Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0282612 (PIN)
 2,291 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The beta-adrenergic receptors (beta-ARs) coupled to pepsinogen secretion on frog esophageal peptic cells have been compared to frog erythrocyte beta-ARs using the radioligand 125I-iodopindolol (125I-PIN). 125I-PIN binding to intact peptic cells was time and temperature dependent. Saturation and competition experiments established that a large component of this binding represented radioligand uptake, which was energy dependent, pH sensitive, Na+ independent, and inhibited by agents that depress cellular ATP or disrupt proton gradients. This uptake system, which was absent from frog erythrocytes, appeared similar to that recently described for a number of mammalian cells. 125I-PIN bound to a single class of sites on peptic cell homogenates with a KD = 64 (+/- 5) pM. Binding to cell homogenates and a proportion of the binding to intact cells was inhibited by beta-agonists and antagonists with pharmacological characteristics similar to typical beta 2-ARs of frog erythrocytes. The number of beta-ARs in these peptic cell preparations was 1300 (+/- 240) sites/cell. Isolated peptic cells were poorly responsive to isoproterenol stimulation even in the presence of the phosphodiesterase inhibitor IBMX (3-isobutyl-1-methylxanthine). Pretreatment of cells with the phorbol ester TPA (12-O-tetra-decanoylphorbol-13-acetate) (100 nM) promoted isoproterenol stimulation of pepsinogen secretion. Catecholamine agonists stimulated pepsinogen secretion with an order of potency: isoproterenol greater than epinephrine much greater than norepinephrine, which was identical to that determined for inhibition of 125I-PIN binding. These findings indicate that frog peptic cells contain beta 2-ARs functionally coupled to pepsinogen secretion.
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PMID:125I-iodopindolol binding to frog esophageal peptic cells. Detection of amine uptake and beta-adrenergic receptors coupled to pepsinogen secretion. 254 27

The aim of this work was to develop an integrated solution to DNA hybridisation monitoring for diagnostics on a monolithic silicon platform. A fabrication process was developed incorporating a gold initiation electrode patterned directly onto a PIN photodiode detector. Patterned interdigitated type electrodes exhibited the smallest reduction in photodiode sensitivity, therefore these were chosen as the ECL initiator design. A novel DNA hybridisation assay was developed based on the displacement of a partially mismatched complementary strand by a perfectly matched labelled complementary strand. Pre-hybridised thiolated oligonucleotide and unlabelled 25% mismatched oligonucleotide were assembled on the gold initiation electrode. On addition of the labelled perfectly complementary oligonucleotide, the mismatched strands were displaced and a signal was generated. The sensitivity of the photodiode to light emitted at 620 nm, the ruthenium emission wavelength, was determined and subsequently, the diode current response to light generated by flow addition of ruthenium solution was found to be measurable to a concentration of 10 fM. Pre-hybridised duplex DNA, consisting of thiolated oligonucleotide and ruthenium labelled complementary oligonucleotide, was assembled on the gold initiation electrode. The difference between the current measured during flow of buffer and the ECL co-reactant TPA was three orders of magnitude, indicating that DNA assembled on the surface comprised sufficient ruthenium to generate a measurable signal. Finally, the displacement of unlabelled partial mismatch oligonucleotide from the sensor surface was monitored on addition of the ruthenium labelled perfectly complementary oligonucleotide in TPA flow and the measured photodiode current response was up to 50 times greater.
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PMID:A monolithic silicon based integrated signal generation and detection system for monitoring DNA hybridisation. 1620 69