Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The synthetic vasopressin analog 1-deamino-8-D-arginine vasopressin (dDAVP) has been shown to influence a wide range of cell-membrane-related events. Accordingly, the effect of dDAVP on membrane transport of various alkylating agents and amino acids was evaluated in L5178Y lymphoblasts in vitro. dDAVP stimulated melphalan uptake but conversely inhibited uptake of nitrogen mustard, choline (the natural transport substrate for the nitrogen mustard carrier), and leucine. No effect on the uptake of cyclophosphamide or glutamine was observed. Increased melphalan uptake was due to effects on both substrate influx and efflux. The effect of dDAVP on melphalan influx was particularly complex: dDAVP stimulated melphalan influx by amino acid transport system ASC but inhibited influx by system L, resulting in a net increase in unidirectional drug influx. Melphalan efflux was inhibited by dDAVP. Decreased uptake of nitrogen mustard, choline and leucine was due, at least in part, to decreased substrate influx. However, the mechanisms of inhibition were dissimilar: inhibition of substrate influx was non-competitive for choline but competitive for leucine. In conclusion, dDAVP induced diverse but apparently specific effects on membrane transport of several alkylating agents and amino acids. Since the accumulation of alkylating agents such as melphalan within tumor cells is a major determinant of cytotoxicity, dDAVP may have a role as a biological response modifier.
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PMID:Modulation of membrane transport of alkylating agents and amino acids by an analog of vasopressin in murine L5178Y lymphoblasts in vitro. 380 Oct 52

Primary cultures of rat hepatocytes respond to hormones or amino acid deprivation by increasing System A-mediated neutral amino acid transport. Previous reports have shown this stimulation to be dependent on RNA and protein synthesis, whereas the present report describes the inhibition of System A by tunicamycin (TM), an inhibitor of asparagine-linked glycoprotein biosynthesis. The basal System A activity, as monitored by Na+-dependent 2-aminoisobutyric acid uptake, was decreased by TM when hepatocytes were cultured for 24 h in the presence of the antibiotic. System Gly activity was also sensitive to TM, whereas the activities of Systems L1, L2, and N were relatively resistant and that of System ASC was only moderately affected. The increase in System A-mediated uptake after incubation of hepatocytes in the absence of amino acids (i.e. adaptive control) was almost completely abolished by including TM. Likewise, stimulation of hepatic 2-aminoisobutyric acid transport by glucagon, dexamethasone, insulin, or vasopressin was also blocked by the inhibitor. When glucagon alone or glucagon plus dexamethasone was added, the inhibition by TM was transient such that the degree of inhibition decreased with incubation time after the initial 2 h. Addition of TM to cells which had been treated previously for 2 h to 4 h with glucagon and dexamethasone blocked any further increase in transport indicating that the glycoprotein component of System A must be continually synthesized to sustain the increase in activity. Treatment of hepatocytes with various lectins did not inhibit 2-aminoisobutyric acid transport.
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PMID:Induction of amino acid transport system A in rat hepatocytes is blocked by tunicamycin. 635 4

In this study we try to simultaneously investigate the response of neurons and astrocytes of rats following hyperosmotic stimulation and test the possibility that the reciprocal pathways between medullary visceral zone (MVZ) and hypothalamic paraventricular nucleus (PVN) or supraoptic nucleus (SON). Hyperosmotic pressure animal model was established by administering 3% sodium chloride as drinking water to rats. The distribution and expression of the HRP retrogradely labeled neurons, Fos, tyrosine hydroxylase (TH) or vasopressin (VP) positive neuron and glial fibrillary acidic protein (GFAP) positive astrocytes in the MVZ, SON and PVN were observed by quadruplicate-labeling methods of WGA-HRP retrograde tracing combined with anti-Fos, TH (or VP) and GFAP immunohistochemical technique. Fos positive neurons within the MVZ, PVN and SON increased markedly. There were also a large number of GFAP positive structures in the brain and their distribution pattern was fundamentally similar or analogous to Fos positive neurons in the above-mentioned areas. The augmented GFAP reactivities took on hypertrophic cell bodies, thicker and longer processes. Quadruplicate immunohistochemical staining showed that a neuron could be closely surrounded by many astrocytes and they formed neuron-astrocytic complex (N-ASC). Fos+/TH+/HRP+/GFAP+ and Fos+/VP+/HRP+/GFAP+ quadruplicate labeled N-ASC could be found in the MVZ, PVN and SON, respectively. The present results indicated that the neurons and astrocytes might be very active following hyperosmotic pressure and N-ASC as a functional unit might serve to modulate osmotic pressure. There were reciprocal osmoregulation pathways between the MVZ and SON or PVN in the brain.
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PMID:Reciprocal pathway between medullary visceral zone and hypothalamic supraoptic nucleus or paraventricular nucleus involved in hyperosmotic regulation. 1872 99

Intracellular Ca(2+) signals are essential for stem cell differentiation due to their ability to control signaling pathways involved in this process. Arginine vasopression (AVP) is a neurohypophyseal hormone that increases intracellular Ca(2+) concentration during adipogenesis via V1a receptors, Gq-proteins and the PLC-IP3 pathway in human adipose-derived stromal/stem cells (hASCs). These Ca(2+) signals originate through calcium release from pools within the endoplasmic reticulum and the extracellular space. AVP supplementation to the adipogenic media inhibits adipogenesis and key adipocyte marker genes. This review focuses on the intersection between AVP, Ca(2+) signals and ASC differentiation.
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PMID:Vasopressin-induced Ca(2+) signals in human adipose-derived stem cells. 2683 Sep 70