Affinage

KIAA0586

Protein TALPID3 · UniProt Q9BVV6

Length
1533 aa
Mass
169.3 kDa
Annotated
2026-06-10
46 papers in source corpus 16 papers cited in narrative 16 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

KIAA0586/TALPID3 is a centrosomal protein that assembles a ring-like structure at the distal end of centrioles (mother centriole/basal body) and is essential for primary cilia formation and Hedgehog signal transduction (PMID:19144723, PMID:24421332). A conserved coiled-coil region encoded by exons 11-12 is required for centrosomal localization and sufficient to rescue ciliogenesis (PMID:19144723), and deletion of these exons in mice abolishes primary cilia and produces hallmark Hedgehog-dependent developmental defects in face, neural tube, left/right asymmetry, and digit number (PMID:21750036). Mechanistically, TALPID3 governs basal body docking to the apical membrane: mutant basal bodies mature but fail to dock and lack ciliary axonemes, and TALPID3 acts upstream of Rab8a, with activated Rab8a rescuing the cilia and photoreceptor outer-segment defects of TALPID3-deficient cells (PMID:24421332, PMID:29396404). It is a component of a CP110-containing complex and controls centriolar satellite dispersal that precedes ciliary vesicle formation (PMID:24421332). Through its interaction with the PKA regulatory subunit PKARIIβ at centrioles, TALPID3 enables PKA-dependent phosphorylation and proper processing of Gli2/Gli3 into activator and repressor forms, providing a cilium-based mechanism for graded Hedgehog output (PMID:16702409, PMID:28673820, PMID:22028029). TALPID3 further interacts with CEP120 and C2CD3 for distal centriole/appendage assembly (PMID:30988386), with ANKRD26 to recruit FBF1 to transition fibers for cilia gating (PMID:32366837), and with Ninein to organize microtubules and maintain adherens junctions during neural progenitor mitosis (PMID:33326788). Its abundance is restrained by Mib1-mediated poly-ubiquitylation, which is held in check by PCM1 tethering at centriolar satellites (PMID:27146717). Biallelic KIAA0586 mutations cause a human ciliopathy, with patient cells showing defective ciliogenesis, abnormal SHH response, and aberrant Gli3 processing rescued by wild-type KIAA0586 (PMID:26166481).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2006 High

    Established that TALPID3 is required for both activator and repressor functions of the Hedgehog pathway by acting on Gli3 processing, placing it at a central regulatory node of Hh output.

    Evidence Genetic rescue and Gli3 processing assays in chicken embryos

    PMID:16702409

    Open questions at the time
    • Cytoplasmic localization defined but subcellular site of action not yet resolved
    • Molecular partners mediating Gli processing unknown
  2. 2009 High

    Identified TALPID3 as a centrosomal protein required for basal body docking to the apical membrane and cilia formation, localizing the Hh defect to a ciliogenesis step.

    Evidence Anti-Talpid3 immunofluorescence, EM, and exon 11-12 deletion rescue in talpid3 mutant chicken embryos

    PMID:19144723

    Open questions at the time
    • Molecular mechanism of docking not defined
    • Interacting partners at the distal centriole unidentified
  3. 2011 High

    Demonstrated in zebrafish and mouse that TALPID3 loss abolishes cilia and disrupts Gli processing and Hh-dependent patterning, confirming a conserved vertebrate cilia-dependent mechanism.

    Evidence Zinc-finger nuclease and gene-deletion mutants with Gli2a localization/processing and limb patterning analysis

    PMID:21750036 PMID:22028029

    Open questions at the time
    • Did not define the biochemical step linking TALPID3 to Gli phosphorylation
    • Cell migration phenotype mechanism unresolved
  4. 2013 Medium

    Showed TALPID3 is required for centrosome migration to the apical surface but not for de novo centriologenesis or axoneme formation, distinguishing its docking role from centriole biogenesis.

    Evidence Immunofluorescence and EM of talpid3 ependymal multiciliate cells

    PMID:23613203

    Open questions at the time
    • Single lab
    • Molecular basis of migration defect not defined
  5. 2014 High

    Defined the centriolar architecture and trafficking mechanism: TALPID3 forms a distal-end ring within a CP110 complex and controls satellite dispersal and Rab8a recruitment to drive ciliary vesicle formation.

    Evidence Co-IP, siRNA depletion, EM, and activated-Rab8a rescue; separate Co-IP mapping Cep120 to daughter centriole via Talpid3

    PMID:24421332 PMID:25251415

    Open questions at the time
    • How TALPID3 activates/recruits Rab8a mechanistically unclear
    • Cep120 interaction from single Co-IP
  6. 2015 Medium

    Linked KIAA0586 to a human ciliopathy and confirmed causality, showing patient cells have defective ciliogenesis, abnormal SHH response, and aberrant Gli3 processing rescued by wild-type protein.

    Evidence Patient fibroblast ciliogenesis/SHH assays, CEP290 pattern, Gli3 western, and wild-type rescue; photoreceptor basal body localization

    PMID:26166481 PMID:26386247

    Open questions at the time
    • Genotype-phenotype correlations not established
    • Single lab for localization data
  7. 2016 High

    Uncovered post-translational control of TALPID3 abundance: PCM1 tethers Mib1 at satellites to prevent Mib1-mediated poly-ubiquitylation and degradation of TALPID3, gating ciliogenesis.

    Evidence PCM1 deletion, ubiquitylation assays, domain rescue, and Mib1-inactivation epistasis in human cells

    PMID:27146717

    Open questions at the time
    • Ubiquitylation sites on TALPID3 not mapped
    • Signals triggering Mib1 activity unclear
  8. 2017 Medium

    Provided a molecular mechanism for Gli processing by showing TALPID3 recruits PKARIIβ to centrioles via its C-terminus to enable PKA-dependent Gli2/Gli3 phosphorylation.

    Evidence Co-IP, domain mapping with N-/C-terminal constructs, and phosphorylation/Gli processing assays

    PMID:28673820

    Open questions at the time
    • Single lab
    • Direct kinase-substrate relationship at centrioles not reconstituted
  9. 2018 Medium

    Extended the Rab8a-upstream model to photoreceptors, showing TALPID3 enables outer-segment formation through basal body docking upstream of Rab8a activation.

    Evidence Zebrafish talpid3 mutant analysis with constitutively active Rab8a rescue and electroretinograms

    PMID:29396404

    Open questions at the time
    • Mechanism of Rab8a activation by TALPID3 unresolved
    • Single lab
  10. 2019 Medium

    Placed TALPID3 within a CEP120-C2CD3 distal centriole module, showing CEP120 recruits both to centriole distal ends for appendage assembly and cilia formation.

    Evidence Co-IP, CRISPR CEP120 knockout in RPE1 cells, and disease-mutant binding assay

    PMID:30988386

    Open questions at the time
    • Single lab
    • Order of assembly among CEP120/C2CD3/TALPID3 not fully defined
  11. 2020 High

    Defined a cilia-gating function and a neurodevelopmental role: TALPID3 forms an ANKRD26-FBF1 complex recruiting FBF1 to transition fibers, and associates with Ninein to organize microtubules and maintain radial glial integrity.

    Evidence C. elegans forward screen, epistasis, and Co-IP for the FBF1 complex; Co-IP, silencing, and live imaging for Ninein and radial glia

    PMID:32366837 PMID:33326788

    Open questions at the time
    • How TALPID3 selects transition fiber vs. distal centriole functions unclear
    • Ninein interaction from single lab
  12. 2023 Medium

    Revealed a tissue-specific requirement in muscle stem cell self-renewal where the regeneration defect is rescued by Wnt rather than Hedgehog activation, indicating context-dependent pathway coupling.

    Evidence Conditional MuSC deletion, scRNA-seq, and pharmacological Wnt vs. Smo rescue in mice

    PMID:37925530

    Open questions at the time
    • Mechanism linking TALPID3/cilia to Wnt regulation undefined
    • Single lab

Open questions

Synthesis pass · forward-looking unresolved questions
  • How TALPID3 mechanistically activates Rab8a and integrates its distal-centriole, transition-fiber, PKA-scaffolding, and Wnt-related roles into a unified molecular function remains unresolved.
  • No structural model of the TALPID3 distal-end ring
  • Direct biochemical activity of TALPID3 not defined
  • Mechanism coupling ciliary function to Wnt signaling unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 4
Localization
GO:0005815 microtubule organizing center 4 GO:0005929 cilium 3 GO:0005829 cytosol 1
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-1266738 Developmental Biology 3 R-HSA-1852241 Organelle biogenesis and maintenance 3 R-HSA-5653656 Vesicle-mediated transport 2
Partners
ANKRD26C2CD3CEP120CP110FBF1NINPRKAR2BRAB8A
Complex memberships
CEP120-C2CD3-TALPID3 distal centriole moduleCP110 complexTALPID3-ANKRD26-FBF1 transition fiber complex

Evidence

Reading pass · 16 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2006 Talpid3/KIAA0586 is absolutely required for both Gli repressor and activator functions in the intracellular Hedgehog pathway; Gli3 processing is abnormal in talpid3 mutant cells, though Gli3 can still translocate to the nucleus. The protein localizes to the cytoplasm. Genetic rescue experiments in chicken embryos, Gli3 processing assays, subcellular localization studies in mutant vs. wild-type cells Genes & development High 16702409
2009 Talpid3/KIAA0586 is a centrosomal protein essential for primary cilia formation; in talpid3 mutant cells, basal bodies mature and dock is attempted but fail to dock with the apical membrane, are misorientated, and almost completely lack ciliary axonemes. A conserved coiled-coil domain region (exons 11-12) is required to rescue primary cilia formation and is sufficient for centrosomal localization. Marked changes in actin organisation were also detected in mutant cells. Immunofluorescence with anti-Talpid3 antibody, electron microscopy (ultrastructural analysis), rescue experiments with deletion constructs in talpid3 mutant embryos, antibody detection of Talpid3 at centrosome Development (Cambridge, England) High 19144723
2014 Talpid3 assembles a ring-like structure at the extreme distal end of centrioles and is a component of a CP110-containing protein complex. Ablation of Talpid3 causes aberrant distribution of centriolar satellites and mislocalization of Rab8a. Expression of activated Rab8a suppresses cilia assembly defects provoked by Talpid3 depletion, indicating Talpid3 affects cilia formation through Rab8a recruitment and/or activation. Talpid3 is also required for centriolar satellite dispersal preceding ciliary vesicle formation. Co-immunoprecipitation to identify CP110 complex, siRNA depletion, immunofluorescence, ultrastructural analysis, rescue with activated Rab8a The Journal of cell biology High 24421332
2016 PCM1 tethers the E3 ubiquitin ligase Mindbomb1 (Mib1) to centriolar satellites. In the absence of PCM1, Mib1 destabilizes Talpid3 through poly-ubiquitylation, suppressing cilium assembly. Loss of PCM1 blocks ciliogenesis by abrogating recruitment of ciliary vesicles associated with Talpid3-binding protein Rab8; this can be reversed by inactivating Mib1. Thus Mib1-mediated poly-ubiquitylation is a post-translational regulatory mechanism controlling Talpid3 abundance. PCM1 gene deletion in human cells, rescue with PCM1 domain constructs, ubiquitylation assays, Mib1 inactivation rescue experiments, immunofluorescence eLife High 27146717
2014 Centrosomal protein Cep120 is asymmetrically localized to the daughter centriole through its physical interaction with Talpid3 (Ta3), another centrosomal protein. Co-immunoprecipitation (pulldown), immunofluorescence localization in cerebellar granule neuron progenitors PloS one Medium 25251415
2017 Talpid3 interacts with PKA regulatory subunit PKARIIβ at centrioles; the centriolar localization region maps to the N-terminal region and the PKA-binding region to the C-terminal region of Ta3. Talpid3 mutation results in failure of PKARIIβ to localize at centrioles, leading to reduced Gli2 and Gli3 phosphorylation and impaired processing. Hedgehog signaling inhibits Gli2 and Gli3 phosphorylation by PKA in cilia. Co-immunoprecipitation (Talpid3–PKARIIβ interaction), immunofluorescence colocalization, domain mapping with N- and C-terminal constructs, phosphorylation assays in mutant vs. wild-type cells, Gli processing western blot Developmental biology Medium 28673820
2019 CEP120 interacts with C2CD3 and Talpid3; loss of CEP120 impairs recruitment of C2CD3 and Talpid3 to the distal ends of centrioles, leading to defects in centriole appendage assembly and cilia formation. A disease-associated CEP120 mutant (I975S) has low affinity for C2CD3 binding and perturbs cilia assembly. Co-immunoprecipitation (CEP120 with C2CD3 and Talpid3), CRISPR/Cas9 CEP120 knockout in RPE1 cells, immunofluorescence, disease-mutant binding assay Scientific reports Medium 30988386
2020 TALPID3 and ANKRD26 form a protein complex with cilia-gating component FBF1 at transition fibers. Co-depletion of TALPID3 and ANKRD26 specifically impairs recruitment of FBF1 to transition fibers, disrupting cilia gating. This function is conserved in both C. elegans (TALP-3/ANKR-26/DYF-19) and mammalian cells (TALPID3/ANKRD26/FBF1). Forward genetic screen in C. elegans, genetic epistasis (co-depletion), co-immunoprecipitation (complex formation), immunofluorescence (FBF1 localization at transition fibers) in both C. elegans and mammalian cells Nature communications High 32366837
2011 In zebrafish talpid3 mutants (MZta3), primary and motile cilia are absent and Hedgehog signaling is aberrant. GFP-tagged Gli2a localizes to basal bodies in the absence of primary cilia, and Gli2a protein is aberrantly processed in MZta3 embryos as shown by western blot, demonstrating a cilia-dependent mechanism for Gli processing. Zinc-finger nuclease mutagenesis, GFP-Gli2a localization by live imaging, western blot for Gli2a processing, germline replacement for maternal depletion Development (Cambridge, England) High 22028029
2011 Deletion of conserved exons 11-12 of KIAA0586/Talpid3 in mice results in embryos lacking primary cilia with face, neural tube, and left/right asymmetry defects. Conditional deletion in limb mesenchyme causes polydactyly and brachydactyly attributable to abnormal Sonic hedgehog and Indian hedgehog signaling. Talpid3 mutant mouse cells migrate more slowly than wild-type cells. Constitutive and conditional gene deletion in mice, primary cilia immunofluorescence, cell migration assays Development (Cambridge, England) High 21750036
2013 TALPID3 is required for centrosomal migration to the apical surface prior to ciliogenesis in ependymal multiciliate cells; talpid3 ependymal cells develop multiple centrosomes but these fail to migrate to the apical cell surface, though axoneme formation was sometimes observed. TALPID3 is not directly required for de novo centriologenesis, multiciliated fate, or axoneme formation. Immunofluorescence for centrosome markers, electron microscopy of ependymal cells, analysis of FOXJ1 expression in talpid3 vs. wild-type chicken embryos Developmental dynamics Medium 23613203
2015 KIAA0586 protein localizes to the basal body in human and mouse photoreceptors, and also in pericentriolar locations. Loss of TALPID3 function in animal models causes abnormal tissue polarity, centrosome length and orientation, and centriolar satellites. Immunofluorescence localization in human and mouse photoreceptors, animal model analysis (chicken and mouse), homozygosity mapping and whole-exome sequencing identifying splice site mutation eLife Medium 26386247
2018 In zebrafish talpid3 mutant photoreceptors, the majority of photoreceptors lack outer segment development due to defects in basal body positioning and docking at the apical cell surface. Overexpression of constitutively active Rab8a rescues outer segment formation in talpid3 mutant photoreceptors, indicating Ta3's role in early ciliogenesis lies upstream of Rab8a activation in photoreceptors. Zebrafish talpid3 mutant analysis, immunofluorescence for Rab8a localization, constitutively active Rab8a rescue experiment, electroretinograms for functional assessment Scientific reports Medium 29396404
2020 Talpid3 is localized to the mother centriole of radial glial cells (RGCs) and is required for their apical mitosis. Talpid3 associates with Ninein to regulate microtubule organization and maintain the integrity of adherens junctions to anchor RGCs. Genetic silencing of Talpid3 causes abnormal RGC delamination and impairs interkinetic nuclear migration in cell-autonomous and non-autonomous manners. Immunofluorescence localization, co-immunoprecipitation (Talpid3-Ninein interaction), genetic silencing (shRNA/conditional KO), adherens junction integrity assays, live imaging of nuclear migration Cell reports Medium 33326788
2023 Conditional deletion of Talpid3 in muscle stem cells (MuSC) impairs muscle regeneration and self-renewal after injury. Single-cell transcriptomics identified deregulation of Hh and Wnt signaling pathways in TA3-depleted MuSC progeny. Pharmacological activation of Wnt (but not Smoothened/Hh pathway activation) restores muscle regeneration in TA3 conditional KO mice. Tamoxifen-inducible conditional deletion in MuSC, cytotoxic injury model, single-cell transcriptomics, pharmacological rescue with Wnt activator and Smo agonist (purmorphamine) Communications biology Medium 37925530
2015 Cells derived from patients with biallelic KIAA0586 mutations show defective ciliogenesis and abnormal response to SHH-signaling activation. Centriolar maturation appeared unaffected in mutant cells, but an abnormal extended pattern of CEP290 (a centriolar satellite protein) was observed. Rescue of cilia defect with full-length wild-type KIAA0586 confirmed the causal link. Gli3 processing is abnormal in mutant cells. Patient-derived fibroblast ciliogenesis assay, SHH stimulation assay, rescue with wild-type KIAA0586, immunofluorescence for CEP290 pattern, Gli3 processing western blot American journal of human genetics Medium 26166481

Source papers

Stage 0 corpus · 46 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2009 The Talpid3 gene (KIAA0586) encodes a centrosomal protein that is essential for primary cilia formation. Development (Cambridge, England) 113 19144723
2006 The chicken talpid3 gene encodes a novel protein essential for Hedgehog signaling. Genes & development 105 16702409
2016 Tethering of an E3 ligase by PCM1 regulates the abundance of centrosomal KIAA0586/Talpid3 and promotes ciliogenesis. eLife 103 27146717
2014 The CP110-interacting proteins Talpid3 and Cep290 play overlapping and distinct roles in cilia assembly. The Journal of cell biology 98 24421332
1999 Expression of ptc and gli genes in talpid3 suggests bifurcation in Shh pathway. Development (Cambridge, England) 76 10225999
2015 Mutations in KIAA0586 Cause Lethal Ciliopathies Ranging from a Hydrolethalus Phenotype to Short-Rib Polydactyly Syndrome. American journal of human genetics 75 26166481
2015 Functional genome-wide siRNA screen identifies KIAA0586 as mutated in Joubert syndrome. eLife 71 26026149
2015 KIAA0586 is Mutated in Joubert Syndrome. Human mutation 69 26096313
2011 Generation of mice with functional inactivation of talpid3, a gene first identified in chicken. Development (Cambridge, England) 63 21750036
2011 Targeted mutation of the talpid3 gene in zebrafish reveals its conserved requirement for ciliogenesis and Hedgehog signalling across the vertebrates. Development (Cambridge, England) 62 22028029
2015 TALPID3 controls centrosome and cell polarity and the human ortholog KIAA0586 is mutated in Joubert syndrome (JBTS23). eLife 50 26386247
2015 Mutations in human homologue of chicken talpid3 gene (KIAA0586) cause a hybrid ciliopathy with overlapping features of Jeune and Joubert syndromes. Journal of medical genetics 46 26386044
2014 Talpid3-binding centrosomal protein Cep120 is required for centriole duplication and proliferation of cerebellar granule neuron progenitors. PloS one 40 25251415
2019 CEP120 interacts with C2CD3 and Talpid3 and is required for centriole appendage assembly and ciliogenesis. Scientific reports 37 30988386
2004 Craniofacial development in the talpid3 chicken mutant. Differentiation; research in biological diversity 35 15554946
2006 Analysis of talpid3 and wild-type chicken embryos reveals roles for Hedgehog signalling in development of the limb bud vasculature. Developmental biology 28 16959240
2017 PKA-mediated Gli2 and Gli3 phosphorylation is inhibited by Hedgehog signaling in cilia and reduced in Talpid3 mutant. Developmental biology 27 28673820
1975 Intercellular adhesion and formation of aggregates in normal and Talpid-3 mutant chick limb mesenchyme. Journal of cell science 27 1141395
2020 TALPID3 and ANKRD26 selectively orchestrate FBF1 localization and cilia gating. Nature communications 23 32366837
2013 Failure of centrosome migration causes a loss of motile cilia in talpid(3) mutants. Developmental dynamics : an official publication of the American Association of Anatomists 23 23613203
1975 Cell proliferation in the developing wing-bud of normal and talpid3 mutant chick embryos. Journal of embryology and experimental morphology 23 1214111
2019 Mice with a conditional deletion of Talpid3 (KIAA0586) - a model for Joubert syndrome. The Journal of pathology 20 30924151
2018 The ciliopathy protein TALPID3/KIAA0586 acts upstream of Rab8 activation in zebrafish photoreceptor outer segment formation and maintenance. Scientific reports 18 29396404
2020 Talpid3-Mediated Centrosome Integrity Restrains Neural Progenitor Delamination to Sustain Neurogenesis by Stabilizing Adherens Junctions. Cell reports 17 33326788
2014 Loss of cilia causes embryonic lung hypoplasia, liver fibrosis, and cholestasis in the talpid3 ciliopathy mutant. Organogenesis 17 24743779
2019 TALPID3 in Joubert syndrome and related ciliopathy disorders. Current opinion in genetics & development 13 31326647
2018 Homozygosity for the c.428delG variant in KIAA0586 in a healthy individual: implications for molecular testing in patients with Joubert syndrome. Journal of medical genetics 13 30120217
2014 The chicken left right organizer has nonmotile cilia which are lost in a stage-dependent manner in the talpid(3) ciliopathy. Genesis (New York, N.Y. : 2000) 11 24700455
1989 The capacity of normal and talpid3 mutant fowl myogenic cells to migrate in quail limb buds. Anatomy and embryology 10 2735533
2020 The splice c.1815G>A variant in KIAA0586 results in a phenotype bridging short-rib-polydactyly and oral-facial-digital syndrome: A case report and literature review. Medicine 7 32080096
2023 Absence of the primary cilia formation gene Talpid3 impairs muscle stem cell function. Communications biology 5 37925530
2021 TALPID3/KIAA0586 Regulates Multiple Aspects of Neuromuscular Patterning During Gastrointestinal Development in Animal Models and Human. Frontiers in molecular neuroscience 4 35002618
1992 Localization of delta-crystallin RNA during lens morphogenesis and differentiation in the normal and talpid3 chick embryo. The International journal of developmental biology 4 1280155
2022 Hippocampals neurogenesis is impaired in mice with a deletion in the coiled coil domain of Talpid3-implications for Joubert syndrome. Human molecular genetics 3 35470378
1999 Expression of transcription factor c-Rel and apoptosis occurrence in polydactylous and syndactylous limb buds of the talpid3 mutant chick embryo. Apoptosis : an international journal on programmed cell death 3 14634293
2024 Pathogenic KIAA0586/TALPID3 variants are associated with defects in primary and motile cilia. iScience 2 39898050
2022 Compound heterozygous splicing variants in KIAA0586 cause fetal short-rib thoracic dysplasia and cerebellar malformation: Use of exome sequencing in prenatal diagnosis. Molecular genetics & genomic medicine 2 36538006
1989 Cell generation times in normal and talpid3 mutant chick limb mesenchyme. Folia morphologica 2 2634607
2025 Prenatal Diagnosis of Joubert Syndrome 23 With Left Isomerism: A Novel Phenotype Associated With Pathogenic KIAA0586 Variant. Prenatal diagnosis 1 41148001
2024 Expanding the Phenotypic Spectrum of Pathogenic KIAA0586 Variants: From Joubert Syndrome to Hydrolethalus Syndrome. International journal of molecular sciences 1 39063141
2025 Molecular treatment options for patients carrying KIAA0586/TALPID3 variants. Molecular therapy. Nucleic acids 0 40951761
2025 Novel Pathogenic Biallelic Variants in KIAA0586 Expand the Variant Spectrum of Ciliopathies. Cytoskeleton (Hoboken, N.J.) 0 41020477
2024 Targeted Deletion in the Basal Body Protein Talpid3 Leads to Loss of Primary Cilia in Embryonic Stem Cells and Defective Lineage-Specific Differentiation. Cells 0 39682705
2022 Corrigendum: TALPID3/KIAA0586 Regulates Multiple Aspects of Neuromuscular Patterning During Gastrointestinal Development in Animal Models and Human. Frontiers in molecular neuroscience 0 35571366
2018 Publisher Correction: The ciliopathy protein TALPID3/KIAA0586 acts upstream of Rab8 activation in zebrafish photoreceptor outer segment formation and maintenance. Scientific reports 0 30120317
1988 Scale development in talpid3 mutant chick embryos. Journal of anatomy 0 3417549

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