Interference of AlF4− with nucleotide and DNA binding of rat histone H1 in vitro. Implications for the pathogenesis of Alzheimer's disease

Oikarinen, Jouko; Mannermaa, Riitta-Maaria; Tarkka, Tatu; Yli-Mäyry, N; Majamaa, Kari

doi:10.1016/0304-3940(91)90294-4

Cited by 9 publications

(2 citation statements)

References 14 publications

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“…A divalent cation, Mg 2+ or Ca 2+ , is at least in most cases involved in the binding of ATP to proteins with ATP‐dependent activity, such as protein kinases and actin [25]. In a previous study Mg 2+ had little effect when the ability to stabilize the binding of nucleoside triphosphate to H1 was investigated [26]. In accordance with those results, Mg 2+ did not produce any change in the folding of H1 in our CD analysis even at a concentration of 1 mM (data not shown).…”

Section: Resultsmentioning

confidence: 99%

Nucleotide and calcium‐induced conformational changes in histone H1

1997

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Section: Resultsmentioning

confidence: 99%

Nucleotide and calcium‐induced conformational changes in histone H1

1997

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“…Both basic ends of HI contain repeats of a motif° Ser.Pro-Lys/Arg-Lys/Arg, with DNA-binding capacity [13,14]. HI also contains a conserved segment with homology to nucleotide binding domains in diverse nucleotide-binding proteins [i [5][6][7][8][9][10][11][12][13][14][15][16][17], and nucleotides can bind to HI [16,18,19]. in this report we analyze the importance of the nucleotide interaction and show that nucleotides differentially affect the DNA binding of HI.…”

Section: Introductionmentioning

confidence: 99%

DNA binding of histone H1 is modulated by nucleotides

et al. 1992

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Hislone HI acts as a general repressor of transcription in eukaryotcs by organizing nueleosomcs into inaccessible condensed forms of chromatin, The capability of HI to bind to DNA with some sequence specificity is Likely to be critical in the control of tl~cse processes. We show I,¢re thai ATP and several other nu¢leotides, including non-hydrolyzable derivatives, can inhibit DNA binding of HI. The results also show thal ATP differentially affects binding of HI to DNA in a fashion enhancing nu¢leotide sequen¢~ specificity of the binding. The study suggests a novel mechanism of modulation of H1 activity that has important implications for lhe role of HI as a traa~:riptional regulator.

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Aluminium and the risk for alzheimer's disease

McLachlan

1995

Environmetrics

186

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SUMMARYThe strength of the evidence implicating aluminium as an important factor in the dementia of Alzheimer's disease (AD) is reviewed. We submit that the weight of the epidemiological and biological arguments is considerable. While a complete understanding has not been achieved, we recommend lowering aluminium exposure in municipal drinking water to below 50 pg/l in at least the province of Ontario. The Ministry of Energy and the Environment of Ontario maintains a drinking water surveillance programme which has provided a database for more than 10 years. This database has permitted assessment of the relative risk for AD using four independent measures of disease prevalence: 1. weighted residential history as a measure of exposure in autopsy-verified AD cases and controls; 2. first admission hospital discharge diagnoses of AD and controls; 3. death certificate rates for AD and presenile dementia; 4. impairments in cognitive function in elderly males. Taken together, many of the criticisms applied to epidemiological studies conducted elsewhere and reaching similar conclusions have been met. A vast experimental database on aluminium neurotoxicity, rapid advances in the understanding of the molecular basis of AD, and comparison studies between human brains exposed to chronic low dose aluminium exposure secondary to renal failure and AD, lend strong biological support to the conclusions reached by the epidemiological studies. The factors initiating AD, how aluminium gains access to the brain in AD, and the relative contributions of food, pharmaceuticals and skin absorption, remain unknown. While a full understanding is not in hand, the devastating nature of the disease, the lack of an effective treatment or prevention and the high cost to the health care system, together with the human costs, weighed against the relative cost of moderately reducing drinking water aluminium concentration to reduce exposure indicate that action is both reasonable and timely. KEY WORDSAlzheimer's disease; aluminium ALZHEIMER'S DISEASE: THE PROBLEMAlzheimer's disease (AD) is a slowly progressive, lethal, brain disorder which affects memory and other cognitive functions. AD is the most common cause of senile dementia and the prevalence in the age group over 65 years has been estimated to range between 9 per cent' and 5-5 per cent.2 The onset of AD is uncommon under the age of 65 (presenile dementia), but no less tragic. About 10 per cent of all cases occur in families (known as familial Alzheimer's disease (FAD)) and are inherited as an autosomal dominant disorder.The AD degenerative process renders victims mentally incompetent with progressive loss of self-help skills. The prolonged clinical course of the disease over ten or more years results in a particularly heavy burden of care upon the next-of-kin, the community social support systems, and, eventially, chronic care institutions, where the terminal phase may last three or more years. The brain changes which distinguish AD from all other causes of senile dementia are loss of neurons...

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Interference of AlF4− with nucleotide and DNA binding of rat histone H1 in vitro. Implications for the pathogenesis of Alzheimer's disease

Cited by 9 publications

References 14 publications

Nucleotide and calcium‐induced conformational changes in histone H1

Nucleotide and calcium‐induced conformational changes in histone H1

DNA binding of histone H1 is modulated by nucleotides

Aluminium and the risk for alzheimer's disease

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