| 2003 |
IFT20 physically interacts with IFT57/Hippi and the kinesin II subunit KIF3B as determined by yeast two-hybrid, and all four IFT proteins (IFT88, IFT57, IFT52, IFT20) co-immunoprecipitate from mouse testis, kidney, and retina lysates, co-fractionating at ~17S. IFT20 appears to bridge kinesin II with the IFT complex. |
Yeast two-hybrid, co-immunoprecipitation, sucrose gradient sedimentation |
The Journal of biological chemistry |
High |
12821668
|
| 2006 |
IFT20 localizes to the Golgi complex, basal body, and cilia. In living cells, fluorescently tagged IFT20 is highly dynamic and moves between the Golgi complex and the cilium as well as along ciliary microtubules. Strong knockdown of IFT20 blocks ciliary assembly; moderate knockdown reduces polycystin-2 localization to cilia without blocking assembly, suggesting IFT20 functions in delivery of ciliary membrane proteins from the Golgi to the cilium. |
Live-cell fluorescence imaging (FRAP and trafficking), siRNA knockdown, immunofluorescence microscopy |
Molecular biology of the cell |
High |
16775004
|
| 2008 |
GMAP210/TRIP11 anchors IFT20 to the Golgi complex; cells lacking GMAP210 have normal Golgi structure but IFT20 is no longer localized to the Golgi. Cilia on GMAP210 mutant cells are shorter and have reduced polycystin-2, indicating GMAP210 and IFT20 function together at the Golgi in sorting/transport of proteins destined for the ciliary membrane. |
Genetic knockout (GMAP210 null mice), immunofluorescence, Western blot, cilium length measurement |
PLoS genetics |
High |
19112494
|
| 2008 |
Kidney-specific deletion of IFT20 prevents cilia formation and causes cystic kidney disease. Dividing collecting duct cells lacking IFT20 fail to orient their mitotic spindles along the tubule, and non-dividing cells misposition their centrosomes. Later-stage cysts show increased canonical Wnt signaling and increased cell proliferation, coupling IFT20 loss to altered Wnt pathway output. |
Conditional knockout (Cre-lox, collecting duct-specific), immunofluorescence for spindle orientation, Wnt signaling assay |
The Journal of cell biology |
High |
18981227
|
| 2009 |
SPEF2 interacts with IFT20 in the testis, as demonstrated by yeast two-hybrid assay and co-immunoprecipitation. The two proteins co-localize in differentiating male germ cells at the Golgi complex, manchette, basal body, and midpiece of the sperm tail. |
Yeast two-hybrid, co-immunoprecipitation, immunofluorescence co-localization |
Biology of reproduction |
Medium |
19889948
|
| 2011 |
IFT20 is required for opsin trafficking from the Golgi to the connecting cilium in photoreceptors. Deletion of IFT20 in cones causes opsin accumulation in the inner segment, and deletion in rods causes rapid rhodopsin accumulation at the Golgi complex. IFT20, acting both as part of the IFT particle and independently, binds to rhodopsin and RG-opsin. |
Conditional knockout (cone-specific and tamoxifen-inducible Cre), co-immunoprecipitation, immunofluorescence |
Molecular biology of the cell |
High |
21307337
|
| 2014 |
IFT20 and IFT140 play distinct roles in opsin transport: acute deletion of IFT20 causes opsin to accumulate at the Golgi complex, whereas acute deletion of IFT140 causes opsin to accumulate in the plasma membrane of inner segments (not Golgi). This supports a model where IFT20 moves opsin from the Golgi to the base of the cilium, and IFT140 carries it through the connecting cilium. |
Conditional knockout (acute tamoxifen-inducible deletion of Ift20 and Ift140), immunofluorescence for opsin localization |
Cytoskeleton (Hoboken, N.J.) |
High |
24619649
|
| 2015 |
IFT20 interacts with the core PCP molecule Vangl2 by co-immunoprecipitation, and deletion of IFT20 results in disruption of asymmetric accumulation of Vangl2 in cochlear cells, causing mis-oriented hair cell stereociliary bundles. IFT20 also localizes to filamentous actin in addition to microtubules, implicating it in selective trafficking of membrane proteins upstream of cytoskeletal reorganization. |
Conditional knockout, co-immunoprecipitation, immunofluorescence for PCP marker asymmetry and bundle orientation |
Development (Cambridge, England) |
Medium |
25605782
|
| 2015 |
In primary CD4+ T cells, IFT20 is required for TCR-mediated signaling and recruitment of the signaling adaptor LAT to the immune synapse. Loss of IFT20 leaves centrosome polarization unaffected but impairs LAT delivery, reducing CD4+ T-cell activation, proliferation, and in vivo antigen-specific T-cell responses and colitis induction. |
Conditional knockout (T-cell-specific), confocal imaging of immune synapse, adoptive transfer experiments |
Proceedings of the National Academy of Sciences of the United States of America |
High |
26715756
|
| 2016 |
Deletion of IFT20 in male germ cells causes infertility with reduced sperm counts and motility, abnormally shaped spermatid heads, disrupted axonemes, and failure to incorporate sperm flagella proteins ODF2 and SPAG16L into sperm tails. ODF2 and SPAG16L form complexes of lighter density in the absence of IFT20. IFT20 is also involved in removing excess cytoplasmic components, possibly through association with autophagy protein ATG16. |
Conditional knockout (germ cell-specific Cre), electron microscopy, sucrose gradient fractionation, immunofluorescence, Western blot |
Molecular biology of the cell |
High |
27682589
|
| 2016 |
A mutation in VPS15 (PIK3R4) impairs IFT20 release from the cis-Golgi; in patient fibroblasts bearing the VPS15-R998Q mutation, IFT20 is restricted to the Golgi and not present in vesicles trafficking to the cilium. VPS15 interacts with golgin GM130 at the Golgi, and this complex facilitates IFT20-dependent sorting and transport of membrane proteins from the cis-Golgi to the primary cilium. |
Patient fibroblast analysis, immunofluorescence, co-immunoprecipitation of VPS15 with GM130, humanized yeast complementation |
Nature communications |
Medium |
27882921
|
| 2017 |
Ror2 receptor tyrosine kinase signaling upregulates IFT20 in tumor cells lacking primary cilia. IFT20 mediates Ror2-induced tumor invasiveness by regulating nucleation of Golgi-derived microtubules through the GM130-AKAP450 complex, promoting Golgi ribbon formation for polarized secretion, and enhancing transport efficiency through the Golgi complex. |
Knockdown/overexpression in cancer cells, Golgi morphology analysis, invadopodia assay, microtubule nucleation assay |
Scientific reports |
Medium |
28127051
|
| 2017 |
IFT20 interacts with E3 ubiquitin ligases c-Cbl and Cbl-b and is required for Cbl-mediated ubiquitination and internalization of PDGFRα for feedback inhibition of receptor signaling at the primary cilium. In IFT20-depleted cells, PDGFRα localizes aberrantly to the plasma membrane and is overactivated after PDGF-AA stimulation because c-Cbl and Cbl-b are destabilized and degraded. |
siRNA knockdown, co-immunoprecipitation, ubiquitination assays, confocal imaging of PDGFRα localization, receptor signaling assays |
The Journal of cell biology |
High |
29237719
|
| 2017 |
Quantitative mass spectrometry of the IFT20 interactome in Jurkat T cells identified IFT57, IFT88, IFT54/TRAF3IP1, GMAP-210/TRIP11, ARPC3, COP9 signalosome subunit-1 (CSN1/GPS1), and ERGIC-53/LMAN1 as binding partners. Direct interactions between IFT20 and IFT54 and between IFT20 and GMAP-210 were confirmed by pulldown assays. Depletion of IFT54, ARPC3, or ERGIC-53 impaired TCR accumulation and phosphotyrosine signaling at the immune synapse. |
Quantitative mass spectrometry (interactome), pulldown assays, RNA interference, confocal imaging of immune synapse |
Journal of cell science |
Medium |
28154159
|
| 2017 |
IFT54's C-terminal coiled-coil (CC) domain binds IFT20, and loss of the CC domain or complete loss of IFT54 destabilizes IFT20 protein. The CC domain of IFT54 is required for IFT54 recruitment to the basal body and incorporation into IFT complexes. |
Domain deletion mutants in Chlamydomonas, immunofluorescence, Western blot to assess IFT20 stability |
Cellular and molecular life sciences : CMLS |
Medium |
28417161
|
| 2019 |
IFT20 is required for lysosome biogenesis and function in T cells by controlling lysosomal targeting of acid hydrolases. This function involves IFT20 regulating retrograde traffic of the cation-independent mannose-6-phosphate receptor (CI-MPR) to the trans-Golgi network by coupling recycling CI-MPRs to the microtubule motor dynein. Loss of IFT20 results in autophagic clearance defect, lipid droplet accumulation, and upregulation of TFEB-dependent lysosomal gene network. |
Conditional knockout (T cell-specific), lysosomal enzyme targeting assays, CI-MPR trafficking analysis, dynein co-immunoprecipitation, TFEB transcriptional assays |
Cell death and differentiation |
High |
31142807
|
| 2019 |
GMAP210 is essential for acrosome biogenesis, normal mitochondrial sheath formation, and male fertility in mice. Loss of GMAP210 in spermatocytes/spermatids significantly reduces IFT20 expression and disrupts its acrosomal localization, confirming GMAP210 as an upstream determinant of IFT20 levels and localization in male germ cells. |
Conditional knockout (Stra8-iCre), immunofluorescence, Western blot, electron microscopy |
American journal of physiology. Cell physiology |
Medium |
31577511
|
| 2020 |
COPS5 (COP9 signalosome subunit 5) is a major binding partner of IFT20 in the testis. Loss of COPS5 in male germ cells leads to dramatic reduction of IFT20 expression and its absence from the acrosome (but retention in Golgi of spermatocytes). Conversely, loss of IFT20 does not change COPS5 localization, establishing a one-directional dependency. |
Co-immunoprecipitation, conditional knockout, immunofluorescence, Western blot |
Biology of reproduction |
Medium |
31373619
|
| 2020 |
Genetic ablation of IFT20 in keratinocytes slows wound healing migration. This is independent of primary cilia and is caused by defective integrin recycling: loss of IFT20 prevents β1 integrins from being transferred out of Rab5+ early endosomes after endocytosis during focal adhesion disassembly, blocking their recycling to the cell surface and impairing focal adhesion reformation. In vivo, IFT20 loss in hair follicle stem cells impairs their migration during wound healing. |
Conditional knockout (keratinocyte and hair follicle stem cell-specific), live-cell imaging of FA dynamics, Rab5 endosome trafficking assays, integrin recycling assays, lineage tracing |
Molecular biology of the cell |
High |
32520638
|
| 2020 |
SPATA1 is an IFT20 binding protein in the testis identified by yeast two-hybrid screening, confirmed by co-immunoprecipitation and co-localization. SPATA1 localizes to the acrosome of developing spermatids. In conditional Ift20 knockout mice, SPATA1 expression level and acrosomal localization are unchanged, indicating SPATA1 is not downstream of IFT20 for its own targeting. |
Yeast two-hybrid, co-immunoprecipitation, immunofluorescence, conditional Ift20 KO |
Developmental dynamics |
Medium |
31816150
|
| 2021 |
IFT20 interacts with ATG16L1 via the WD40 domain of ATG16L1 and a Y-E-F-I motif in IFT20, and they are co-transported to the primary cilium during ciliogenesis. Perturbation of the ATG16L1/IFT20 complex alters INPP5E trafficking to the primary cilium, causing aberrant ciliary phosphoinositide composition (accumulation of PI4,5P2, loss of PI4P). ATG16L1 also interacts with INPP5E. |
Co-immunoprecipitation, domain mutagenesis (WD40, Y-E-F-I motif), confocal imaging, phosphoinositide staining |
Cell reports |
Medium |
33910006
|
| 2021 |
IFT20 promotes autophagosome biogenesis in T cells by recruiting ATG16L1 to early endosomes tagged by the BECLIN1/VPS34/Rab5 complex, resulting in local LC3 accumulation. IFT20's CC domain is essential for its pro-autophagic activity. IFT20 also interacts with GMAP210 at the Golgi and Rab5 at early endosomes to mediate ATG16L1 localization; GMAP210 depletion disperses ATG16L1 from Golgi but does not affect basal autophagy. |
siRNA knockdown, co-immunoprecipitation, confocal imaging of ATG16L1 and LC3 localization, domain mutagenesis (CC domain) |
Frontiers in cell and developmental biology |
Medium |
33829015
|
| 2021 |
IFT20 localizes at the trans-Golgi and TGN in breast cancer cells lacking primary cilia and mediates vesicular transport of cell migration regulators (Numb and Ctnnal1) from the TGN to the plasma membrane via Rab8a-positive vesicles. IFT20 directly interacts with Ctnnal1 and Numb as shown by Strep-Tactin pulldown. Loss of IFT20 promotes EMT, lamellipodia formation, and cell migration. |
BioID proximity labeling, Strep-Tactin pulldown, confocal colocalization, CRISPR knockout |
Frontiers in cell and developmental biology |
Medium |
33748116
|
| 2022 |
MEIG1 is required for IFT20 and IFT88 localization to the manchette in elongating spermatids. In Meig1 knockout mice, IFT20 and IFT88 are absent from the manchette despite normal localization in spermatocytes and round spermatids. MEIG1, IFT20, and IFT88 form a complex as shown by co-immunoprecipitation from mouse testis extracts. Loss of MEIG1 also shifts IFT20 and IFT88 to lighter density fractions in sucrose gradient and significantly reduces their mRNA and protein levels. |
Conditional and conventional knockout (Meig1 KO), co-immunoprecipitation, immunofluorescence, sucrose gradient sedimentation, Western blot |
Developmental biology |
Medium |
35257720
|
| 2022 |
IFT20 controls mesenchymal stem cell (MSC) lineage allocation by regulating glucose metabolism through the TGF-β-Smad2/3-Glut1 signaling axis. Loss of IFT20 in MSCs decreases TGF-β-Smad2/3 activity and reduces Smad2/3 binding to the Glut1 promoter, thereby downregulating Glut1 expression, suppressing glucose uptake and ATP/lactate production, and promoting adipocyte over osteoblast formation. |
Conditional knockout (MSC-specific), ChIP for Smad2/3 binding to Glut1 promoter, glucose uptake assay, metabolic flux assay, signaling pathway analysis |
Redox biology |
Medium |
35751983
|
| 2023 |
IFT20 interacts with TSG101 (a protein involved in ubiquitinated TCR endocytosis), and this IFT20-TSG101 interaction promotes SMAC formation at the immune synapse, amplifying AKT-mTOR signaling in CD4+ T cells. IFT20-deficient CD4+ T cells show SMAC malformation, reduced proliferation, impaired aerobic glycolysis, and diminished cellular respiration. Mice with T-cell-specific IFT20 deficiency have reduced allergen-induced airway inflammation. |
Co-immunoprecipitation (IFT20-TSG101), conditional knockout, immune synapse imaging, AKT-mTOR signaling assays, metabolic assays, in vivo allergy model |
Cellular & molecular immunology |
Medium |
37029318
|
| 2023 |
IFT20 drives paclitaxel resistance in breast cancer cells by triggering β-arrestin-1 to bind ASK1, promoting ASK1 ubiquitination and degradation, thereby attenuating ASK1-JNK signaling and allowing cells to escape apoptosis. IFT20 knockdown enhances paclitaxel-induced apoptosis. |
Co-immunoprecipitation (IFT20 with β-arrestin-1), ubiquitination assay for ASK1, knockdown/overexpression, apoptosis assays |
Molecular cancer research : MCR |
Medium |
36573960
|
| 2024 |
IFT20 interacts with TGF-β receptor type II (TβRII) and enhances TβRII stability by blocking c-Cbl-mediated ubiquitination and degradation of TβRII in osteoblasts. Loss of both IFT20 and WWTR1 synergistically inhibits osteogenesis and promotes adipogenesis. |
Co-immunoprecipitation, ubiquitination assay, conditional double KO in osteoblasts |
Research square (preprint)preprint |
Low |
38562782
|
| 2024 |
DLG1 functions upstream of SDCCAG3 and IFT20 to control ciliary targeting of polycystin-2 (PC2) in kidney epithelial cells. Loss of DLG1 reduces SDCCAG3, IFT20, and PC2 in cilia. Biochemical approaches and AlphaFold modeling indicate SDCCAG3 and IFT20 form a complex that associates indirectly with DLG1. |
Conditional knockout (Dlg1), proximity labeling proteomics, immunofluorescence, biochemical co-precipitation, AlphaFold modeling |
EMBO reports |
Medium |
38849673
|
| 2025 |
IFT20 is required for MPR recycling to the trans-Golgi network, proper granzyme B (GZMB) localization to lytic granules (LGs), and CTL killing capability. IFT20 deficiency impairs LG biogenesis and activates compensatory upregulation of lysosomal and LG genes via TFEB. Modulation of TFEB alters LG-related gene expression and CTL-mediated cytotoxicity. |
Conditional knockout (CTL-specific), immunofluorescence for MPR and GZMB localization, cytotoxicity assays, TFEB modulation, gene expression analysis |
Cell death & disease |
Medium |
40389449
|
| 2025 |
IFT20 loss in lymphatic endothelial cells causes accumulation of VE-cadherin in Rab5+ early endosomes and impairs its recycling to adherens junctions, leading to discontinuous junctions, enhanced and sustained VEGFR-3 signaling after VEGF-C treatment, excessive lymphangiogenesis, and impaired lymph drainage in mice. |
IFT20 knockdown/KO (lymphatic-specific), immunofluorescence for VE-cadherin and Rab5 localization, VEGFR-3 signaling assays, in vivo lymphangiogenesis models |
bioRxivpreprint |
Low |
bio_10.1101_2025.01.15.631989
|
| 2025 |
IFT20 depletion in RPE cells impairs photoreceptor outer segment phagocytosis by reducing outer segment binding and altering apical membrane morphology, and causes mitochondrial metabolic alterations. Loss of IFT88 produces a similar phenotype whereas loss of Bbs6 does not, placing IFT20 and IFT88 in a specific phagocytosis-enabling pathway. |
Conditional KO/siRNA depletion in RPE-J cells, phagocytosis binding assays, proteomics, mitochondrial metabolism assays |
bioRxivpreprint |
Low |
bio_10.1101_2025.10.16.682843
|
| 2025 |
IFT20 knockout reduces the protein levels of both IFT88 and IFT140 and abrogates IFT88 localization at the basal body and ciliary axoneme; IFT140 localization at the ciliary axoneme is also impaired but its basal body localization is unaffected. IFT20 does not affect CP110 removal from the mother centriole or MKS3 recruitment to the transition zone. Mass spectrometry of IFT20 interactors confirms IFT components as the main binding partners. |
CRISPR-Cas9 knockout, immunofluorescence, immunoblotting, mass spectrometry |
Journal of clinical laboratory analysis |
Medium |
40192002
|