Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The endopeptidase, post-proline cleaving enzyme, has been purified 10,500-fold in an overall yield of 18% from lamb kidney. The enzyme possesses a specific activity of 45 mumol/mg/min as tested with the substrate Z-Gly-Pro-Leu-Gly (Km = 6.0 X 10(-5)), has a molecular weight of 115,000, is comprised of two subunits with a molecular weight of 57,000, and exhibits maximal activity at pH 7.5 to 8.0. With the exception of the -Pro-Pro linkage, the -Pro-X-peptide bond (X equals L- and D-amino acid residues) located internally in the peptide sequence can be hydrolyzed (cleavage occurs faster when X = lipophilic side chain as compared to X = acidic side chain). The appropriate -Pro-X- bonds in zinc-free porcine insulin, oxytocin, arginine vasopressin, angiotensin II, bradykinin-potentiating factor were cleaved. Human gastrin, adrenocorticotropic hormone, denatured guinea pig skin collagen, and ascaris cuticle collagen were not degraded. Dipeptides with the structure Z-Pro-LD-X competitively inhibit post-proline cleaving enzyme.
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PMID:Post-proline cleaving enzyme. Purification of this endopeptidase by affinity chromatography. 1 73

Immunocytochemical localization of neuropeptides (beta-endorphin, substance P, arginine vasopressin, oxytocin), pituitary hormones (adrenocorticotropin, prolactin, growth hormone, follicle stimulating hormone (FSH), gonadal inhibin, gastrin, and human chorionic gonadotrophin (hCG)) was carried out in marmoset testis during development. Both intensity of immunostaining and distribution of these peptides in testicular compartments viz. seminiferous tubules and Leydig cells changed dramatically during development. In vitro biosynthesis of inhibin and FSH was increased by hCG, whereas prolactin (5 micrograms) and prostatic inhibin peptide suppressed the synthesis of these hormones.
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PMID:Immunocytochemical localization of bioregulatory peptides in marmoset testes. 138 Feb 34

Peptide receptor-activated membrane currents were studied in two mouse fibroblast cell lines, Swiss and Balb/c 3T3 cells, using a patch-electrode voltage-clamp technique. About 50% of the Swiss 3T3 cells examined responded to bombesin (Bn; 10(-9) to 10(-6) M), either by inducing outward current flow or inward current flow at the membrane holding potential (Vh) of -60 mV. The outward current type was more common (approximately 70%) than the inward current type (30%). The Bn-induced outward current (IBn) was reversed as the Vh was held to more negative than -90 mV (avg reversal potential, Erev = -82 mV). This Erev was closer to the equilibrium potential for K+ and shifted by altering the extracellular-to-intracellular K+ concentration ratio, in a Nernst-like relationship. The chance of recording this type of IBn was greatly reduced when K+ conductance blockers were present in the bathing solution (i.e., tetraethylammonium, Ba2+) or in the pipette solution (i.e., Cs). It was also reduced by recording with the pipette containing 5-10 mM ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid. Application of Ca2+ ionophore A23187 (5 microM) induced a similar membrane current with conductance increase. Thus the outward IBn in Swiss 3T3 cells appears to be induced by the intracellular Ca2(+)-dependent K+ conductance increase. Applications of bradykinin (Bk), arginine vasopressin (AVP), neuromedin B (NmB), and gastrin releasing peptide (GRP) to Swiss 3T3 cells also induced receptor-activated currents similar to IBn. Balb/c 3T3 cells rarely generated outward currents in response to Bn, GRP, and NmB but did not respond to both AVP and Bk with outward current flows.
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PMID:Bombesin-like peptides induce Ca2(+)-activated K+ conductance increases in mouse fibroblasts. 201 7

Several factors are involved in the persistence of endocrine alterations after renal transplantation, among which the following are to be mentioned: (1) duration of chronic uraemia before renal transplantation; (2) residual function of the patients' native kidneys; (3) quality of function of the renal graft; (4) modulation of secretion, transport, and degradation of hormones, and/or (5) altered target organ responsiveness to hormones induced by immunosuppressive drugs (glucocorticoids, azathioprine, cyclosporin A) or altered internal environment. In kidney transplant patients the following endocrine abnormalities are to be mentioned: dissociation of the physiological relationship between aldosterone synthesis and function of the renin-angiotensin system, abnormal volumetric regulation of arginine vasopressin secretion, suppressed responsiveness of cortisol secretion to stimulatory manoeuvres, persistent secondary hyperparathyroidism, relative deficiency of insulin (induced by glucocorticoid therapy), with consequent carbohydrate intolerance or even diabetes mellitus, suppressed response of gastrin and pancreatic hormone secretion to a test meal, and reduced responsiveness of atrial natriuretic peptide secretion to central hypervolaemia. Episodes of acute graft rejection are characterized by endocrine alterations similar to those seen in patients with acute or chronic renal failure.
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PMID:Endocrine alterations in kidney transplant patients. 219 17

Short-latency emetic responses were induced in dogs by injecting angiotensin II (AII), arginine vasopressin (AVP), and neurotensin (NTN) into cerebroventricular (ICV) and cisternal (ICT) sites also responsive to the emetic effects of apomorphine (APO). Angiotensin III, bradykinin, bombesin, oxytocin, adrenocorticotropic hormone, substance P, gastrin-related peptide and cholecystokinin were ineffective. The results suggest a possible dopaminergic mediation of peptide-induced emesis by receptors in the area postrema (AP).
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PMID:Emetic effects of centrally administered angiotensin II, arginine vasopressin and neurotensin in the dog. 404 79

Most neuropeptides can now be assayed in human cerebrospinal fluid (CSF). Some, such as beta-endorphin and arginine vasopressin, seem to be secreted directly into CSF. Others may reach CSF from plasma either by passage through the blood-brain barrier or by absorption through the circumventricular organs, which lack a blood-brain barrier. The role of neuropeptides in CSF is still unclear. Thyrotropin-releasing hormone, somatostatin, arginine vasopressin, angiotensin II, substance P, vasoactive intestinal polypeptide, beta-endorphin, gastrin, and cholecystokinin are all present in assayable quantities in human CSF. Their functions in this fluid are liable to be as diverse as their functions elsewhere in the body. The release of hypothalamic releasing factors into the CSF may be part of the pathway of pituitary hormone release. Pituitary hormones may function in CSF as part of a feedback loop from the hypothalamus. Other neuropeptides may affect receptors in the central nervous system far away from their release site. Intraventricular neuropeptide injection, anatomical and physiological ablation experiments, receptor studies, and neurobiological techniques now being developed will allow a more complete understanding of CSF neuropeptide function in the future.
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PMID:Neuropeptides in cerebrospinal fluid. 675 95

Several factors are involved in the persistence of endocrine alterations after renal transplantation, among which the following are to be mentioned: 1) duration of chronic uraemia before renal transplantation; 2) residual function of the patients' native kidneys; 3) quality of function of the renal graft; 4) modulation of secretion, transport, and degradation of hormones, and/or 5) altered target organ responsiveness to hormones induced by immunosuppressive drugs (glucocorticoids, azathioprine, cyclosporin A) or altered internal environment. In kidney transplant patients the following endocrine abnormalities are to be mentioned: dissociation of the physiological relationship between aldosterone synthesis and function of the renin-angiotensin system, abnormal volumetric regulation of arginine vasopressin secretion, suppressed responsiveness of cortisol secretion to stimulatory manoeuvres, persistent secondary hyperparathyroidism, relative deficiency of insulin (induced by glucocorticoid therapy), with consequent carbohydrate intolerance or even diabetes mellitus, suppressed response of gastrin and pancreatic hormone secretion to a test meal, and reduced responsiveness of atrial natriuretic peptide secretion to central hypervolaemia. Episodes of acute graft rejection are characterized by endocrine alterations similar to those seen in patients with acute or chronic renal failure.
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PMID:Function of endocrine organs in kidney transplant patients. 986 33

The circadian pacemaker of the suprachiasmatic nucleus (SCN) is likely to control the timing of the sleep-wake cycle in mammals by modulating the daily activity patterns of brain regions important in sleep and wakefulness. One such brain region is the paraventricular nucleus of the thalamus (PVT). In both nocturnal rats and the diurnal rodent Arvicanthis niltoicus (Nile grass rat), expression of Fos (the product of the immediate-early gene c-fos) in the PVT increases at times of day when the animals are most active. To compare the projections of the SCN to the PVT in these two species, the retrograde tracer cholera toxin (beta subunit; CTbeta) was microinjected into the PVT and the SCN was examined to identify labeled neurons. Further, the PVT-projecting SCN cells containing either arginine vasopressin (AVP) or gastrin releasing peptide (GRP) were also compared between species. In both nocturnal rats and diurnal Nile grass rats, the SCN sends a substantial projection to the PVT. In both species, many PVT-projecting SCN neurons contain AVP, and few contain GRP. Other work has shown that some AVP-containing neurons of the SCN function differently in rats and Nile grass rats. Projections from functionally distinct SCN neurons to the PVT may contribute to the difference in the temporal distribution of sleep and wakefulness seen between these two species.
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PMID:Suprachiasmatic nucleus projections to the paraventricular thalamic nucleus in nocturnal rats (Rattus norvegicus) and diurnal nile grass rats (Arviacanthis niloticus). 1096 May 99

Autocrine and paracrine signaling leading to stimulation of tumor cell growth is a common theme in human cancers. In addition to polypeptide growth factors such as EGF family members which signal through receptor tyrosine kinases, accumulating evidence supports the autocrine and paracrine involvement of specific neuropeptides with defined physiologic actions as neurotransmitters and gut hormones in lung, gastric, colorectal, pancreatic and prostatic cancers. These neuropeptides, including gastrin-releasing peptide, neuromedin B, neurotensin, gastrin, cholecystokinin and arginine vasopressin bind seven transmembrane-spanning receptors that couple to heterotrimeric G proteins. Studies with human small cell lung cancer (SCLC) cells support a requirement for balanced signaling through G(q) and G(12/13) proteins leading to intracellular Ca2+ mobilization, PKC activation and regulation of the ERK and JNK MAP kinase pathways. While specific neuropeptide antagonists offer promise for interrupting the single neuropeptide autocrine systems operating in pancreatic and prostatic cancers, SCLC is exemplified by multiple, redundant neuropeptide autocrine systems such that tumor growth cannot be inhibited with a single specific antagonist. However, a novel class of neuropeptide derivatives based on the substance P sequence have been defined that exhibit broad specificity for neuropeptide receptors and induce apoptosis in SCLC by functioning as biased agonists that stimulate discordant signal transduction. Thus, interruption of autocrine and paracrine neuropeptide signaling with specific antagonists or broad-spectrum biased agonists offer promising new therapeutic approaches to the treatment of human cancers.
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PMID:Autocrine and paracrine signaling through neuropeptide receptors in human cancer. 1131 3

Small-cell lung cancer (SCLC) synthesises a wide range of neuropeptides and their corresponding receptors. Together, these can form autocrine growth loops. Non-small-cell lung cancer (NSCLC) does not generally share this neuroendocrine phenotype. In this study, we tested the hypothesis that multiple neuropeptides and their receptors are co-expressed in SCLC, constituting potential autocrine loops. Expression of mRNA for arginine vasopressin, gastrin, cholecystokinin, gastrin-releasing peptide, endothelin and neurotensin, together with their cognate receptors, was evaluated by reverse transcriptase-polymerase chain reaction (RT-PCR) in a panel of human lung cancer cell lines. We have assessed those neuropeptides and neuropeptide receptors that could be used as potential early markers to detect lung cancer cells both as micrometastases in blood and within dysplasia in bronchial biopsies. We establish that although no cell line expressed all neuropeptides, co-expression of neuropeptides and their receptors is common in SCLC but not in NSCLC. We conclude that mRNA for the neuropeptides gastrin-releasing peptide and arginine vasopressin and the cholecystokinin receptor B were most SCLC-specific and RT-PCR for these markers could be used to distinguish between SCLC and NSCLC.
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PMID:Use of RT-PCR to detect co-expression of neuropeptides and their receptors in lung cancer. 1142 90


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