ArticleDevelopment (Cambridge, England)2014
ATMIN is a transcriptional regulator of both lung morphogenesis and ciliogenesis.
Article in Development (Cambridge, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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
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Who cites it
31 citing papers in PubMed, 46 citations in OpenAlex.
- CPLANE protein INTU regulates growth and patterning of the mouse lungs through cilia-dependent Hh signaling.Developmental biology · 2024Article
- Transcription factor ATMIN facilitates chemoresistance in nasopharyngeal carcinoma.Cell death & disease · 2024Article
- Primary cilia as dynamic and diverse signalling hubs in development and disease.Nature reviews. Genetics · 2023Review
- LRRK1-mediated NDEL1 phosphorylation promotes cilia disassembly via dynein-2-driven retrograde intraflagellar transport.Journal of cell science · 2022Article
- ATMIN enhances invasion by altering PARP1 in MSS colorectal cancer.American journal of cancer research · 2022Article
- ATMIN Suppresses Metastasis by Altering the WNT-Signaling Pathway via PARP1 in MSI-High Colorectal Cancer.Annals of surgical oncology · 2021Article
- The ASCIZ-DYNLL1 Axis Is Essential for TLR4-Mediated Antibody Responses and NF-κB Pathway Activation.Molecular and cellular biology · 2021Article
- Mucociliary Respiratory Epithelium Integrity in Molecular Defense and Susceptibility to Pulmonary Viral Infections.Biology · 2021Review
- TRIM68, PIKFYVE, and DYNLL2: The Possible Novel Autophagy- and Immunity-Associated Gene Biomarkers for Osteosarcoma Prognosis.Frontiers in oncology · 2021Article
- Ciliary exclusion of Polycystin-2 promotes kidney cystogenesis in an autosomal dominant polycystic kidney disease model.Nature communications · 2019Article
- Atmin modulates Pkhd1 expression and may mediate Autosomal Recessive Polycystic Kidney Disease (ARPKD) through altered non-canonical Wnt/Planar Cell Polarity (PCP) signalling.Biochimica et biophysica acta. Molecular basis of disease · 2019Article
- PPARγ Interaction with UBR5/ATMIN Promotes DNA Repair to Maintain Endothelial Homeostasis.Cell reports · 2019Article
- Dynein-2 intermediate chains play crucial but distinct roles in primary cilia formation and function.eLife · 2018Article
- Article
- The established and the predicted roles of dynein light chain in the regulation of mitochondrial apoptosis.Cell cycle (Georgetown, Tex.) · 2018Article
- Dynein light chain regulates adaptive and innate B cell development by distinctive genetic mechanisms.PLoS genetics · 2017Article
- Article
- Review
- The Biology of Ciliary Dynamics.Cold Spring Harbor perspectives in biology · 2017Review
- Microtubule Motors Drive Hedgehog Signaling in Primary Cilia.Trends in cell biology · 2017Review
Corrections and comments
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Authors and funding
22 authors at 5 institutions in 3 countries.
Funding
Abstract
Initially identified in DNA damage repair, ATM-interactor (ATMIN) further functions as a transcriptional regulator of lung morphogenesis. Here we analyse three mouse mutants, Atmin(gpg6/gpg6), Atmin(H210Q/H210Q) and Dynll1(GT/GT), revealing how ATMIN and its transcriptional target dynein light chain LC8-type 1 (DYNLL1) are required for normal lung morphogenesis and ciliogenesis. Expression screening of ciliogenic genes confirmed Dynll1 to be controlled by ATMIN and further revealed moderately altered expression of known intraflagellar transport (IFT) protein-encoding loci in Atmin mutant embryos. Significantly, Dynll1(GT/GT) embryonic cilia exhibited shortening and bulging, highly similar to the characterised retrograde IFT phenotype of Dync2h1. Depletion of ATMIN or DYNLL1 in cultured cells recapitulated the in vivo ciliogenesis phenotypes and expression of DYNLL1 or the related DYNLL2 rescued the effects of loss of ATMIN, demonstrating that ATMIN primarily promotes ciliogenesis by regulating Dynll1 expression. Furthermore, DYNLL1 as well as DYNLL2 localised to cilia in puncta, consistent with IFT particles, and physically interacted with WDR34, a mammalian homologue of the Chlamydomonas cytoplasmic dynein 2 intermediate chain that also localised to the cilium. This study extends the established Atmin-Dynll1 relationship into a developmental and a ciliary context, uncovering a novel series of interactions between DYNLL1, WDR34 and ATMIN. This identifies potential novel components of cytoplasmic dynein 2 and furthermore provides fresh insights into the molecular pathogenesis of human skeletal ciliopathies.
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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.