ArticleScientific reports2019
ERICH3 in Primary Cilia Regulates Cilium Formation and the Localisations of Ciliary Transport and Sonic Hedgehog Signaling Proteins.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- Bridging the gap: an emerging link between tubulinopathies and ciliopathies.NPJ genomic medicine · 2026Review
- Analysis of Transcriptome and Differentially Expressed Genes in Chicken Primordial Germ Cells.Animals : an open access journal from MDPI · 2026Article
- Integrated multi-omic analysis unravels the characteristics of the metabolism-related intratumoral microbes and establishes a novel signature for predicting prognosis and therapeutic response in lung adenocarcinoma.Translational cancer research · 2025Article
- Defective IFT57 underlies a novel cause of Bardet-Biedl syndrome.Human molecular genetics · 2025Article
- Regionalized Protein Localization Domains in the Zebrafish Hair Cell Kinocilium.Journal of developmental biology · 2023Article
- The ERK activator, BCI, inhibits ciliogenesis and causes defects in motor behavior, ciliary gating, and cytoskeletal rearrangement.Life science alliance · 2023Article
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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
Intraflagellar transport (IFT) is essential for the formation and function of the microtubule-based primary cilium, which acts as a sensory and signalling device at the cell surface. Consisting of IFT-A/B and BBSome cargo adaptors that associate with molecular motors, IFT transports protein into (anterograde IFT) and out of (retrograde IFT) the cilium. In this study, we identify the mostly uncharacterised ERICH3 protein as a component of the mammalian primary cilium. Loss of ERICH3 causes abnormally short cilia and results in the accumulation of IFT-A/B proteins at the ciliary tip, together with reduced ciliary levels of retrograde transport regulators, ARL13B, INPP5E and BBS5. We also show that ERICH3 ciliary localisations require ARL13B and BBSome components. Finally, ERICH3 loss causes positive (Smoothened) and negative (GPR161) regulators of sonic hedgehog signaling (Shh) to accumulate at abnormally high levels in the cilia of pathway-stimulated cells. Together, these findings identify ERICH3 as a novel component of the primary cilium that regulates cilium length and the ciliary levels of Shh signaling molecules. We propose that ERICH3 functions within retrograde IFT-associated pathways to remove signaling proteins from cilia.
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