| 2011 |
Cobl forms a complex with the F-BAR protein syndapin I in vivo; syndapin I recruits Cobl to membranes via its FCH-F-BAR lipid-binding domain, and this interaction is required for cortical localization of Cobl and for dendritic arbor development in neurons. Additionally, endogenous Cobl, syndapin I, and the Arp2/3 activator N-WASP were found in one complex, linking Cobl to Arp2/3-based actin dynamics. |
Coimmunoprecipitation, colocalization, subcellular fractionation, in vitro reconstitution, RNAi loss-of-function in neurons |
The EMBO journal |
High |
21725280
|
| 2012 |
Cobl physically associates with the F-actin-binding protein Abp1; F-actin-anchored Cobl/Abp1 complexes are critical for dendritic branching in hippocampal neurons and for Purkinje cell arborization. A Cobl mutant deficient for Abp1 binding and an Abp1 mutant lacking F-actin binding both fail to rescue respective loss-of-function phenotypes, demonstrating that both interactions are functionally required. |
Subcellular fractionation, protein interaction analyses, subcellular reconstitution, colocalization, gene gun transfection knockdown and rescue in neurons and tissue slices |
The Journal of neuroscience |
High |
23223303
|
| 2012 |
In zebrafish, Cobl and syndapin I colocalize at the base of forming cilia and act together to form ciliated sensory hair cells (both kinocilia and stereocilia) in the lateral line organ. Rescue experiments showed that Cobl's syndapin I-binding Cobl homology domain and its actin-nucleating C-terminus are both required for proper sensory hair cell rosette formation. |
Morpholino knockdown in zebrafish, scanning electron microscopy, rescue experiments with domain-specific mutants, colocalization |
Journal of cell science |
High |
23203810
|
| 2015 |
Cobl is directly regulated by Ca²⁺/Calmodulin (CaM): CaM binds Cobl at multiple sites, modulates Cobl's actin-binding properties, and promotes Cobl's interaction with syndapin I. Cobl-induced dendritic branch initiation is preceded by Ca²⁺ signals and is strictly dependent on CaM activity. CaM-binding-deficient Cobl mutants fail to rescue Cobl loss-of-function phenotypes. |
In vitro binding assays, CaM inhibitor studies, overexpression and rescue experiments with CaM-binding-deficient Cobl mutants in primary neurons and tissue slices, live Ca²⁺ imaging |
PLoS biology |
High |
26334624
|
| 2018 |
Cobl is post-translationally regulated by arginine methylation: the protein arginine methyltransferase PRMT2 associates with Cobl via an SH3 domain-dependent interaction and methylates Cobl's actin-nucleating C-terminal domain. Methylation is required for Cobl's actin-binding activity and dendritogenesis; PRMT2's catalytic domain and SH3 domain are both required for these effects. |
Coprecipitation, coimmunoprecipitation, in vitro reconstitution, cellular reconstitution, gain- and loss-of-function studies in neurons, PRMT2 catalytic mutant analyses |
Developmental cell |
High |
29689199
|
| 2018 |
Cobl acts as an effector of planar cell polarity (PCP) signaling during postnatal cochlear hair cell development. Cobl KO mice show mispositioned basal bodies and centrioles, reduced cortical F-actin beneath the sensory apparatus, and premature kinocilium retraction. The pericentriolar scaffold defects were shown to be actin polymerization dependent and calcium/calmodulin signaling dependent. |
Cobl knockout mice, confocal and electron microscopy, pharmacological inhibition of actin polymerization and CaM signaling |
Cell reports |
High |
30157434
|
| 2021 |
Cobl and Cobl-like act interdependently in dendritic arbor development, physically linked by syndapin I. Syndapin I forms nanodomains at convex plasma membrane areas at the base of protrusive structures, and interacts with three motifs in Cobl-like, one of which is Ca²⁺/CaM-regulated. The N-terminal CaM-binding site of Cobl-like and the Ca²⁺/CaM-responsive syndapin-binding motif are critical for Cobl-like's functions, demonstrating that coordinated actin nucleation by both factors is required for dendritogenesis. |
Loss-of-function studies, protein interaction mapping, super-resolution microscopy of syndapin I nanodomains, rescue with domain-specific mutants |
eLife |
High |
34264190
|
| 2021 |
Cobl is required for poststroke dendritic arbor repair in penumbral neurons. After middle cerebral artery occlusion, Cobl levels decline due to calpain-mediated proteolysis, but are rapidly restored by increased mRNA expression. In Cobl KO mice, the dendritic repair window (day 2–4 post-stroke) passes without any regrowth, demonstrating that Cobl's actin nucleation activity is causally required for stroke recovery. |
Middle cerebral artery occlusion in Cobl KO and WT mice, dendritic morphology quantification, calpain inhibition experiments, mRNA expression analysis |
PLoS biology |
High |
34898601
|
| 2020 |
COBL interacts with and is stabilized by IGFN1 in skeletal muscle; IGFN1 and COBL colocalize at the Z-disc. IGFN1 prevents COBL from forming actin ruffles in COS7 cells, indicating IGFN1 modulates COBL's actin nucleation activity. COBL is expressed in differentiating C2C12 myoblasts but COBL loss-of-function does not abolish myoblast fusion. |
Pull-down with proteomics, coimmunoprecipitation, colocalization in muscle, COS7 overexpression assay, COBL KO C2C12 clones |
Experimental cell research |
Medium |
32768501
|
| 2025 |
Cobl is expressed in ameloblasts during the secretory phase of amelogenesis and colocalizes with cortical F-actin. Cobl KO causes increased ameloblast height, altered apical F-actin density (increased at P0, reduced during maturation phase), and changes in enamel composition (increased carbon content), demonstrating that Cobl controls actin cytoskeletal organization and morphology of enamel-forming cells. |
Cobl KO mice, confocal microscopy with F-actin staining, morphometric analyses, energy dispersive X-ray spectroscopy for enamel composition |
Cells |
Medium |
40072087
|
| 2025 |
Cobl KO mice show layer- and age-restricted deficits in cortical dendritic arborization, revealing that Cobl is required for a transient dendritic arbor expansion during emerging adulthood (layer II/III) and for associated changes in dendritic spine length. This identifies Cobl as a molecular driver of cortical rewiring during brain maturation. |
Cobl KO mice, dendritic morphology quantification across cortical layers and ages, Golgi staining and confocal microscopy |
The Journal of neuroscience |
Medium |
40555515
|