Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1332347 (ADH)
 2,230 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alterations in gene expression during early stages of dormancy release in grapevine buds were analyzed to facilitate the identification of gene products that may mediate the signal transduction of a dormancy-release signal, or derepression of meristematic activity. In the present report we describe the identification of GDBRPK, a transcript for an SNF-like protein kinase that is up-regulated upon chemical induction of dormancy release by hydrogen cyanamide (HC). Since SNF and SNF-like protein kinases are known as sensors of stress signals, we hypothesize that GDBRPK may be involved in the perception of a stress signal induced by HC. We also describe a simultaneous and remarkable induction of both PDC and ADH transcripts that was observed shortly after HC application, and was of a transient nature. These data may imply that HC application leads to a transient respiratory stress, which likely results in a temporary increase in the AMP/ATP ratio. Since AMP is known as a stress signal that is sensed by SNF-like kinases, we suggest that the SNF-like GDBRPK could serve as the sensor of this signal.
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PMID:The transduction of the signal for grape bud dormancy breaking induced by hydrogen cyanamide may involve the SNF-like protein kinase GDBRPK. 1105

The European Medicines Agency approved tolvaptan to slow cyst growth and renal failure progression in adults with ADPKD, glomerular filtration 60 mL/min x 1.73 m2 and rapidly progressive disease. In a multicenter 3-year study, conducted on 1,445 patients with non-genotyped ADPKD, ages 18-50 years, predicted creatinine clearance 60 mL/min and kidney total volume 750 mL, tolvaptan slowed kidney failure progression (-23%-46% for different objectives) and reduced kidney volume increase and pain without effects on hypertension and albuminuria.Tolvaptan induced reversible idiosyncratic hepatopathy in 4% of patients (1% in placebo). Tolvaptan antagonizes ADH effects, reduces cyclic-AMP generation in distal nephron, and induces water diuresis. It has high protein-binding and 8-hour half-life. Dosage is 60-120 mg/day in two different doses (for instance 45/15 or 60/30 mg). Treatment starts using lower dose and continues with cautious up-titolation. Data are insufficient for severe hepatopathy or nephropathy. There is no antidote against overdose. Dialysis should not remove tolvaptan. Aquaretic effects require high fluid intake to prevent dehydration. Treatment should be reduced or suspended in case of inadequate fluid intake or dehydration. Weight, natremia and plasma osmolality can inform on dehydration risks. Efficacy is not yet investigated on end-stage renal disease, non-renal ADPKD-related disorders, and mortality.
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PMID:[Treatment of autosomal dominant polycystic kidney disease (ADPKD) - Tolvaptan]. 2779 22


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