ArticleBiology open2016
Identification of a novel putative interaction partner of the nucleoporin ALADIN.
Article in Biology open, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- The Retina in Patients With Triple A Syndrome: A Window Into Neurodegeneration?Frontiers in endocrinology · 2021Trial
- Rare forms of genetic paediatric adrenal insufficiency: Excluding congenital adrenal hyperplasia.Reviews in endocrine & metabolic disorders · 2023Review
- Review
- What Do We Know about Classical and Non-Classical Progesterone Receptors in the Human Female Reproductive Tract? A Review.International journal of molecular sciences · 2021Review
- Review
- Article
- Allgrove syndrome and motor neuron disease.Neurology international · 2018Article
- Compensation for chronic oxidative stress in ALADIN null mice.Biology open · 2018Article
- Triple A patient cells suffering from mitotic defects fail to localize PGRMC1 to mitotic kinetochore fibers.Cell division · 2018Article
- Phenotype-genotype spectrum of AAA syndrome from Western India and systematic review of literature.Endocrine connections · 2017Article
- The roles of the nuclear pore complex in cellular dysfunction, aging and disease.Seminars in cell & developmental biology · 2017Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been shown that the nucleoporin ALADIN plays a significant role in the redox homeostasis of the cell, but its function in steroidogenesis contributing to adrenal atrophy in triple A syndrome remains largely unknown. In an attempt to identify new interaction partners of ALADIN, co-immunoprecipitation followed by proteome analysis was conducted in different expression models using the human adrenocortical tumour cell line NCI-H295R. Our results suggest an interaction of ALADIN with the microsomal protein PGRMC2. PGRMC2 is shown to be activity regulator of CYP P450 enzymes and, therefore, to be a possible target for adrenal dysregulation in triple A syndrome. We show that there is a sexual dimorphism regarding the expression of Pgrmc2 in adrenals and gonads of wild-type (WT) and Aaas knock-out (KO) mice. Female Aaas KO mice are sterile due to delayed oocyte maturation and meiotic spindle assembly. A participation in meiotic spindle assembly confirms the recently investigated involvement of ALADIN in mitosis and emphasises an interaction with PGRMC2 which is a regulator of the cell cycle. By identification of a novel interaction partner of ALADIN, we provide novel aspects for future research of the function of ALADIN during cell cycle and for new insights into the pathogenesis of triple A syndrome.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.