| scholarly article | Q13442814 |
| P356 | DOI | 10.1007/S00109-010-0661-Y |
| P698 | PubMed publication ID | 20706703 |
| P2093 | author name string | Angela Huebner | |
| Barbara Kind | |||
| Katrin Koehler | |||
| Dana Landgraf | |||
| Manuela Krumbholz | |||
| P2860 | cites work | Achalasia of the Cardia in Allgroveʼs (Triple A) Syndrome: Histopathologic Study of 10 Cases | Q73322636 |
| The nuclear pore complex protein ALADIN is mislocalized in triple A syndrome | Q24301071 | ||
| Proteomic analysis of the mammalian nuclear pore complex | Q24305242 | ||
| Mutation in nuclear pore component NUP155 leads to atrial fibrillation and early sudden cardiac death | Q24323900 | ||
| Rapid evolution of animal mitochondrial DNA | Q24597162 | ||
| Triple A syndrome is caused by mutations in AAAS, a new WD-repeat protein gene | Q28142907 | ||
| Mutant WD-repeat protein in triple-A syndrome | Q28142964 | ||
| Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases | Q28269333 | ||
| The serial cultivation of human diploid cell strains | Q29547356 | ||
| Topology of superoxide production from different sites in the mitochondrial electron transport chain | Q29619855 | ||
| Mitochondrial dysfunction accounts for the stochastic heterogeneity in telomere-dependent senescence | Q33283342 | ||
| Deficiency of ferritin heavy-chain nuclear import in triple a syndrome implies nuclear oxidative damage as the primary disease mechanism | Q33512291 | ||
| Neurological and adrenal dysfunction in the adrenal insufficiency/alacrima/achalasia (3A) syndrome | Q33623544 | ||
| ALADINI482S causes selective failure of nuclear protein import and hypersensitivity to oxidative stress in triple A syndrome | Q34478864 | ||
| Mitochondria, metabolic disturbances, oxidative stress and the kynurenine system, with focus on neurodegenerative disorders | Q34653971 | ||
| From the Hayflick mosaic to the mosaics of ageing. Role of stress-induced premature senescence in human ageing | Q34801705 | ||
| Mitochondria and neuronal activity. | Q36648486 | ||
| Oxidative stress, mitochondrial DNA mutation, and apoptosis in aging. | Q36803297 | ||
| Mitochondrial dysfunction in neurodegenerative disorders. | Q36979746 | ||
| Crosstalk signaling between mitochondrial Ca2+ and ROS. | Q37196065 | ||
| Familial glucocorticoid deficiency with achalasia of the cardia and deficient tear production | Q39492662 | ||
| Flow cytometric analysis of mitochondrial membrane potential using JC-1. | Q39943420 | ||
| Cellular localization of 17 natural mutant variants of ALADIN protein in triple A syndrome - shedding light on an unexpected splice mutation | Q40293550 | ||
| Real-time DNA quantification of nuclear and mitochondrial DNA in forensic analysis | Q40638567 | ||
| Infection-triggered familial or recurrent cases of acute necrotizing encephalopathy caused by mutations in a component of the nuclear pore, RANBP2. | Q41855140 | ||
| Mutated nup62 causes autosomal recessive infantile bilateral striatal necrosis | Q42497102 | ||
| Assay of mitochondrial ATP synthesis in animal cells | Q43623400 | ||
| Intracellular distribution of the fluorescent dye nonyl acridine orange responds to the mitochondrial membrane potential: implications for assays of cardiolipin and mitochondrial mass | Q44068682 | ||
| Increase in mitochondrial mass in human fibroblasts under oxidative stress and during replicative cell senescence | Q44174532 | ||
| Restoration of nuclear-import failure caused by triple A syndrome and oxidative stress | Q45343949 | ||
| Axonal neuropathy with unusual pattern of amyotrophy and alacrima associated with a novel AAAS mutation p.Leu430Phe | Q46482605 | ||
| Oxygen and ion concentrations in normoxic and hypoxic brain cells | Q48304992 | ||
| Allgrove syndrome: an autosomal recessive syndrome of ACTH insensitivity, achalasia and alacrima | Q67915711 | ||
| Adrenocorticotropic hormone insensitivity associated with autonomic nervous system disorders | Q68256694 | ||
| Growth rate of control and beta-interferon-treated human fibroblast populations over the course of their in vitro life span | Q71350034 | ||
| P433 | issue | 12 | |
| P304 | page(s) | 1233-1242 | |
| P577 | publication date | 2010-08-13 | |
| P1433 | published in | Journal of Molecular Medicine | Q6295593 |
| P1476 | title | Intracellular ROS level is increased in fibroblasts of triple A syndrome patients | |
| P478 | volume | 88 |
| Q48241860 | "Crying without tears" as an early diagnostic sign-post of triple A (Allgrove) syndrome: two case reports. |
| Q48181436 | Compensation for chronic oxidative stress in ALADIN null mice |
| Q37644970 | Deficiency of ALADIN impairs redox homeostasis in human adrenal cells and inhibits steroidogenesis. |
| Q37502230 | Identification of a novel putative interaction partner of the nucleoporin ALADIN. |
| Q58557206 | Moonlighting nuclear pore proteins: tissue-specific nucleoporin function in health and disease |
| Q33709973 | Oxidative stress and adrenocortical insufficiency |
| Q28260340 | Role of ALADIN in human adrenocortical cells for oxidative stress response and steroidogenesis |
| Q36115382 | The nucleoporin ALADIN regulates Aurora A localization to ensure robust mitotic spindle formation. |
| Q53744365 | Triple A Syndrome: Preliminary Response to the Antioxidant N-Acetylcysteine Treatment in a Child. |
| Q59136995 | Triple A patient cells suffering from mitotic defects fail to localize PGRMC1 to mitotic kinetochore fibers |
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