 mediated inhibition of hemolysis and the C4 mediated inhibition of immune precipitation. This study shows that mAb AII-1 has no effect on C4-mediated hemolysis or its ability to inhibit the rate of immune precipitate formation. The lack of interference by AII-1 in these assays could not be explained by low affinity interaction between antibody and C4A showing that mAb AII-1 does not affect the covalent binding activity of C4A. Furthermore, results from epitope mapping studies show that AII-1 binds to Leu1105 and Asp1106 suggesting that these residues are not critical for amide bond formation by C4A.

Amino Acid Sequence↗
PubMed1983

Nickel(II) binding to glycylglycyl-L-tyrosine-N-methyl amide, a peptide mimicking the NH2-terminal nickel(II)-binding site of dog serum albumin: a 1H- and 13C-nuclear magnetic resonance investigation.

The nonspecificity of dog serum albumin (DSA) for Ni(II) is mimicked by the simplest tripeptide, glycylglycyl-L-tyrosine-N-methyl amide, which forms a planar complex at high pH. In this study, the 1H and 13C nuclear magnetic resonance (nmr) spectra of the free and complexed peptide are reported. As the pH is increased for the free peptide, the deprotonation of the terminal amino group (pKa = 7.94) is reflected most strongly by the chemical shift changes of the NH2-terminal -CH2CO- unit. Large upfield and downfield shifts for the tyrosine C xi, C epsilon and C gamma carbon resonances occur on the ionization of the phenolic hydroxyl group. The planar Ni(II) complex is in slow exchange on the nmr time scale and is of 1:1 stoichiometry. The greater chemical shift changes on Ni(II) coordination are observed from the protons nearest the peptide and amino nitrogens:amide CH3 (-0.704), Tyr(3) alpha-CH (-0.667), Gly(1) alpha-CH2 (-0.382), and Gly(2) alpha-CH2 (-0.519, -0.487). In the 13C spectrum, the Gly(1) C alpha (+7.58) is most affected. The Ni(II) ion is therefore at the center of four coordinating nitrogens. Changes in the coupling constants for the Tyr(3) -CH-CH2- moiety suggests a mainly gauche conformation with the tyrosyl ring positioned above the plane of coordination and a weak bonding interaction with the Ni(II) ion is indicated. These results provide structural information regarding the reduced affinity of DSA for Ni(II).

Animals↗
PubMed1989

Non-amidated forms of VIP (glycine-extended VIP and VIP-free acid) have full bioactivity on smooth muscle.

The aim of the present study was to elucidate the importance of the C-terminal amide group for the biological activity of vasoactive intestinal peptide (VIP). Two synthetic peptides lacking the amide group: VIP having a carboxyl group at the C-terminus and the intermediate biosynthetic precursor, glycine-extended VIP were compared with VIP itself regarding the ability to inhibit spontaneous activity in smooth muscle strips from rat stomach and human Fallopian tube. Both the glycine-extended VIP and VIP having a carboxyl group at the C-terminus caused a significant and dose-dependent inhibition of smooth muscle activity and displayed dose-response curves similar to VIP. The potencies of the VIP variants did not differ significantly from that of VIP. Thus, alpha-carboxyamidation of VIP is not a prerequisite for biological activity.

Animals↗
PubMed1995

Binding and agonist/antagonist actions of M35, galanin(1-13)-bradykinin(2-9)amide chimeric peptide, in Rin m 5F insulinoma cells.

The chimeric peptide M35 [galanin(1-13)-bradykinin(2-9) amide] is a high-affinity galanin receptor ligand acting as a galanin receptor antagonist in the rat spinal cord, rat hippocampus and isolated mouse pancreatic islets. We have radiolabelled M35 and performed equilibrium binding studies with [125I]M35 on the rat pancreatic beta-cell line Rin m 5F, whereby we show the existence of high-affinity binding site (KD = 0.9 +/- 0.1 nM) with a Bmax of 72 +/- 3 fmol/mg protein. Galanin displaces [125I]M35 with the same affinity (KD = 1 nM) as it displaces [125I]galanin. Displacement of [125I]galanin by M35 from Rin m 5F cell membranes shows the presence of two binding sites for M35 with KD-values of 0.3 +/- 0.1 nM and 0.52 +/- 0.03 microM, respectively. The GTP- and pertussis toxin-sensitivity of M35 binding to Rin m 5F membranes shows that binding of [125I]M35 is almost completely abolished by the presence of GTP or after pertussis toxin treatment of the cells, indicating an agonist-like binding of M35 to the galanin receptors. M35 has a dual effect on the galanin mediated inhibition of forskolin stimulated cyclic AMP production in Rin m 5F cells: at low concentrations M35 antagonises the effect of galanin, whereas at concentrations above 10 nM M35 acts as a galanin receptor agonist. These agonist-like effects of galanin and M35 are not additive, thus the mixed agonist/antagonist properties arise from the chimeric nature of M35[galanin(1-13)-bradykinin(2-9)amide] acting solely at galanin receptors.

Animals↗
PubMed1994

Stabilized NMR structure of the hypercalcemia of malignancy peptide PTHrP[Ala-26](1-34)amide.

The structure of the biologically active mutant PTHrP[Ala-26](1-34)amide in 10% trifluoroethanol was studied by two-dimensional proton NMR spectroscopy. Complete assignments of all backbone and side chain hydrogens were made with the aid of totally correlated and nuclear Overhauser effect spectroscopy. The NMR data were utilized in the distance geometry algorithm (DIANA) and the resulting family of structures further refined using dynamic simulated annealing (X-PLOR). The major structural features include two segments of alpha-helix extending from Glu-4 to Lys-13 and from Phe-21/Phe-22 to Ala-34, with a turn from Gln-16 to Arg-19 and a hinge around Ser-14/Ile-15. A close resemblance to the structure of PTH(1-34)amide in water was noted. A comparison of the structural features common to PTH and PTHrP in different solvents was made which enabled the key structural features likely to be involved in PTH receptor binding to be identified.

Amino Acid Sequence↗
PubMed1992

Comparison of subcutaneously administered soluble insulin and des-(B26-B30)-insulin-B25-amide in rabbit, pig and healthy man.

Subcutaneous injections of soluble human insulin and of the monomeric insulin analogue des-(B26-B30)-insulin-B25-amide were given to fasted rabbits, pigs and healthy man. The time course of blood glucose decline and the rate of appearance of the hormones in the peripheral circulation were studied for doses of 0.35 and 0.7 nmol/kg. In rabbits an identical time course with early glucose nadirs between 45 and 60 min and hormone peaks at about 20 min were observed for both hormones. Similar results were obtained for insulin and the analogue in pigs. When injected into humans, slightly earlier peaks of the analogue at 30 to 45 min were measured compared to insulin peaks at 60 min. In addition, a trend towards faster decline in blood glucose could be demonstrated after analogue injection. In contrast to monomeric insulin analogues produced by recombinant DNA technology, s.c. injections of des-(B26-B30)-insulin-B25-amide do not appear to meet mealtime insulin requirements better than soluble insulin.

Adult↗
PubMed1996

Peptide amidating activity in human bronchoalveolar lavage fluid.

Monitoring respiratory epithelial biology may reveal individuals with incipient lung cancer. The expression of neuroendocrine (NE) markers in pulmonary epithelium is thought to be central to lung development, repair of injury and may contribute to carcinogenesis. In this study, we evaluate several candidate NE markers to determine the feasibility of prospective analysis of clinical specimens. The potential NE markers include the enzyme L-DOPA decarboxylase (DDC), the neuropeptide gastrin releasing peptide (GRP), and peptidyl-glycine alpha-amidating monooxygenase (PAM), the bifunctional enzyme responsible for the final bioactivation step of many neuropeptides. A comparison of PAM activity and DDC levels in 30 lung cancer cell lines indicated that peptide amidating activity may be an indicator of NE status. Bronchoalveolar lavage (BAL) fluid from subjects at risk of developing second primary lung cancer and from volunteers was obtained. The activity of the first PAM enzyme, peptidylglycine alpha-hydroxylating monooxygenase (PHM), ranged from not detectable to 507 pmol/h/mg protein in 57 specimens. The second PAM enzyme, peptidylamidoglycolate lyase (PAL), ranged from not detectable to 414 pmol/h/mg protein in 56 specimens. Using cluster analysis by the average linkage method, a group of enzyme values with PHM greater than 230 pmol/h/mg protein was determined. Long-term follow-up of these patients for new second primary lung cancers may help to determine the potential predictive value of PAM detected in the BAL fluid.

Biomarkers, Tumor↗
PubMed1988

Structural aspects of gastrin/CCK-like insect leucosulfakinins and FMRF-amide.

The leucosulfakinins (LSKs), isolated from head extracts of the cockroach Leucophaea maderae, are sulfated neuropeptides with homology to gastrin and cholecystokinin. The undecapeptide LSK and decapeptide LSK-II stimulate contractions of the isolated cockroach hindgut. Several structural aspects of the two gastrin/CCK-like insect leucosulfakinins (LSKs) and their relation to FMRF-amide are discussed. Replacement of the oxidation sensitive Met residue with isosteric norleucine leads to an analog with retention of biological activity. The Arg residue of the LSKs is critical for cockroach hindgut contractile stimulatory activity, as its introduction into gastrin II transforms the inactive peptide into an active analog. As demonstrated by the equipotent [His14,Arg16]gastrin II, the His8 and Asp5 residues of LSK are not critical for activity. The common C-terminal tetrapeptide of the LSKs ([8-11]LSK) is inactive. Taken together with a comparison of the two LSK structures, the data suggest that the LSK active core resides between [8-11]LSK and [4-11]LSK. This is confirmed by considerable activity displayed by the sulfate analog of LSK-II, which contains an extra sulfate group on the Ser2 residue in the N-terminal region. Homology between the LSKs and molluscan cardioacceleratory and rectum contractile neuropeptide FMRF-amide and Met-enkephalin-Arg6-Phe7 is discussed. The insect LSKs may represent a molecular evolutionary link between the vertebrate gastrin/CCK family and this mammalian enkephalin.

Amino Acid Sequence↗
PubMedDate not supplied

Albuminamide: a novel peptide amide isolated from bovine serum.

During a systemic search for peptides that possess the C-terminal amide structure, a novel heptapeptide with isoleucine amide was isolated from bovine serum by sequential steps of reversed phase HPLC. Microsequence and amino acid analyses revealed the structure: Asp-Thr-His-Lys-Ser-Glu-Ile-NH2. Since this peptide has the identical sequence to N-terminal (1-7) fragment of bovine serum albumin (BSA), we have designated it albuminamide. The final HPLC step yielded 10 micrograms of homogeneous peptide preparation from 1 liter of bovine serum.

Amino Acid Sequence↗
PubMedDate not supplied

Biological effects of human gastrin I and II chemically modified at the C-terminal tetrapeptide amide.

Binding to gastrin receptors and gastric acid secretion experiments were performed with gastrin derivatives modified at the C-terminal tetrapeptide amide from HG-13 sequence. 1. When the ultimate phenylalanine amide was replaced by a phenethylester or a phenetylamide moiety, the resulting compound bound to gastrin receptors (Kd approximately 10 nM) and exhibited antagonist activity on gastrin-induced acid secretion in the anesthetized rat. 2. Changing the peptide bond between Trp and Leu residues to a -omega(CH2-NH)- bond resulted in a compound which also bound to gastrin receptors (Kd approximately 10 nM) but presented agonist activity on acid secretion in the rat. In contrast, when the peptide bond between Leu and Asp residues was replaced by a -omega(CH2-NH)- bond, the resulting compound was devoid of any affinity for gastrin receptor (Kd greater than 10(-6) M) and of any biological activity. 3. The HG-13 derivatives were synthesized in sulfated and unsulfated forms: O-sulfation of the HG-13 tyrosine residue did not change its intrinsic in vivo activity but enhanced its affinity for gastrin receptors (Kd approximately 0.3 nM). On the contrary, O-sulfation of the various chemically modified HG-13 had no significant effect in either in vitro or in vivo experiments. 4. Finally, no significant difference between binding on parietal (F3) and nonparietal (F1) cells was observed, in agreement with the presence of a gastrin-type receptor in these two cell populations.

Amino Acid Sequence↗
PubMed1992

Secretion of peptidylglycine alpha-amidating monooxygenase (PAM) from rat salivary glands.

Peptidylglycine alpha-amidating monooxygenase (PAM) is a regulating enzyme to synthesize the biologically active hormones having carboxy-terminal amide. In the present study we investigated secretion of the enzyme from rat saliva. Property of PAM in the saliva was similar to that in the submandibular gland. Both enzymes showed similar pH optimum at 5.0 and optimal ascorbic acid concentration at 2.5 mM. But molecular size of PAM in the saliva was 75 kDa in the gel permeation chromatography on Superose 12 column, while the size in the submandibular gland was 25 kDa. After the treatment with trypsin, PAM in the saliva was converted to a small size molecule, which is similar to the size in rat submandibular gland. These and other data indicate that a native molecular size of PAM is secreted into saliva and plays some physiological roles.

Aging↗
PubMed1994

Further studies on the adjuvanticity of stearyl tyrosine and amide analogues.

Stearly tyrosine has been described in the literature as a candidate adjuvant for human vaccines. More recently, other stearyl esters have been reported to be adjuvant-active. This preliminary study assesses the adjuvanticity of stearyl amides, including the amide analogue of stearyl tyrosine: tyrosyl stearylamine. This study indicates that phenylalanylethanolamine O-stearate induces a significant antibody response and a favourable isotype distribution.

Adjuvants, Immunologic↗
PubMed1991

Processing of pro-opiomelanocortin-derived amidated joining peptide and glycine-extended precursor in monkey pituitary.

The molecular forms of proopiomelanocortin (POMC) derived amidated and C-terminal glycine-extended joining peptide from monkey (Macaca mulatta) pituitary were determined. The predominant forms of joining peptide found were the low molecular peptides POMC(76-105) and POMC(76-106), respectively. Significant amounts of N-terminally truncated POMC(78-105) and POMC(78-106) were also detected in the posterior-intermediate lobe. No N-terminal extended forms were detected. The relative amount of amidated joining peptide to total joining peptide was 6-35%. It is concluded that not only is the primary sequence of monkey and human POMC extremely conserved, but also the processing patterns are similar. The monkey therefore serves as a suitable model for studying regulation of the processing of POMC and the hypothalamus-pituitary-adrenal axis in man.

Amino Acid Sequence↗
PubMed1995

Exacerbation of acetaminophen hepatotoxicity by thalidomide and protection by nicotinic acid amide.

1. The effects of racemic thalidomide (D[+]/L[-] alpha-phthalimido-glutarimide) on acetaminophen (AAP)-induced hepatitis were tested in male NMRI mice (n = 133) and quantified as serum activities of glutamate-oxaloacetate transaminase (GOT) and glutamate-pyruvate transaminase (GPT). 2. A 2.1-fold increase of GOT and a 1.9-fold increase of GPT activities (P < 0.001) were observed in mice treated perorally with 500 mg/kg of AAP plus 150 mg/kg of thalidomide (Thal). In the absence of AAP, Thal did not display any detectable hepatotoxic effects. 3. The Thal-induced exacerbation of AAP hepatotoxicity was completely inhibited by nicotinic acid amide, a selective inhibitor of poly(ADP-ribose) polymerase (PARP) (P < 0.0001), suggesting a possible influence of Thal on the hepatic metabolism of NAD-adenoribosylation. 4. We see the main application of nicotinic acid amide as for the combinational use in pharmaceutical preparations of AAP in order to avoid hepatic damage in patients treated with AAP and Thal.

Acetaminophen↗
PubMed1992

Liquid chromatography-mass spectrometry of hydroxy and non-hydroxy fatty acids as amide derivatives.

A useful method for analyzing fatty acids by liquid chromatography-mass spectrometry with an atmospheric-pressure chemical-ionization interface system has been developed. The sensitivity of six kinds of palmitamide derivatives monitored by a single ion of [M+H]+ was, in decreasing order: N-n-propylamide greater than anilide greater than N,N-diethylamide, amide greater than N,N-diphenylamide greater than N-1-naphthylamide. Individual fatty acids were identified from a mixture of amide derivatives of authentic fatty acids from C16:0 to C30:0 on a mass chromatogram. This method was used to detect both hydroxy and non-hydroxy fatty acids. Many kinds of fatty acid, including hydroxy fatty acids of the rat brain, were detected in a single run.

Animals↗