ArticlePloS one2014
NDK-1, the homolog of NM23-H1/H2 regulates cell migration and apoptotic engulfment in C. elegans.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
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Who cites it
20 citing papers in PubMed, 26 citations in OpenAlex.
- CED-6/GULP and components of the clathrin-mediated endocytosis machinery act redundantly to correctly display CED-1 on the cell membrane in Caenorhabditis elegans.G3 (Bethesda, Md.) · 2024Article
- Mechanisms of action of NME metastasis suppressors - a family affair.Cancer metastasis reviews · 2023Review
- NDK/NME proteins: a host-pathogen interface perspective towards therapeutics.Current genetics · 2022Review
- NME/NM23/NDPK and Histidine Phosphorylation.International journal of molecular sciences · 2020Review
- The Function of NM23-H1/NME1 and Its Homologs in Major Processes Linked to Metastasis.Pathology oncology research : POR · 2020Review
- Expression of nm23-H1, p53, and integrin β1 in endometriosis and their clinical significance.International journal of clinical and experimental pathology · 2020Article
- MiR-35 buffers apoptosis thresholds in the C. elegans germline by antagonizing both MAPK and core apoptosis pathways.Cell death and differentiation · 2019Article
- The nucleoside diphosphate kinase NDK-1/NME1 promotes phagocytosis in concert with DYN-1/Dynamin.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- AWD regulates timed activation of BMP signaling in intestinal stem cells to maintain tissue homeostasis.Nature communications · 2019Article
- Modulation of small GTPase activity by NME proteins.Laboratory investigation; a journal of technical methods and pathology · 2018Review
- The 'known-knowns', and 'known-unknowns' of extracellular Nm23-H1/NDPK proteins.Laboratory investigation; a journal of technical methods and pathology · 2018Review
- NM23 proteins: innocent bystanders or local energy boosters for CFTR?Laboratory investigation; a journal of technical methods and pathology · 2018Review
- The NDPK/NME superfamily: state of the art.Laboratory investigation; a journal of technical methods and pathology · 2018Article
- The dosage-dependent effect exerted by the NM23-H1/H2 homolog NDK-1 on distal tip cell migration in C. elegans.Laboratory investigation; a journal of technical methods and pathology · 2018Review
- Invading, Leading and Navigating Cells inGenetics · 2018Review
- The advantage of channeling nucleotides for very processive functions.F1000Research · 2017Review
- Article
- Nucleoside diphosphate kinases (NDPKs) in animal development.Cellular and molecular life sciences : CMLS · 2015Review
- Progress on Nme (NDP kinase/Nm23/Awd) gene family-related functions derived from animal model systems: studies on development, cardiovascular disease, and cancer metastasis exemplified.Naunyn-Schmiedeberg's archives of pharmacology · 2015Article
- Janus-faces of NME-oncoprotein interactions.Naunyn-Schmiedeberg's archives of pharmacology · 2015Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
Abstract
Abnormal regulation of cell migration and altered rearrangement of cytoskeleton are characteristic of metastatic cells. The first described suppressor of metastatic processes is NM23-H1, which displays NDPK (nucleoside-diphosphate kinase) activity. To better understand the role of nm23 genes in cell migration, we investigated the function of NDK-1, the sole Caenorhabditis elegans homolog of group I NDPKs in distal tip cell (DTC) migration. Dorsal phase of DTC migration is regulated by integrin mediated signaling. We find that ndk-1 loss of function mutants show defects in this phase. Epistasis analysis using mutants of the α-integrin ina-1 and the downstream functioning motility-promoting signaling module (referred to as CED-10 pathway) placed NDK-1 downstream of CED-10/Rac. As DTC migration and engulfment of apoptotic corpses are analogous processes, both partially regulated by the CED-10 pathway, we investigated defects of apoptosis in ndk-1 mutants. Embryos and germ cells defective for NDK-1 showed an accumulation of apoptotic cell corpses. Furthermore, NDK-1::GFP is expressed in gonadal sheath cells, specialized cells for engulfment and clearence of apoptotic corpses in germ line, which indicates a role for NDK-1 in apoptotic corpse removal. In addition to the CED-10 pathway, engulfment in the worm is also mediated by the CED-1 pathway. abl-1/Abl and abi-1/Abi, which function in parallel to both CED-10/CED-1 pathways, also regulate engulfment and DTC migration. ndk-1(-);abi-1(-) double mutant embryos display an additive phenotype (e. g. enhanced number of apoptotic corpses) which suggests that ndk-1 acts in parallel to abi-1. Corpse number in ndk-1(-);ced-10(-) double mutants, however, is similar to ced-10(-) single mutants, suggesting that ndk-1 acts downstream of ced-10 during engulfment. In addition, NDK-1 shows a genetic interaction with DYN-1/dynamin, a downstream component of the CED-1 pathway. In summary, we propose that NDK-1/NDPK might represent a converging point of CED-10 and CED-1 pathways in the process of cytoskeleton rearrangement.
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