ArticleThe Journal of biological chemistry2012
Intestinal cell kinase (ICK) promotes activation of mTOR complex 1 (mTORC1) through phosphorylation of Raptor Thr-908.
Article in The Journal of biological chemistry, 2012. 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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Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- Progressive tooth pattern changes in Cilk1-deficient mice depending on Hedgehog signaling.International journal of oral science · 2025Article
- Genetic Animal Models of Idiopathic Generalized Epilepsies: What Can We Learn from Them?Biomedicines · 2025Review
- Ciliogenesis-associated Kinase 1 Promotes Breast Cancer Cell Proliferation and Chemoresistance via Phosphorylating ERK1.International journal of biological sciences · 2024Article
- The role of Raptor in lymphocytes differentiation and function.Frontiers in immunology · 2023Review
- Phosphosite T674A mutation in kinesin family member 3A fails to reproduce tissue and ciliary defects characteristic of CILK1 loss of function.Developmental dynamics : an official publication of the American Association of Anatomists · 2021Article
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- Proteomics of Long-Lived Mammals.Proteomics · 2020Review
- Activation of sonic hedgehog signaling by a Smoothened agonist restores congenital defects in mouse models of endocrine-cerebro-osteodysplasia syndrome.EBioMedicine · 2019Article
- Ciliogenesis associated kinase 1: targets and functions in various organ systems.FEBS letters · 2019Review
- Targeting mTOR for cancer therapy.Journal of hematology & oncology · 2019Review
- LF4/MOK and a CDK-related kinase regulate the number and length of cilia in Tetrahymena.PLoS genetics · 2019Article
- A CCRK and a MAK Kinase Modulate Cilia Branching and Length via Regulation of Axonemal Microtubule Dynamics in Caenorhabditis elegans.Current biology : CB · 2019Article
- Fibroblast growth factor receptor influences primary cilium length through an interaction with intestinal cell kinase.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Subtle Brain Developmental Abnormalities in the Pathogenesis of Juvenile Myoclonic Epilepsy.Frontiers in cellular neuroscience · 2019Review
- Reciprocal Regulation of the TOR Kinase and ABA Receptor Balances Plant Growth and Stress Response.Molecular cell · 2018Article
- Primary cilia in energy balance signaling and metabolic disorder.BMB reports · 2015Review
- Intestinal cell kinase, a protein associated with endocrine-cerebro-osteodysplasia syndrome, is a key regulator of cilia length and Hedgehog signaling.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Regulation of cilium length and intraflagellar transport by the RCK-kinases ICK and MOK in renal epithelial cells.PloS one · 2014Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Intestinal cell kinase (ICK), named after its cloning origin, the intestine, is actually a ubiquitously expressed and highly conserved serine/threonine protein kinase. Recently we reported that ICK supports cell proliferation and G(1) cell cycle progression. ICK deficiency significantly disrupted the mammalian target of rapamycin (mTOR) complex 1 (mTORC1) signaling events. However, the biological substrates that mediate the downstream signaling effects of ICK in proliferation and the molecular mechanisms by which ICK interacts with mTORC1 are not well defined. Our prior studies also provided biochemical evidence that ICK interacts with the mTOR/Raptor complex in cells and phosphorylates Raptor in vitro. In this report, we investigated whether and how ICK targets Raptor to regulate the activity of mTORC1. Using the ICK substrate consensus sequence [R-P-X-S/T-P/A/T/S], we identified a putative phosphorylation site, RPGT908T, for ICK in human Raptor. By mass spectrometry and a phospho-specific antibody, we showed that Raptor Thr-908 is a novel in vivo phosphorylation site. ICK is able to phosphorylate Raptor Thr-908 both in vitro and in vivo and when Raptor exists in protein complexes with or without mTOR. Although expression of the Raptor T908A mutant did not affect the mTORC1 integrity, it markedly impaired the mTORC1 activation by insulin or by overexpression of the small GTP-binding protein RheB under nutrient starvation. Our findings demonstrate an important role for ICK in modulating the activity of mTORC1 through phosphorylation of Raptor Thr-908 and thus implicate a potential signaling mechanism by which ICK regulates cell proliferation and division.
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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.