| 2002 |
PCM-1 localizes to centriolar satellites and is required for microtubule- and dynactin-dependent recruitment of centrin, pericentrin, and ninein to the centrosome; depletion of PCM-1 by antibody microinjection, dominant-negative overexpression, or siRNA disrupts radial microtubule organization without affecting microtubule nucleation. |
Antibody microinjection, dominant-negative overexpression, siRNA depletion, immunofluorescence microscopy |
The Journal of cell biology |
High |
12403812
|
| 1994 |
PCM-1 is a 228-kDa centrosomal protein that associates tightly with the centrosome during G1, S, and early G2, then dissociates in late G2 and remains dispersed throughout mitosis, re-associating with centrosomes in G1 daughter cells, demonstrating cell cycle-dependent dynamics of pericentriolar material composition. |
Immunofluorescence microscopy with anti-recombinant PCM-1 antibodies across cell cycle stages |
The Journal of cell biology |
High |
8120099
|
| 2003 |
PCM-1 granules (centriolar satellites) are formed by self-aggregation of PCM-1 through two distinct N-terminal regions; overexpressed C-terminal deletion mutants bind each other and recruit endogenous PCM-1 into large aggregates; granule assembly is cell-cycle regulated, disassembling during mitosis and reassembling in interphase. |
Overexpression of deletion mutants, immunofluorescence microscopy, cell cycle synchronization |
Journal of cell science |
High |
12571289
|
| 2001 |
PCM-1 and pericentrin-B (kendrin) co-immunoprecipitate, indicating they form a functional complex; binding of both proteins to salt-stripped centrosomes requires intact microtubules, and immunodepletion of either protein does not inhibit microtubule nucleation from centrosomes. |
Co-immunoprecipitation, immunodepletion, microtubule nucleation assay, salt-stripped centrosome reconstitution |
Journal of cell science |
Medium |
11171385
|
| 2005 |
PCM-1-containing centriolar satellites are required for centrosomal recruitment of Nek2 kinase and its substrate C-Nap1; Nek2 particles partially colocalize with PCM-1 and depletion of PCM-1 by siRNA reduces centrosomal Nek2; Nek2 recruitment also involves microtubule transport and localized proteasomal degradation. |
siRNA depletion of PCM-1, FRAP, immunofluorescence colocalization, co-immunoprecipitation |
Molecular biology of the cell |
High |
15659651
|
| 2008 |
CEP290 interacts with PCM-1 and localizes to centriolar satellites in a PCM-1- and microtubule-dependent manner; CEP290 knockdown disrupts PCM-1 distribution and protein complex formation; both CEP290 and PCM-1 are required for ciliogenesis and ciliary targeting of Rab8. |
Co-immunoprecipitation, siRNA knockdown, immunofluorescence microscopy, ciliogenesis assay |
Human molecular genetics |
High |
18772192
|
| 2008 |
PCM1 forms a complex with DISC1 and BBS4 at the centrosome through discrete binding domains in each protein; DISC1 and BBS4 are required synergistically for targeting PCM1 and cargo proteins (e.g., ninein) to the centrosome; suppression of PCM1 in the developing cerebral cortex causes neuronal migration defects phenocopied by DISC1 or BBS4 suppression. |
Co-immunoprecipitation, immunofluorescence, in utero RNAi, domain mapping |
Archives of general psychiatry |
High |
18762586
|
| 2010 |
Hook3 is recruited to pericentriolar satellites through direct interaction with PCM1; disruption of the Hook3-PCM1 interaction in vivo impairs interkinetic nuclear migration in embryonic neural progenitors, causing overproduction of neurons and premature depletion of the neural progenitor pool. |
Co-immunoprecipitation, in utero electroporation, immunofluorescence, in vivo dominant-negative perturbation |
Neuron |
High |
20152126
|
| 2011 |
Wild-type huntingtin (HTT) interacts with PCM1 through HAP1 to regulate retrograde trafficking of PCM1 to the centrosome and normal ciliogenesis; loss of Htt impairs PCM1 retrograde trafficking and reduces primary cilia formation; pathogenic polyQ-expanded HTT causes centrosomal accumulation of PCM1 and abnormally long primary cilia. |
Co-immunoprecipitation, conditional knockout mouse models, live-cell imaging, immunofluorescence, ciliogenesis assay |
The Journal of clinical investigation |
High |
21985783
|
| 2013 |
PCM1 acts upstream of Plk1 and recruits it to the pericentriolar matrix in a dynein-dynactin-dependent manner; this interaction is phosphorylation-dependent with CDK1 as the priming kinase; centrosomal Plk1 then activates HDAC6 to promote ciliary deacetylation and primary cilia disassembly before mitotic entry. |
shRNA depletion, co-immunoprecipitation, kinase assays, phosphorylation-dependent interaction analysis, immunofluorescence |
Journal of cell science |
High |
23345402
|
| 2016 |
PCM1 is essential for tethering the E3 ubiquitin ligase Mindbomb1 (Mib1) to centriolar satellites; in the absence of PCM1, Mib1 poly-ubiquitylates and destabilizes Talpid3, blocking recruitment of Rab8-associated ciliary vesicles and ciliogenesis; an N-terminal domain of PCM1 is sufficient for restoring satellite localization of certain proteins and ciliogenesis. |
PCM1 gene deletion (CRISPR), domain mapping, ubiquitylation assay, co-immunoprecipitation, rescue experiments, immunofluorescence |
eLife |
High |
27146717
|
| 2016 |
Plk4 kinase phosphorylates PCM1 at the conserved S372 residue, promoting PCM1 dimerization and interaction with other satellite components; non-phosphorylatable PCM1-S372A recapitulates Plk4 depletion phenotypes (satellite dispersal, ciliogenesis defects), while phosphomimetic S372E partially rescues satellite organization and ciliogenesis in PCM1-depleted cells. |
In vitro kinase assay, phosphomimetic/alanine mutants, immunofluorescence, ciliogenesis assay, co-immunoprecipitation |
EMBO reports |
High |
26755742
|
| 2019 |
SNX17 recruits the deubiquitinating enzyme USP9X to antagonize MIB1-induced ubiquitination and proteasomal degradation of PCM1; SNX17 deficiency leads to enhanced degradation of USP9X and PCM1 and disrupts ciliogenesis upon serum starvation. |
Co-immunoprecipitation, ubiquitination assay, siRNA knockdown, immunofluorescence, ciliogenesis assay |
Cells |
Medium |
31671755
|
| 2019 |
Zika virus infection increases Mindbomb1 (MIB1) levels, which promotes MIB1-mediated poly-ubiquitination and proteasomal degradation of PCM1 and CEP131, causing dispersion of centriolar satellite granules while leaving centrioles intact; MIB1 knockout cells are refractory to ZIKV-induced PCM1 degradation and satellite dispersion. |
Viral infection, MIB1 knockout cells, proteasome inhibitor (MG132), Western blot, immunofluorescence |
The Journal of biological chemistry |
Medium |
31666336
|
| 2020 |
Trichoplein (TCHP) localizes to centriolar satellites and binds PCM1, stabilizing it; loss of TCHP causes delocalization and proteasome-dependent degradation of PCM1 and loss of PCM1's binding partner GABARAP, impairing autophagic flux under basal conditions. |
Co-immunoprecipitation, siRNA/knockout, immunofluorescence, autophagic flux assay, proteasome inhibitor treatment |
EMBO reports |
Medium |
32337819
|
| 2020 |
Ablation of PCM1 in mice leads to progressive ciliary defects, and PCM1 associates with dopamine D2 receptors (D2Rs) as shown by immunoprecipitation; PCM1-null mice show decreased available D2R levels and failure of antipsychotic drugs to rescue adult behavioral defects. |
Mouse PCM1 knockout, immunoprecipitation, behavioral assays, RNAseq |
Nature communications |
Medium |
33214552
|
| 2024 |
Necrosulfonamide (NSA) functions as a redox cycler that oxidizes and aggregates PCM1 alongside select satellite partners independently of MLKL; NSA-mediated ROS production disrupts ciliogenesis and leads to accumulation of autophagy markers, effects partially alleviated by PCM1 deletion, identifying PCM1 as a redox sensor in centriolar satellite biology. |
Chemical perturbation, ROS assays, PCM1 deletion (CRISPR), immunofluorescence, autophagy flux assays |
iScience |
Medium |
38600973
|
| 2025 |
In zebrafish radial glia progenitors, Pcm1 is asymmetrically distributed at centrosomes and detected on Notch ligand-containing endosomes in a complex with polarity regulator Par-3 and dynein motor; loss of pcm1 disrupts Rab5b-to-Rab11a endosome transition and Par-3/dynein macromolecular complex assembly, increasing neuronal differentiation at the expense of progenitor self-renewal; PARD3-PCM1-CEP83-RAB11 associations are conserved in human cortical brain organoids. |
In vivo time-lapse imaging, nanoscale expansion microscopy, co-immunoprecipitation, clonal analysis, zebrafish pcm1 knockout, human brain organoids |
Nature communications |
High |
41315244
|
| 2025 |
PCM1 orchestrates centrosomal and flagellar protein transport during sperm maturation; Pcm1 knockout mice exhibit disorganized manchette and head-tail coupling apparatus, defective flagellogenesis, and male infertility; PCM1 binds centrosomal proteins and governs their translocation via intra-manchette transport for centrosome remodeling and axoneme biogenesis. |
Pcm1 knockout mice, co-immunoprecipitation, immunofluorescence, electron microscopy, ICSI experiments |
Communications biology |
Medium |
40481240
|
| 2025 |
Centriolar satellites assemble via a hierarchical pathway initiated by PCM1 scaffold multimerization followed by regulated client recruitment; PCM1 intrinsically assembles into granules through self-multimerization modulated by the cytoskeleton; PCM1 and its clients occupy distinct subdomains with different compositions and dynamics; perturbing PCM1 multimerization impairs ciliary signaling. |
In vitro biogenesis assays, cellular assembly assays, high-resolution imaging, spatiotemporal quantification of granule properties |
bioRxivpreprint |
Medium |
|
| 2005 |
The t(8;9)(p22;p24) translocation fuses PCM1 coiled-coil domains to the entire tyrosine kinase domain of JAK2, producing a PCM1-JAK2 chimeric protein; the predicted coiled-coil domains of PCM1 likely promote JAK2 oligomerization and constitutive tyrosine kinase activation. |
RT-PCR, RACE-PCR, FISH, sequence analysis, prediction of constitutive activation by coiled-coil oligomerization |
Cancer research |
Medium |
15805263
|
| 2013 |
PCM1-JAK2 fusion signals through STAT5 to upregulate SOCS2 and SOCS3; lentiviral knockdown of PCM1-JAK2 inhibited these top upregulated genes, and treatment with a selective JAK2 inhibitor confirmed JAK2 as the active kinase moiety; GATA3 expression silenced in aggressive lymphoma cells is partially restored by PCM1-JAK2 knockdown. |
Lentiviral shRNA knockdown, JAK2 inhibitor treatment, gene expression profiling, PCM1-JAK2 fusion cell lines |
PloS one |
Medium |
23372669
|
| 2025 |
CCHCR1 interacts with PCM1 and OFD1; the centrosomal localization of CCHCR1 is determined by both OFD1 and PCM1; CCHCR1 recruits P-body proteins (via EDC4) to the centrosome and depletion of CCHCR1 or P-body components impairs ciliogenesis, placing PCM1 upstream of CCHCR1 centrosomal targeting. |
BioID-mass spectrometry, co-immunoprecipitation, GST pulldown, AB-FRET, siRNA/CRISPR knockdown/knockout, immunofluorescence |
Cellular & molecular biology letters |
Medium |
40883668
|