Affinage

PRICKLE1

Prickle-like protein 1 · UniProt Q96MT3

Length
831 aa
Mass
94.3 kDa
Annotated
2026-06-10
39 papers in source corpus 18 papers cited in narrative 18 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

PRICKLE1 is a core WNT/planar cell polarity (PCP) scaffold protein that organizes cortical cytoskeletal architecture and cell polarity across multiple developmental and morphogenetic contexts (PMID:19706528, PMID:35512799). It acts genetically downstream of the noncanonical WNT5A-ROR2 axis and the core PCP gene Vangl2 to establish apical-basal polarity, orient mitotic spindles, and direct polarized extracellular matrix deposition during epiblast and tissue morphogenesis (PMID:19706528, PMID:25190059). PRICKLE1 binds Dishevelled proteins through its LIM domain, an interaction that underlies its control of cell polarity, neurite outgrowth, and chondrocyte maturation [PMID:22218901, PMID:34423861, PMID:bio_10.1101_2025.03.24.644882]. Mechanistically, PRICKLE1 regulates the actomyosin cortex: diffuse cytoplasmic PRICKLE1 increases cortical F-actin and tension acting upstream of casein kinase II, while at the apical cortex of neuroepithelial cells it drives actomyosin accumulation and apical constriction to power convergence and EMT-driven cell ingression (PMID:35512799, PMID:42045189). It also governs migration through a membrane-localized pool that promotes focal adhesion disassembly via CLASP1/2 and LL5β and assembles a complex with MINK1 and the mTORC2 component RICTOR to activate AKT and drive cancer cell dissemination (PMID:27184734, PMID:27378169). PRICKLE1 controls cadherin switching during epithelial-to-mesenchymal transition and polarized basement membrane secretion via microtubule-dependent vesicle trafficking (PMID:30721665, PMID:33144400, PMID:38185785). In the nervous system PRICKLE1 binds SYNAPSIN I and stabilizes the transcriptional repressor REST; the epilepsy/ASD-associated R104Q mutation that disrupts the PRICKLE1–REST interaction reduces excitatory synapse density, lowers seizure threshold, and impairs cognition, establishing PRICKLE1 as a human epilepsy gene (PMID:18976727, PMID:24312498, PMID:34597683). PRICKLE1 protein stability is itself regulated by USP7-mediated deubiquitination and by estrogen-receptor/EZH2-dependent transcriptional repression (PMID:34331380, PMID:39314474).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 2006 High

    Established that PRICKLE1 negatively regulates canonical WNT/β-catenin signaling by targeting Dishevelled for degradation, defining a molecular mechanism for its pathway role.

    Evidence Co-IP, ubiquitination assay, D-box mutagenesis, and β-catenin reporter in hepatocellular carcinoma cells

    PMID:17030191

    Open questions at the time
    • Based on enforced overexpression; physiological relevance to endogenous DVL3 levels not established
    • E3 ligase mediating DVL3 ubiquitination not identified
  2. 2008 Medium

    Identified REST as a direct PRICKLE1 binding partner and linked PRICKLE1 to human epilepsy via the R104Q mutation that disrupts this interaction.

    Evidence In vitro interaction-blocking assay and zebrafish overexpression functional assay

    PMID:18976727

    Open questions at the time
    • Interaction shown in vitro; functional consequence of REST binding not yet mechanistically resolved
    • Did not establish whether epilepsy arises from REST destabilization or noncanonical WNT defects
  3. 2009 High

    Defined PRICKLE1 as essential for apical-basal epiblast polarity acting downstream of Vangl2 in the PCP pathway, establishing its in vivo developmental role.

    Evidence Conditional knockout mice, genetic epistasis with Vangl2, and Xenopus dominant-negative ΔPK/LIM with PKCζ imaging

    PMID:19706528

    Open questions at the time
    • Molecular effectors linking PRICKLE1 to spindle orientation not defined
    • How PRICKLE1 couples to Vangl2 mechanistically not resolved
  4. 2012 Medium

    Showed PRICKLE1 promotes neurite outgrowth through a DVL1-dependent mechanism, extending its DVL antagonism to neuronal morphogenesis.

    Evidence Co-IP, overexpression/knockdown, and neurite outgrowth assays in C1300 neuroblastoma cells

    PMID:22218901

    Open questions at the time
    • Cell-line-based; in vivo relevance not tested
    • Downstream cytoskeletal effectors not identified
  5. 2013 Medium

    Connected PRICKLE1 to synaptic vesicle biology by identifying SYNAPSIN I as a binding partner through the SYN1 region mutated in ASD/epilepsy.

    Evidence Yeast two-hybrid screen, neuronal co-IP/co-localization, and dense-core vesicle size assay in PC12 cells

    PMID:24312498

    Open questions at the time
    • Mechanism by which PRICKLE1 controls vesicle size unresolved
    • Reciprocal validation of the interaction in native neurons limited
  6. 2014 Medium

    Placed Prickle1 genetically downstream of WNT5A-ROR2 noncanonical signaling and showed it is a proteasomal target of WNT5A, integrating its degradation into pathway regulation.

    Evidence Multiple mouse mutant alleles, epistasis with Wnt5a/Ror2, proteasome inhibitor assays, and DVL2 immunostaining

    PMID:25190059

    Open questions at the time
    • E3 ligase and signal transducing WNT5A degradation not identified
    • Direct versus indirect DVL2 misregulation not distinguished
  7. 2016 High

    Revealed a PRICKLE1–MINK1–RICTOR complex driving AKT activation and cancer cell dissemination, defining a noncanonical signaling output coupled to mTORC2.

    Evidence Reciprocal Co-IP, proximity ligation, focal adhesion imaging, and xenograft dissemination assays

    PMID:27184734

    Open questions at the time
    • Whether PRICKLE1 directly activates mTORC2 kinase activity not resolved
    • Structural basis of the complex not defined
  8. 2016 High

    Demonstrated a membrane-localized, farnesylation-dependent pool of PRICKLE1 that promotes focal adhesion disassembly via CLASP1/2 and LL5β, linking it to microtubule-targeted adhesion turnover.

    Evidence TIRF/FRAP live imaging, Co-IP, siRNA with focal adhesion turnover assay, and farnesylation mutant analysis

    PMID:27378169

    Open questions at the time
    • How PRICKLE1 recruits CLASPs mechanistically not defined
    • Relationship between this membrane pool and the RICTOR complex unclear
  9. 2019 Medium

    Established PRICKLE1 as a regulator of cadherin switching during EMT and collective neural crest migration in vivo.

    Evidence pk1a/pk1b mutant zebrafish, live time-lapse imaging, and E-/N-Cadherin immunofluorescence

    PMID:30721665

    Open questions at the time
    • Molecular link between PRICKLE1 and cadherin transcription/turnover not defined
    • Whether effect is cell-autonomous not fully resolved
  10. 2020 Medium

    Showed PRICKLE1 is required for polarized basement membrane deposition during tear duct elongation, tying it to vesicular and cytoskeletal trafficking of ECM.

    Evidence Prickle1 mutant mouse analysis with laminin/BM, cytoskeletal, and vesicular transport markers

    PMID:33144400

    Open questions at the time
    • Trafficking machinery directly controlled by PRICKLE1 not identified
    • Cause of cytoplasmic laminin accumulation mechanistically unresolved
  11. 2021 Medium

    Dissected PRICKLE1 LIM1-domain-mediated DVL2/DVL3 binding as the basis for chondrocyte polarity and maturation, with a disease-associated missense mutation reducing the interaction.

    Evidence In vivo Co-IP, proximity ligation, and primary cilia/polarity immunofluorescence in growth plates

    PMID:34423861

    Open questions at the time
    • How reduced DVL binding randomizes polarity mechanistically not resolved
    • Downstream chondrocyte maturation effectors not defined
  12. 2021 Medium

    Identified USP7 as a deubiquitinase that stabilizes PRICKLE1, coupling PRICKLE1 abundance to mTORC2 complex integrity and AKT/PKCα signaling in migration.

    Evidence USP7 overexpression/inhibitor, ubiquitination assays, proteasome vs lysosome inhibitor discrimination, and Co-IP

    PMID:34331380

    Open questions at the time
    • E3 ligase opposing USP7 not identified
    • Direct versus indirect USP7–PRICKLE1 interaction not fully resolved
  13. 2021 Medium

    Provided in vivo causal evidence that the PRICKLE1–REST interaction underlies synaptic and behavioral phenotypes relevant to epilepsy and ASD.

    Evidence CRISPR R104Q knock-in mice with Co-IP, synaptic marker quantification, and behavioral/seizure-threshold assays

    PMID:34597683

    Open questions at the time
    • How REST destabilization reduces excitatory synapse density mechanistically not defined
    • Whether noncanonical WNT functions also contribute not separated
  14. 2024 Medium

    Separated PRICKLE1's basement-membrane secretion function from its apicobasal polarity function using rescue experiments, showing BM deposition depends on microtubule-based vesicle trafficking.

    Evidence iPSC-derived embryoid body rescue, microtubule network analysis, and vesicle trafficking assays

    PMID:38185785

    Open questions at the time
    • Molecular cargo adaptors used by PRICKLE1 for BM secretion not identified
    • Why polarity is not rescued by PRICKLE1 reintroduction unexplained
  15. 2024 Medium

    Placed PRICKLE1 in an estrogen-receptor/EZH2 transcriptional circuit and established it as required for REST protein stability in myometrial cells.

    Evidence ChIP for EZH2/H3K27me3 at the PRICKLE1 promoter, EZH2 siRNA, PRICKLE1 overexpression, and conditional knockout mice (preprint)

    PMID:39314474

    Open questions at the time
    • Mechanism by which PRICKLE1 stabilizes REST protein not defined
    • Preprint status; requires peer-reviewed confirmation
  16. 2025 Low

    Mapped the PRICKLE1 proximity interactome and challenged the model that PRICKLE1 regulates DVL2/DVL3 levels or phosphorylation under near-physiological expression.

    Evidence miniTurboID proximity biotinylation with mass spectrometry in an inducible expression system (preprint)

    PMID:bio_10.1101_2025.03.24.644882

    Open questions at the time
    • Negative result for DVL regulation awaits independent replication
    • Single preprint; physiological expression levels need validation against earlier overexpression studies
  17. 2026 Medium

    Defined an apical-cortex pool of PRICKLE1 that drives actomyosin accumulation and apical constriction to power convergence and EMT-driven ingression independently of classical planar polarity.

    Evidence Quantitative live imaging in transgenic quail embryos with loss-of-function and actomyosin/polarity marker readouts

    PMID:42045189

    Open questions at the time
    • Molecular link between cortical PRICKLE1 and actomyosin recruitment not defined
    • Relationship to casein-kinase-II-dependent cortical regulation not integrated

Open questions

Synthesis pass · forward-looking unresolved questions
  • Whether PRICKLE1's distinct outputs — DVL antagonism, mTORC2/AKT signaling, REST stabilization, cortical actomyosin control, and ECM secretion — reflect a single unifying biochemical activity or separable context-specific modules remains unresolved.
  • No structural model unifies the LIM/farnesyl-dependent interactions
  • Mechanism by which PRICKLE1 stabilizes REST protein remains unknown
  • The reported negative DVL-regulation result conflicts with earlier overexpression findings and is unreconciled

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 3 GO:0008092 cytoskeletal protein binding 2 GO:0098772 molecular function regulator activity 2
Localization
GO:0005856 cytoskeleton 3 GO:0005829 cytosol 2 GO:0005886 plasma membrane 2
Pathway
R-HSA-1266738 Developmental Biology 4 R-HSA-162582 Signal Transduction 3 R-HSA-392499 Metabolism of proteins 2
Partners
DVL1DVL2DVL3MINK1RESTRICTORSYN1USP7
Complex memberships
PRICKLE1–MINK1–RICTOR (mTORC2-associated) complex

Evidence

Reading pass · 18 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2008 A missense mutation in PRICKLE1 (R104Q) blocks the PRICKLE1–REST interaction in vitro, identifying REST as a direct binding partner of PRICKLE1 and placing PRICKLE1 in the noncanonical WNT signaling pathway as the first member directly implicated in human epilepsy. In vitro protein interaction assay (blocking of PRICKLE1–REST interaction); zebrafish overexpression functional assay American journal of human genetics Medium 18976727
2006 PRICKLE1 binds Dishevelled3 (DVL3) and promotes its ubiquitination and proteasomal degradation through destruction-box (D-box) motifs on PRICKLE1, thereby negatively regulating the WNT/β-catenin pathway in hepatocellular carcinoma cells. Co-immunoprecipitation, ubiquitination assay, enforced expression/knockdown with β-catenin reporter assay, D-box motif mutagenesis Gastroenterology High 17030191
2009 Mouse Prickle1 (mpk1) is essential for apical-basal polarity of the epiblast; loss of mpk1 causes abnormal cell shapes, mislocalized ECM proteins, and disrupted mitotic spindle orientation. Genetic interaction with Vangl2 (another core PCP gene) was demonstrated, placing Prickle1 downstream in the PCP pathway for epiblast polarity. Dominant-negative ΔPK/LIM construct in Xenopus disrupted apical marker PKCζ localization, confirming a direct role in cortical polarity. Conditional knockout mice, genetic epistasis with Vangl2, Xenopus dominant-negative overexpression with apical marker (PKCζ) imaging Proceedings of the National Academy of Sciences of the United States of America High 19706528
2016 PRICKLE1 forms a complex with MINK1 (serine/threonine kinase) and RICTOR (an mTORC2 component); integrity of this PRICKLE1–MINK1–RICTOR complex is required for AKT activation, focal adhesion regulation, and cancer cell migration/dissemination. Disruption of the PRICKLE1–RICTOR interaction strongly impairs breast cancer cell dissemination in xenograft assays. Co-immunoprecipitation, proximity ligation, xenograft in vivo dissemination assay, focal adhesion imaging Developmental cell High 27184734
2016 PRICKLE1 accumulates at cell retraction sites near focal adhesions, where it promotes focal adhesion disassembly by associating with CLASP1/2 and LL5β (PHLDB2) and enabling LL5β-dependent accumulation of CLASPs at the cell edge to drive microtubule targeting of focal adhesions. Membrane localization via a farnesyl moiety is required for these functions. Live-cell imaging (TIRF/FRAP), co-immunoprecipitation, siRNA knockdown with focal adhesion turnover assay, farnesylation mutant analysis Journal of cell science High 27378169
2013 PRICKLE1 physically interacts with SYNAPSIN I (SYN1) in neurons, co-localizing with endogenous Syn1. The interaction is through the SYN1 region mutated in ASD and epilepsy. A PRICKLE1 mutation disrupts its ability to increase the size of dense-core vesicles in PC12 cells, implicating PRICKLE1 in synaptic vesicle regulation. Yeast two-hybrid screen (human brain cDNA library), co-immunoprecipitation/co-localization in neurons, dense-core vesicle size assay in PC12 cells PloS one Medium 24312498
2014 Prickle1 is a proteasomal target of WNT5A signaling in mice; complete Prickle1 loss leads to misregulation of DVL2 (a WNT5A target), and Prickle1 mutants phenocopy Wnt5a and Ror2 mutants, placing Prickle1 downstream of WNT5A-ROR2 in the noncanonical WNT pathway. Multiple Prickle1 mutant alleles in mice, epistasis with Wnt5a/Ror2 mutants, proteasome inhibitor experiments to assess Prickle1 degradation, immunostaining of DVL2 Biology open Medium 25190059
2012 Prickle1 associates with Dishevelled1 (DVL1), and overexpression of Prickle1 reduces DVL1 protein levels; overexpression of DVL1 blocks Prickle1-induced neurite-like process formation, demonstrating that Prickle1 promotes neurite outgrowth via a DVL1-dependent mechanism. Co-immunoprecipitation, overexpression and knockdown in C1300 neuroblastoma cells, neurite outgrowth assay Methods in molecular biology Medium 22218901
2022 In Xenopus prechordal mesoderm, cytoplasmic (diffuse) Prickle1 upregulates cortical F-actin content, antagonizing DVL2-mediated cortex downregulation; both factors act upstream of casein kinase II to modulate cortical tension, affecting cell migration and rearrangement during radial intercalation. Punctate/plaque forms of Pk1 are associated with localized depletion of cortical F-actin, suggesting opposite roles for diffuse versus punctate Pk1. Xenopus live imaging, F-actin quantification, cortical tension measurements, dominant-negative and overexpression constructs, epistasis with casein kinase II The Journal of cell biology High 35512799
2021 The Prickle1 LIM1 domain mediates protein–protein interactions with DVL2 and DVL3 in chondrocytes; a missense mutation in the LIM1 domain (Prickle1Bj) reduces these interactions, causing randomized chondrocyte polarity (assessed by primary cilia and PRICKLE1/DVL localization) and precocious maturation with stalled terminal differentiation. In vivo co-immunoprecipitation, proximity ligation assay, immunofluorescence of primary cilia/polarity markers in growth plates Journal of bone and mineral research Medium 34423861
2019 In zebrafish, Prickle1a and Prickle1b are required for epithelial-to-mesenchymal transition (EMT) and collective migration of cranial neural crest cells; loss of Pk1b elevates E-Cadherin and reduces N-Cadherin levels, indicating Prickle1 regulates cadherin switching during EMT. pk1a/pk1b mutant zebrafish analysis, live-cell time-lapse imaging, immunofluorescence for E-Cadherin and N-Cadherin Developmental biology Medium 30721665
2021 USP7 (ubiquitin-specific protease 7) deubiquitinates and stabilizes PRICKLE1 protein; morin inhibits USP7, leading to increased PRICKLE1 ubiquitination and proteasomal degradation (blocked by MG132 but not the lysosomal inhibitor BafA1), which in turn disrupts the PRICKLE1–mTORC2 complex and AKT/PKCα activation to impair cell migration. USP7 overexpression/inhibitor experiments, ubiquitination assay, proteasome/lysosome inhibitor treatment, co-immunoprecipitation Molecular nutrition & food research Medium 34331380
2020 Prickle1 is required for polarized basement membrane deposition during tear duct elongation; Prickle1 disruption causes loss of basement membrane deposition and aberrant cytoplasmic accumulation of laminin, with associated defects in cell adhesion, cytoskeletal and vesicular transport, and cell axis orientation. Prickle1 mutant mouse analysis, immunofluorescence for laminin/BM components, cytoskeletal and vesicular transport markers Development (Cambridge, England) Medium 33144400
2024 In iPSC-derived embryoid bodies, Prickle1 directs secretion of basement membrane components through a proper microtubule network and vesicle trafficking in visceral endoderm cells; reintroduction of Prickle1 in mutant EBs rescues BM formation but not apicobasal polarity, demonstrating BM deposition and apicobasal polarity are separable Prickle1 functions. iPSC-derived embryoid body system, Prickle1 rescue experiments, microtubule network analysis, vesicle trafficking assays, immunofluorescence Cell proliferation Medium 38185785
2021 The Prickle1 R104Q mutation impairs the interaction between PK1 and REST, reduces excitatory synapse density in hippocampus, decreases seizure threshold, and impairs social interaction and cognition in mice, linking the PK1–REST interaction to epilepsy/ASD-related synaptic phenotypes. CRISPR-Cas9 knock-in mouse (R104Q), co-immunoprecipitation for PK1–REST interaction, immunostaining of synaptic markers, behavioral assays Experimental neurology Medium 34597683
2024 Estrogen receptor alpha (ERα), acting through EZH2-mediated H3K27 methylation at the PRICKLE1 promoter, represses PRICKLE1 expression; reduced PRICKLE1 destabilizes REST protein. Conversely, PRICKLE1 overexpression restores REST in leiomyoma smooth muscle cells, establishing PRICKLE1 as required for REST protein stability in myometrial cells. Chromatin immunoprecipitation (ChIP) for EZH2 and H3K27me3 at PRICKLE1 promoter, siRNA knockdown of EZH2, overexpression of PRICKLE1, conditional knockout mice (Lhb, Esr1) bioRxivpreprint Medium 39314474
2025 PRICKLE1 interactome mapping (miniTurboID proximity biotinylation + MS) reveals PRICKLE1 localizes intracellularly and interacts with DVL2/DVL3 as binding partners in the WNT/PCP pathway. Notably, unlike PRICKLE3, PRICKLE1 does not influence levels or phosphorylation status of DVL2 and DVL3 under near-physiological expression conditions, contradicting earlier overexpression-based findings. miniTurboID proximity biotinylation combined with mass spectrometry, inducible expression system bioRxivpreprint Low bio_10.1101_2025.03.24.644882
2026 In quail junctional neural tube, PRICKLE1 is enriched at the apical cortex of medial neuroepithelial cells where it drives actomyosin accumulation and apical constriction to orchestrate mediolateral convergence and EMT-driven cell ingression, independently of classical planar polarity axis establishment. High-resolution quantitative live imaging in transgenic quail embryos, loss-of-function with actomyosin and polarity marker readout Nature communications Medium 42045189

Source papers

Stage 0 corpus · 39 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2008 A homozygous mutation in human PRICKLE1 causes an autosomal-recessive progressive myoclonus epilepsy-ataxia syndrome. American journal of human genetics 170 18976727
2003 Identification and characterization of human PRICKLE1 and PRICKLE2 genes as well as mouse Prickle1 and Prickle2 genes homologous to Drosophila tissue polarity gene prickle. International journal of molecular medicine 159 12525887
2006 Prickle-1 negatively regulates Wnt/beta-catenin pathway by promoting Dishevelled ubiquitination/degradation in liver cancer. Gastroenterology 109 17030191
2009 Mouse prickle1, the homolog of a PCP gene, is essential for epiblast apical-basal polarity. Proceedings of the National Academy of Sciences of the United States of America 96 19706528
2016 PRICKLE1 Contributes to Cancer Cell Dissemination through Its Interaction with mTORC2. Developmental cell 64 27184734
2011 Identification and characterization of novel rare mutations in the planar cell polarity gene PRICKLE1 in human neural tube defects. Human mutation 64 21901791
2007 Mouse Prickle1 and Prickle2 are expressed in postmitotic neurons and promote neurite outgrowth. FEBS letters 46 17868671
2016 Prickle1 mutation causes planar cell polarity and directional cell migration defects associated with cardiac outflow tract anomalies and other structural birth defects. Biology open 43 26883626
2014 Null and hypomorph Prickle1 alleles in mice phenocopy human Robinow syndrome and disrupt signaling downstream of Wnt5a. Biology open 41 25190059
2013 Prickle1 is expressed in distinct cell populations of the central nervous system and contributes to neuronal morphogenesis. Human molecular genetics 37 23420014
2016 Prickle1 promotes focal adhesion disassembly in cooperation with the CLASP-LL5β complex in migrating cells. Journal of cell science 35 27378169
2013 PRICKLE1 interaction with SYNAPSIN I reveals a role in autism spectrum disorders. PloS one 34 24312498
2017 Prickle1 regulates neurite outgrowth of apical spiral ganglion neurons but not hair cell polarity in the murine cochlea. PloS one 29 28837644
2013 Analysis of PRICKLE1 in human cleft palate and mouse development demonstrates rare and common variants involved in human malformations. Molecular genetics & genomic medicine 29 24689077
2019 Prickle1 is required for EMT and migration of zebrafish cranial neural crest. Developmental biology 22 30721665
2018 Prickle1 regulates differentiation of frontal bone osteoblasts. Scientific reports 21 30575813
2014 Prickle1 is necessary for the caudal migration of murine facial branchiomotor neurons. Cell and tissue research 18 24927917
2018 A de novo mutation in PRICKLE1 associated with myoclonic epilepsy and autism spectrum disorder. Journal of neurogenetics 16 29790814
2021 Morin Acts as a USP7 Inhibitor to Hold Back the Migration of Rheumatoid Arthritis Fibroblast-Like Synoviocytes in a "Prickle1-mTORC2" Dependent Manner. Molecular nutrition & food research 12 34331380
2018 PRICKLE1-related early onset epileptic encephalopathy. American journal of medical genetics. Part A 12 30345727
2016 A de novo mutation in PRICKLE1 in fetal agenesis of the corpus callosum and polymicrogyria. Journal of neurogenetics 11 26727662
2022 Cell cortex regulation by the planar cell polarity protein Prickle1. The Journal of cell biology 9 35512799
2019 A very rare form of autosomal dominant progressive myoclonus epilepsy caused by a novel variant in the PRICKLE1 gene. Seizure 9 31035234
2012 Role of Prickle1 and Prickle2 in neurite outgrowth in murine neuroblastoma cells. Methods in molecular biology (Clifton, N.J.) 9 22218901
2021 PRICKLE1 × FOCAD Interaction Revealed by Genome-Wide vQTL Analysis of Human Facial Traits. Frontiers in genetics 8 34434215
2017 Prickle1 as positive regulator of oligodendrocyte differentiation. Neuroscience 8 28935237
2022 Distinct overlapping functions for Prickle1 and Prickle2 in the polarization of the airway epithelium. Frontiers in cell and developmental biology 7 36176272
2021 Chondrocyte Polarity During Endochondral Ossification Requires Protein-Protein Interactions Between Prickle1 and Dishevelled2/3. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 7 34423861
2021 Mutation of the murine Prickle1 (R104Q) causes phenotypes analogous to human symptoms of epilepsy and autism. Experimental neurology 6 34597683
2024 Estrogen receptor alpha mediated repression of PRICKLE1 destabilizes REST and promotes uterine fibroid pathogenesis. bioRxiv : the preprint server for biology 5 39314474
2021 PRICKLE1 promotes gastric cancer metastasis by activating mTOR signaling. American journal of translational research 5 34150013
2020 Ontogenesis of the tear drainage system requires Prickle1-driven polarized basement membrane deposition. Development (Cambridge, England) 4 33144400
2018 Sudden unexpected death with rare compound heterozygous variants in PRICKLE1. Neurogenetics 4 30564977
2025 Loss of PRICKLE1 leads to abnormal endometrial epithelial architecture, decreased embryo implantation, and reduced fertility in mice. PNAS nexus 3 39917256
2024 Prickle1-driven basement membrane deposition of the iPSC-derived embryoid bodies is separable from the establishment of apicobasal polarity. Cell proliferation 2 38185785
2023 PRICKLE1 gene methylation and abnormal transcription in Chinese patients with ankylosing spondylitis. Immunobiology 2 37742487
2025 Loss of PRICKLE1 leads to subfertility, aberrant extracellular matrix and abnormal myometrial architecture in mice. Reproduction (Cambridge, England) 1 39679867
2026 Quantitative live imaging reveals PRICKLE1 controls junctional neural tube morphogenesis independent of Planar Cell Polarity. Nature communications 0 42045189
2024 Loss of PRICKLE1 leads to abnormal endometrial epithelial architecture, decreased embryo implantation, and reduced fertility in mice. bioRxiv : the preprint server for biology 0 39211179

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