Heme deficiency may be a factor in the mitochondrial and neuronal decay of aging. - Wikidata - awgldk - TriplyDB

Heme deficiency may be a factor in the mitochondrial and neuronal decay of aging.

Heme deficiency may be a factor in the mitochondrial and neuronal decay of aging.

http://www.wikidata.org/entity/Q34379668

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Biomarkers in autism Amyloid-beta peptide binds with heme to form a peroxidase: relationship to the cytopathologies of Alzheimer's disease Heme regulates gene expression by triggering Crm1-dependent nuclear export of Bach1 Mitochondrial dysfunction in autism spectrum disorders: a systematic review and meta-analysis From the lab to the land.Heme deficiency in Alzheimer's disease: a possible connection to porphyria Heme is involved in microRNA processing Tissue-specific expression of ALA synthase-1 and heme oxygenase-1 and their expression in livers of rats chronically exposed to ethanol Iron deficiency accelerates Helicobacter pylori-induced carcinogenesis in rodents and humans An ATP and oxalate generating variant tricarboxylic acid cycle counters aluminum toxicity in Pseudomonas fluorescens.A possible link between iron deficiency and gastrointestinal carcinogenesis.Defining a role for hemoglobin in Parkinson's disease Prevention of mutation, cancer, and other age-associated diseases by optimizing micronutrient intake.An enthusiasm for metabolism.Therapeutic approaches to delay the onset of Alzheimer's disease GAPDH regulates cellular heme insertion into inducible nitric oxide synthase Increasing longevity by tuning up metabolism. To maximize human health and lifespan, scientists must abandon outdated models of micronutrients.An alternatively-spliced exon in the 5'-UTR of human ALAS1 mRNA inhibits translation and renders it resistant to haem-mediated decay.The jaundice of the cell.Transition between acute and chronic hepatotoxicity in mice is associated with impaired energy metabolism and induction of mitochondrial heme oxygenase-1.Frataxin, iron-sulfur clusters, heme, ROS, and aging.Impaired iron status in aging research Iron accumulation during cellular senescence in human fibroblasts in vitro Heme Stabilization of α-Synuclein Oligomers during Amyloid Fibril Formation.PpsR, a regulator of heme and bacteriochlorophyll biosynthesis, is a heme-sensing protein.Measurement of Heme Synthesis Levels in Mammalian Cells Mechanism of hypochlorous acid-mediated heme destruction and free iron release.Reducing mitochondrial decay with mitochondrial nutrients to delay and treat cognitive dysfunction, Alzheimer's disease, and Parkinson's disease.A complex dietary supplement augments spatial learning, brain mass, and mitochondrial electron transport chain activity in aging mice.Both human ferredoxins 1 and 2 and ferredoxin reductase are important for iron-sulfur cluster biogenesis Dynamin-like protein 1 reduction underlies mitochondrial morphology and distribution abnormalities in fibroblasts from sporadic Alzheimer's disease patients.Genetic variants influencing biomarkers of nutrition are not associated with cognitive capability in middle-aged and older adults Cloning, expression, and biochemical properties of CPOX4, a genetic variant of coproporphyrinogen oxidase that affects susceptibility to mercury toxicity in humans A role for heme in Alzheimer's disease: heme binds amyloid beta and has altered metabolism.Heme reversibly damps PERIOD2 rhythms in mouse suprachiasmatic nucleus explants.The emerging role of iron dyshomeostasis in the mitochondrial decay of aging.Novel drug targets based on metallobiology of Alzheimer's disease.The regulatory role of heme in neurons.Regulatory Fe(II/III) heme: the reconstruction of a molecule's biography.Increased iron supplied through Fet3p results in replicative life span extension of Saccharomyces cerevisiae under conditions requiring respiratory metabolism

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P2860

Heme deficiency may be a factor in the mitochondrial and neuronal decay of aging.

http://www.wikidata.org/entity/Q34379668

description

2002 nî lūn-bûn

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2002 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

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2002 թվականի նոյեմբերին հրատարակված գիտական հոդված

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2002年の論文

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2002年論文

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2002年論文

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2002年論文

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name

Heme deficiency may be a factor in the mitochondrial and neuronal decay of aging.

@ast

Heme deficiency may be a factor in the mitochondrial and neuronal decay of aging.

@en

Heme deficiency may be a factor in the mitochondrial and neuronal decay of aging.

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type

label

Heme deficiency may be a factor in the mitochondrial and neuronal decay of aging.

@ast

Heme deficiency may be a factor in the mitochondrial and neuronal decay of aging.

@en

Heme deficiency may be a factor in the mitochondrial and neuronal decay of aging.

@nl

prefLabel

Heme deficiency may be a factor in the mitochondrial and neuronal decay of aging.

@ast

Heme deficiency may be a factor in the mitochondrial and neuronal decay of aging.

@en

Heme deficiency may be a factor in the mitochondrial and neuronal decay of aging.

@nl

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Proceedings of the National Academy of Sciences of the United States of America

P1476

Heme deficiency may be a factor in the mitochondrial and neuronal decay of aging.

@en

P2093

Alison Nisbet Killilea

http://www.w3.org/2001/XMLSchema#string

Bruce N Ames

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David W Killilea

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Hani Atamna

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P2860

The amyloid precursor protein-binding protein APP-BP1 drives the cell cycle through the S-M checkpoint and causes apoptosis in neurons

Alzheimer's disease: genes, proteins, and therapy

The beta-amyloid precursor protein APP is tyrosine-phosphorylated in cells expressing a constitutively active form of the Abl protoncogene

Selective accumulation of aluminum and iron in the neurofibrillary tangles of Alzheimer's disease: a laser microprobe (LAMMA) study.

Nitrosative and oxidative modulation of iron regulatory proteins.

In vivo evaluation of brain iron in Alzheimer disease using magnetic resonance imaging.

The antioxidant properties of zinc.

Energetics in the pathogenesis of neurodegenerative diseases.

Neuroglobin is up-regulated by and protects neurons from hypoxic-ischemic injury.

Cord serum ferritin concentrations and mental and psychomotor development of children at five years of age.

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14807-14812

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10.1073/PNAS.192585799

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23

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99

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2002-11-04T00:00:00Z

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8396542

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12417755

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137500

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