Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.6.1.1 (adenylate cyclase)
 19,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The native plasma of patients suffering from renal insufficiency inhibited the parathyroid hormone (PTH), the vasopressin (VP) and the NaF-activated adenylate cyclase (AC) in bovine renal plasma membranes. A crude immunoglobulin fraction, prepared by (NH4)2SO4 precipitation, decreased only the hormone, but not the NaF activated AC. Chromatography of the native plasma on a AcA 34 column revealed two peaks inhibiting the PTH and to a lesser extent the VP dependent AC. Only the second peak reduced the NaF stimulated cAMP production. None of the column samples inhibited the isoproterenol stimulated adenylate cyclase in turkey red blood cells. Further purification of the first peak on a Sepharose 6B column confirmed previous results that immunoglobulins may block the PTH receptor in the kidney. Repurification of the second peak of inhibition on a Bio-Gel P10 column suggested that small peptides crossreacting in the radioimmunoassay for PTH may desensitize the hormonal receptor.
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PMID:Inhibition of renal adenylate cyclase by plasma from uremic patients. 715 74

An elevation of intracellular cyclic adenosine 3', 5'-monophosphate (cAMP) is known to stimulate proliferation and expression of surface galactocerebroside (galC) in cultured Schwann cells from newborn rats and mice. We investigated the age-related differences in proliferative and differentiating responses of Schwann cells to forskolin, an adenylate cyclase activator, in mice at postnatal days (P) 3, 10 and 30. The proportion of surface galC-positive cells decreased progressively with time in all ages during the initial three days in vitro (DIV) but the proportion of Schwann cells expressing surface galC at P30 was lower than that at P3 or P10. Administration of 50 microM forskolin in the media on the four DIV induced surface galC expression in Schwann cells from P3 and P10 mice but not from P30 mice. Forskolin also stimulated the proliferation of Schwann cells from P3 and P10 mice in media containing 2% fetal bovine serum (FBS) but not those from P30 mice, which, however, proliferated in media containing 10% FBS. These results suggest that Schwann cells in suckling mice are more sensitive to cAMP in both proliferative and differentiating responses than in adult. These different responses in vitro may reflect differences in the intrinsic metabolic status of Schwann cells in vivo since myelin-forming Schwann cells proliferate actively prior to myelination but cease or become less active in proliferation once myelination progresses.
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PMID:Age-related differences in mouse Schwann cell response to cyclic AMP. 878 79

Pituitary adenylate cyclase-activating polypeptide (PACAP) is a neuropeptide which was first isolated from ovine hypothalamic tissue by screening for pituitary adenylate cyclase stimulating activity. Our previous data showed that radioimmunoassayable PACAP and PACAP-binding sites were detected in the whole rat brain as early as embryonic day 14(E14). In order to understand more precisely the developmental pattern of the synthesis of PACAP and its receptors in the brain, we studied the expression of PACAP and its receptor genes in the prenatal and postnatal mouse brain using RNase protection assay. The mRNAs for both PACAP and its receptor were detected as early as 9.5 days of gestation (E9.5) in the whole head of mouse embryos. The levels of PACAP mRNA in the brain increased during the prenatal period peaking at postnatal day 0 (P0). On the other hand, the levels of PACAP receptor mRNA gradually increased after E9.5. The levels sharply increased at P6 (479.0 +/- 82.5% of P0 levels), and then fell to the P3 levels at P10. These data together with our previous study on the ontogeny of PACAP immunoreactivity and its binding sites in the rat brain support the view that PACAP plays an important regulatory role in the development of brain.
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PMID:Ontogeny of pituitary adenylate cyclase activating polypeptide and its receptor mRNA in the mouse brain. 895 77

Twitcher (twi/twi) is a murine model of genetic demyelinating disease globoid cell leukodystrophy (GLD). Available data suggest that demyelination in GLD is caused by degeneration or dysfunction of myelin-forming cells resulting from an accumulation of psychosine, a toxic substrate of galactosylceramidase and a potent inhibitor of protein kinase C (PKC). We investigated proliferation and differentiation of twi/twi Schwann cells in response to forskolin, an adenylate cyclase activator. In twi/twi Schwann cells isolated at the postnatal day (P) 10 prior to the onset of demyelination, proliferation and an expression of the surface galactocerebroside (galC) in response to forskolin were similar to those of +/+ mice. However, in twi/twi Schwann cells isolated from demyelinating sciatic nerves at P20 or P30, fewer numbers of cells expressed surface galC compared to age matched control (+/+) Schwann cells. In all Schwann cells, surface galC expression was lost after 3 days in vitro (DIV). However, with an administration of 50 microM forskolin in the media containing 1% fetal bovine serum (FBS) on the 4 DIV, surface galC could be reexpressed in all +/+ and P10 twi/twi Schwann cells but not in P20 or P30 twi/twi cells. In the media containing 10% FBS, forskolin also stimulated proliferation of Schwann cells from P10 twi/twi, and P10 and P30+/+ mice but not those from P30 twi/twi mice. These results are consistent with a metabolic perturbation of twi/twi Schwann cells that may be reflecting cellular dysfunctions by inhibition of the PKC.
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PMID:Responses to cyclic AMP is impaired in the twitcher Schwann cells in vitro. 987 48