ArticleMolecular and cellular biology2004
Phosphorylation of critical serine residues in Gem separates cytoskeletal reorganization from down-regulation of calcium channel activity.
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 37 papers.
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Who cites it
37 citing papers in PubMed, 73 citations in OpenAlex.
- OXTR-mediated signaling in astrocytes contributes to anxiolysis.Molecular psychiatry · 2025Article
- Rad protein: An essential player in L-type Ca2+ channel localization and modulation in cardiomyocytes.The Journal of general physiology · 2024Article
- The C-terminus of Rad is required for membrane localization and L-type calcium channel regulation.The Journal of general physiology · 2024Article
- Decreased expression of GEM in osteoarthritis cartilage regulates chondrogenic differentiation via Wnt/β-catenin signaling.Journal of orthopaedic surgery and research · 2023Article
- Article
- Expression profile analysis to predict potential biomarkers for glaucoma: BMP1, DMD and GEM.PeerJ · 2020Article
- A potent voltage-gated calcium channel inhibitor engineered from a nanobody targeted to auxiliary CaeLife · 2019Article
- Rad GTPase is essential for the regulation of bone density and bone marrow adipose tissue in mice.Bone · 2017Article
- Rad and Rem are non-canonical G-proteins with respect to the regulatory role of guanine nucleotide binding in Ca(V)1.2 channel regulation.The Journal of physiology · 2015Article
- Functional assessment of three Rem residues identified as critical for interactions with Ca(2+) channel β subunits.Pflugers Archiv : European journal of physiology · 2015Article
- Nerve injury induces a Gem-GTPase-dependent downregulation of P/Q-type Ca2+ channels contributing to neurite plasticity in dorsal root ganglion neurons.Pflugers Archiv : European journal of physiology · 2015Article
- RGK regulation of voltage-gated calcium channels.Science China. Life sciences · 2015Review
- Molecular mechanisms of activity-dependent changes in dendritic morphology: role of RGK proteins.Trends in neurosciences · 2014Review
- Gem-induced cytoskeleton remodeling increases cellular migration of HTLV-1-infected cells, formation of infected-to-target T-cell conjugates and viral transmission.PLoS pathogens · 2014Article
- Ancient origins of RGK protein function: modulation of voltage-gated calcium channels preceded the protostome and deuterostome split.PloS one · 2014Article
- Regulation of voltage-dependent calcium channels by RGK proteins.Biochimica et biophysica acta · 2013Review
- CaMKII-dependent phosphorylation of the GTPase Rem2 is required to restrict dendritic complexity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Increased expression of Gem after rat sciatic nerve injury.Journal of molecular histology · 2013Article
- Molecular determinants of Gem protein inhibition of P/Q-type Ca2+ channels.The Journal of biological chemistry · 2012Article
- Activity-dependent subcellular cotrafficking of the small GTPase Rem2 and Ca2+/CaM-dependent protein kinase IIα.PloS one · 2012Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Gem is a small GTP-binding protein that has a ras-like core and extended chains at each terminus. The primary structure of Gem and other RGK family members (Rad, Rem, and Rem2) predicts a GTPase deficiency, leading to the question of how Gem functional activity is regulated. Two functions for Gem have been demonstrated, including inhibition of voltage-gated calcium channel activity and inhibition of Rho kinase-mediated cytoskeletal reorganization, such as stress fiber formation and neurite retraction. These functions for Gem have been ascribed to its interaction with the calcium channel beta subunit and Rho kinase beta, respectively. We show here that these functions are separable and regulated by distinct structural modifications to Gem. Phosphorylation of serines 261 and 289, located in the C-terminal extension, is required for Gem-mediated cytoskeletal reorganization, while GTP and possibly calmodulin binding are required for calcium channel inhibition. In addition to regulating cytoskeletal reorganization, phosphorylation of serine 289 in conjunction with serine 23 results in bidentate 14-3-3 binding, leading to increased Gem protein half-life. Evidence presented shows that phosphorylation of serine 261 is mediated via a cdc42/protein kinase Czeta-dependent pathway. These data demonstrate that phosphorylation of serines 261 and 289, outside the GTP-binding region of Gem, controls its inhibition of Rho kinase beta and associated changes in the cytoskeleton.
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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 Socratic graph.