ArticleStem cells (Dayton, Ohio)2015
Loss of Faap20 Causes Hematopoietic Stem and Progenitor Cell Depletion in Mice Under Genotoxic Stress.
Article in Stem cells (Dayton, Ohio), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Genome-Wide Association Study of Vertical Jump Performance Among Elite Badminton Players.International journal of molecular sciences · 2026Article
- Fancl-mutant mice reveal central role of monoubiquitination in Fanconi anemia and a model for therapeutic gene editing.Blood advances · 2026Article
- Double jeopardy: howFrontiers in cell and developmental biology · 2026Review
- Gene loss in Antarctic icefish: evolutionary adaptations mimicking Fanconi Anemia?BMC genomics · 2024Article
- Fanconi anemia associated protein 20 (FAAP20) plays an essential role in homology-directed repair of DNA double-strand breaks.Communications biology · 2023Article
- Hypomorphic Brca2 and Rad51c double mutant mice display Fanconi anemia, cancer and polygenic replication stress.Nature communications · 2023Article
- PrimPol-mediated repriming facilitates replication traverse of DNA interstrand crosslinks.The EMBO journal · 2021Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
20-kDa FANCA-associated protein (FAAP20) is a recently identified protein that associates with the Fanconi anemia (FA) core complex component, FANCA. FAAP20 contains a conserved ubiquitin-binding zinc-finger domain and plays critical roles in the FA-BRCA pathway of DNA repair and genome maintenance. The function of FAAP20 in animals has not been explored. Here, we report that deletion of Faap20 in mice led to a mild FA-like phenotype with defects in the reproductive and hematopoietic systems. Specifically, hematopoietic stem and progenitor cells (HSPCs) from Faap20(-) (/) (-) mice showed defects in long-term multilineage reconstitution in lethally irradiated recipient mice, with milder phenotype as compared to HSPCs from Fanca(-) (/) (-) or Fancc(-) (/) (-) mice. Faap20(-) (/) (-) mice are susceptible to mitomycin C (MMC)-induced pancytopenia. That is, acute MMC stress induced a significant progenitor loss especially the erythroid progenitors and megakaryocyte-erythrocyte progenitors in Faap20(-) (/) (-) mice. Furthermore, Faap20(-) (/) (-) HSPCs displayed aberrant cell cycle pattern during chronic MMC treatment. Finally, using Faap20(-) (/) (-) Fanca(-) (/) (-) double-knockout mice, we demonstrated a possible dominant effect of FANCA in the interaction between FAAP20 and FANCA. This novel Faap20 mouse model may be valuable in studying the regulation of the FA pathway during bone marrow failure progress in FA patients.
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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.