ArticleScientific reports2017
Atp6ap2 ablation in adult mice impairs viability through multiple organ deficiencies.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 26 citations in OpenAlex.
- Homozygous overexpression of ATP6AP2 in female mice and its impact on running-induced modulation of the adult hippocampus.Cell and tissue research · 2026Article
- Targeting the High-Density Lipoprotein Proteome for the Treatment of Post-Acute Sequelae of SARS-CoV-2.International journal of molecular sciences · 2024Article
- The Rogdi knockout mouse is a model for Kohlschütter-Tönz syndrome.Scientific reports · 2024Article
- Cellular senescence triggers intracellular acidification and lysosomal pH alkalinized via ATP6AP2 attenuation in breast cancer cells.Communications biology · 2023Article
- Expanding the phenotype and metabolic basis of ATP6AP2-congenital disorder of glycosylation in a Chinese patient with a novel variant c.185G>A (p.Gly62Glu).Frontiers in genetics · 2023Article
- NK-cell dysfunction of acute myeloid leukemia in relation to the renin-angiotensin system and neurotransmitter genes.Open medicine (Warsaw, Poland) · 2022Article
- Loss of Soluble (Pro)renin Receptor Attenuates Angiotensin-II Induced Hypertension and Renal Injury.Circulation research · 2021Article
- V-ATPase-associated prorenin receptor is upregulated in prostate cancer after PTEN loss.Oncotarget · 2019Article
- The (pro)renin receptor: an emerging player in hypertension and metabolic syndrome.Kidney international · 2019Review
- Roles and functions of Atp6ap2 in the brain.Neural regeneration research · 2018Review
- Collecting duct principal, but not intercalated, cell prorenin receptor regulates renal sodium and water excretion.American journal of physiology. Renal physiology · 2018Article
- HMedical molecular morphology · 2018Article
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ATP6AP2 codes for the (pro)renin receptor and is an essential component of vacuolar H+ ATPase. Activating (pro)renin for conversion of Angiotensinogen to Angiotensin makes ATP6AP2 attractive for drug intervention. Tissue-specific ATP6AP2 inactivation in mouse suggested a strong impact on various organs. Consistent with this, we found that embryonic ablation of Atp6ap2 resulted in both male hemizygous lethality and female haploinsufficiency. Next, we examined the phenotype of an induced inactivation in the adult animal, most akin to detect potential effect of functional interference of ATP6AP2 through drug therapy. Induced ablation of Atp6ap2, even without equal efficiency in all tissues (aorta, brain and kidney), resulted in rapid lethality marked by weight loss, changes in nutritional as well as blood parameters, leukocyte depletion, and bone marrow hypoplasia. Upon Atp6ap2 ablation, the colon demonstrated a rapid disruption of crypt morphology, aberrant proliferation, cell-death activation, as well as generation of microadenomas. Consequently, disruption of ATP6AP2 is extremely poorly tolerated in the adult, and severely affects various organ systems demonstrating that ATP6AP2 is an essential gene implicated in basic cellular mechanisms and necessary for multiple organ function. Accordingly, any potential drug targeting of this gene product must be strictly assessed for safety.
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