ArticleMolecular and cellular biology2004
Role for the pleckstrin homology domain-containing protein CKIP-1 in phosphatidylinositol 3-kinase-regulated muscle differentiation.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 62 citations in OpenAlex.
- Modulating PAK1: Accessory Proteins as Promising Therapeutic Targets.Biomolecules · 2025Review
- Ckip-1 3'UTR alleviates prolonged sleep deprivation induced cardiac dysfunction by activating CaMKK2/AMPK/cTNI pathway.Molecular biomedicine · 2024Article
- Spatiotemporal resolution of germinal center Tfh cell differentiation and divergence from central memory CD4Nature communications · 2023Article
- m6A and miRNA jointly regulate the development of breast muscles in duck embryonic stages.Frontiers in veterinary science · 2022Article
- MircroRNA Let-7a-5p in Airway Smooth Muscle Cells is Most Responsive to High Stretch in Association With Cell Mechanics Modulation.Frontiers in physiology · 2022Article
- Ckip-1 regulates C3H10T1/2 mesenchymal cell proliferation and osteogenic differentiation via Lrp5.Experimental and therapeutic medicine · 2021Article
- CKIP-1 regulates the immunomodulatory function of mesenchymal stem cells.Molecular biology reports · 2019Article
- PLEKHO1 knockdown inhibits RCC cell viability in vitro and in vivo, potentially by the Hippo and MAPK/JNK pathways.International journal of oncology · 2019Article
- CKIP-1 limits foam cell formation and inhibits atherosclerosis by promoting degradation of Oct-1 by REGγ.Nature communications · 2019Article
- Myocardial CKIP-1 Overexpression Protects from Simulated Microgravity-Induced Cardiac Remodeling.Frontiers in physiology · 2018Article
- Association of CKIP-1 P21A polymorphism with risk of chronic heart failure in a Chinese population.Oncotarget · 2017Article
- A novel role of CKIP-1 in promoting megakaryocytic differentiation.Oncotarget · 2017Article
- Guidelines for the Use of Protein Domains in Acidic Phospholipid Imaging.Methods in molecular biology (Clifton, N.J.) · 2016Review
- The Role of the Pleckstrin Homology Domain-containing Protein CKIP-1 in Activation of p21-activated Kinase 1 (PAK1).The Journal of biological chemistry · 2015Article
- Enhanced MyoD-induced transdifferentiation to a myogenic lineage by fusion to a potent transactivation domain.ACS synthetic biology · 2015Article
- Capping protein regulators fine-tune actin assembly dynamics.Nature reviews. Molecular cell biology · 2014Review
- CKIP-1 acts as a colonic tumor suppressor by repressing oncogenic Smurf1 synthesis and promoting Smurf1 autodegradation.Oncogene · 2014Article
- CKIP-1 regulates macrophage proliferation by inhibiting TRAF6-mediated Akt activation.Cell research · 2014Article
- CKIP-1 is an intrinsic negative regulator of T-cell activation through an interaction with CARMA1.PloS one · 2014Article
- Crystallization and preliminary X-ray crystallographic analysis of the human CKIP-1 pleckstrin homology domain.Acta crystallographica. Section F, Structural biology and crystallization communications · 2013Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this work, we report the implication of the pleckstrin homology (PH) domain-containing protein CKIP-1 in phosphatidylinositol 3-kinase (PI3-K)-regulated muscle differentiation. CKIP-1 is upregulated during muscle differentiation in C2C12 cells. We show that CKIP-1 binds to phosphatidylinositol 3-phosphate through its PH domain and localizes to the plasma membrane in a PI3-K-dependent manner. Activation of PI3-K by insulin or expression of an active form of PI3-K p110 induces a rapid translocation of CKIP-1 to the plasma membrane. Conversely, expression of the 3-phosphoinositide phosphatase myotubularin or PI3-K inhibition by LY294002, wortmannin, or mutant p85 abolishes CKIP-1 binding to the membrane. Upon induction of differentiation in low-serum medium, CKIP-1 overexpression in C2C12 myoblasts first promotes proliferation and then stimulates the expression of myogenin and cell fusion in a manner reminiscent of the dual positive effect of insulin-like growth factors on muscle cells. Interference with the PI3-K pathway impedes the effect of CKIP-1 on C2C12 cell differentiation. Finally, silencing of CKIP-1 by RNA interference abolishes proliferation and delays myogenin expression. Altogether, these data strongly implicate CKIP-1 as a new component of PI3-K signaling in muscle differentiation.
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