| 2003 |
IFT20 physically interacts with IFT57/Hippi (strong yeast two-hybrid interaction) and with kinesin II subunit KIF3B, and co-immunoprecipitates with IFT88, IFT57, and IFT52 from mouse testis, kidney, and retina lysates, suggesting IFT20 bridges kinesin II with the IFT-B complex. The IFT complex co-fractionates at ~17S in bovine photoreceptor outer segments. |
Yeast two-hybrid, co-immunoprecipitation, sucrose gradient fractionation |
The Journal of biological chemistry |
High |
12821668
|
| 2006 |
IFT20 localizes to the Golgi complex, basal body, and cilia in mammalian cells. Fluorescently tagged IFT20 dynamically moves between the Golgi and the cilium and along ciliary microtubules in living cells. Strong knockdown blocks ciliary assembly; moderate knockdown reduces polycystin-2 in cilia without blocking assembly, suggesting IFT20 functions in delivery of ciliary membrane proteins from the Golgi to the cilium. |
Live-cell fluorescence imaging (FRAP/dynamics), siRNA knockdown, immunofluorescence microscopy |
Molecular biology of the cell |
High |
16775004
|
| 2008 |
IFT20 is anchored to the Golgi complex by the golgin GMAP210/TRIP11. Cells lacking GMAP210 have normal Golgi structure but lose IFT20 Golgi localization; these cells form shorter cilia with reduced polycystin-2, indicating that GMAP210-mediated Golgi anchoring of IFT20 is required for proper sorting of ciliary membrane proteins. |
Mouse knockout (GMAP210), immunofluorescence, co-immunoprecipitation, genetic epistasis |
PLoS genetics |
High |
19112494
|
| 2008 |
Kidney-specific deletion of IFT20 prevents primary cilia formation, causes misorientation of the mitotic spindle in collecting duct cells, and leads to rapid postnatal cystic kidney disease. Non-dividing cells lacking cilia also misposition their centrosomes, and later-stage cyst cells show increased canonical Wnt signaling and proliferation. |
Conditional knockout mouse (floxed Ift20 x collecting duct Cre), immunofluorescence, histology |
The Journal of cell biology |
High |
18981227
|
| 2009 |
SPEF2 (an IFT-associated protein essential for sperm tail development) directly interacts with IFT20 in the testis, as demonstrated by yeast two-hybrid and co-immunoprecipitation. Both proteins co-localize in differentiating male germ cells at the Golgi complex, manchette, basal body, and midpiece. |
Yeast two-hybrid, co-immunoprecipitation, immunofluorescence co-localization |
Biology of reproduction |
Medium |
19889948
|
| 2011 |
IFT20 binds directly to rhodopsin and RG-opsin (cone opsins), acting both as part of the IFT particle and independently. Acute deletion of IFT20 in cones causes opsin accumulation in the inner segment/Golgi even when the connecting cilium is still intact, establishing IFT20's role in trafficking opsins from the Golgi to the base of the cilium. |
Conditional knockout mouse (cone-specific and tamoxifen-inducible Cre), co-immunoprecipitation (IFT20-rhodopsin binding), immunofluorescence |
Molecular biology of the cell |
High |
21307337
|
| 2014 |
Acute deletion of IFT20 (but not IFT140) causes rhodopsin/opsin accumulation at the Golgi complex, while IFT140 deletion causes opsin accumulation in the inner segment plasma membrane. This genetic epistasis places IFT20 in opsin transport from the Golgi to the ciliary base, distinct from IFT140's role in transport through the connecting cilium. |
Conditional knockout mouse (IFT20 and IFT140 separate deletions), immunofluorescence, genetic epistasis |
Cytoskeleton (Hoboken, N.J.) |
High |
24619649
|
| 2015 |
IFT20 interacts with the core planar cell polarity protein Vangl2 (by co-immunoprecipitation) and its deletion in the cochlea disrupts asymmetric Vangl2 accumulation in cochlear cells and causes misoriented hair cell stereociliary bundles. IFT20 localizes to filamentous actin as well as microtubules in cochlear cells. |
Conditional knockout mouse, co-immunoprecipitation, immunofluorescence |
Development (Cambridge, England) |
Medium |
25605782
|
| 2015 |
In primary CD4+ T cells lacking IFT20, TCR-mediated signaling and recruitment of the signaling adaptor LAT to the immune synapse are reduced, while centrosome polarization is unaffected. Conditional IFT20-deficient mice fail to mount effective antigen-specific T-cell responses in vivo, demonstrating IFT20's role in delivering the intracellular LAT pool to the immune synapse. |
Conditional knockout mouse (T cell-specific Cre), immunofluorescence, in vivo T cell response assays, adoptive transfer colitis model |
Proceedings of the National Academy of Sciences of the United States of America |
High |
26715756
|
| 2016 |
IFT20 is essential for spermiogenesis and male fertility. Germ cell-specific Ift20 deletion causes infertility with reduced sperm counts, abnormal spermatid head shaping, disrupted axonemes, and failure to incorporate sperm flagellar proteins ODF2 and SPAG16L into tails. IFT20 loss also reduces assembly of IFT complexes to lighter density fractions and decreases ATG16L expression in testis. |
Conditional knockout mouse (Stra8-Cre), electron microscopy, immunofluorescence, sucrose gradient fractionation, Western blot |
Molecular biology of the cell |
High |
27682589
|
| 2016 |
A VPS15 patient mutation (R998Q) impairs Golgi trafficking; in patient fibroblasts, IFT20 fails to localize to vesicles trafficking to the cilium and is restricted to the Golgi. VPS15 interacts with the golgin GM130 and this complex is required for IFT20-dependent sorting from the cis-Golgi to the primary cilium. |
Patient fibroblasts, co-immunoprecipitation (VPS15-GM130), immunofluorescence, yeast humanization complementation assay |
Nature communications |
Medium |
27882921
|
| 2017 |
Ror2 receptor tyrosine kinase signaling upregulates IFT20 in tumor cells lacking cilia. IFT20 promotes Golgi ribbon formation by affecting the GM130-AKAP450 complex that nucleates Golgi-derived microtubules, and enhances transport efficiency through the Golgi to drive polarized secretion for cell migration and invasion. |
Knockdown/overexpression in tumor cell lines, immunofluorescence (Golgi morphology, microtubule nucleation assays), co-immunoprecipitation, invasion assays |
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 ciliary receptor signaling. In IFT20-depleted cells, c-Cbl and Cbl-b are destabilized and degraded, causing PDGFRα to localize aberrantly to the plasma membrane and become overactivated. |
siRNA knockdown, co-immunoprecipitation, ubiquitination assays, immunofluorescence, receptor activation 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, CSN1/GPS1, and ERGIC-53/LMAN1 as IFT20 binding partners. Direct interaction of IFT20 with IFT54 and GMAP-210 was confirmed by pulldown. Depletion of IFT54, ARPC3, or ERGIC-53 impaired TCR accumulation and phosphotyrosine signaling at the immune synapse. |
Quantitative mass spectrometry, pulldown assays, RNAi knockdown, confocal imaging of antigen-specific conjugates |
Journal of cell science |
High |
28154159
|
| 2019 |
IFT20 is required for lysosome biogenesis in T cells by controlling the retrograde trafficking of the cation-independent mannose-6-phosphate receptor (CI-MPR) to the trans-Golgi network, coupling recycling CI-MPRs to the microtubule motor dynein. IFT20 deficiency impairs lysosomal targeting of acid hydrolases and causes TFEB-dependent upregulation of lysosomal gene expression. |
siRNA/conditional KO, CI-MPR trafficking assays, dynein co-immunoprecipitation, lysosome function assays (acid hydrolase activity), TFEB reporter assays |
Cell death and differentiation |
High |
31142807
|
| 2019 |
GMAP210 deletion in spermatocytes/spermatids reduces IFT20 expression and disrupts its acrosomal localization, causing acrosome biogenesis defects and reduced male fertility. This confirms GMAP210 determines IFT20 levels and localization in germ cells, analogous to its Golgi-anchoring role in somatic cells. |
Conditional knockout mouse (Stra8-iCre x floxed Gmap210), immunofluorescence, electron microscopy, Western blot |
American journal of physiology. Cell physiology |
Medium |
31577511
|
| 2020 |
COPS5 (COP9 signalosome subunit 5) is a major binding partner of IFT20 in the testis (identified by interaction screen). In Cops5 conditional KO testes, IFT20 expression is reduced and it is no longer present in the acrosome. Conversely, in conditional Ift20 KO mice, COPS5 localization and expression are unchanged, placing COPS5 upstream of IFT20 acrosomal localization. |
Co-immunoprecipitation, conditional knockout mouse, immunofluorescence, Western blot |
Biology of reproduction |
Medium |
31373619
|
| 2020 |
IFT20 is required for β1-integrin recycling and focal adhesion (FA) dynamics during polarized cell migration, independently of the primary cilium. Loss of Ift20 prevents β1-integrins endocytosed during FA disassembly from exiting Rab5+ early endosomes, disrupting integrin recycling to the cell surface and impeding FA reformation. In vivo, IFT20 is required for hair follicle stem cell migration during wound healing. |
Conditional knockout (keratinocyte/hair follicle stem cell specific), live-cell imaging of FA dynamics, integrin trafficking assays (endocytosis/recycling), lineage tracing, wound healing assays |
Molecular biology of the cell |
High |
32520638
|
| 2021 |
IFT20 interacts with ATG16L1 (requiring the WD40 domain of ATG16L1 and a Y-E-F-I motif in IFT20) and co-transports with ATG16L1 to the primary cilium upon serum deprivation. Perturbation of the ATG16L1/IFT20 complex impairs INPP5E trafficking to the cilium and disrupts ciliary phosphoinositide composition (accumulation of PI4,5P2, loss of PI4P). |
Co-immunoprecipitation, domain mutagenesis (WD40 and Y-E-F-I motif), immunofluorescence, lipid composition analysis |
Cell reports |
High |
33910006
|
| 2021 |
IFT20 recruits ATG16L1 to early endosomes (tagged by BECLIN1/VPS34/Rab5 complex) to promote autophagosome biogenesis under basal conditions in T cells. IFT20 interacts with GMAP210 at the Golgi and Rab5 at early endosomes; its CC domain is essential for pro-autophagic activity. GMAP210 depletion disperses ATG16L1 from the Golgi but does not impair basal autophagy, whereas IFT20 loss does. |
siRNA knockdown, co-immunoprecipitation (IFT20-Rab5, IFT20-ATG16L1), domain mutagenesis (CC domain), autophagic flux assays, immunofluorescence |
Frontiers in cell and developmental biology |
High |
33829015
|
| 2021 |
IFT20 localizes at the trans-Golgi/TGN in breast cancer cells and mediates transport of migration regulators Numb and Ctnnal1 from the TGN to the plasma membrane via Rab8a-positive vesicles; IFT20 directly interacts with Ctnnal1 and Numb (Strep-Tactin pulldown). Loss of IFT20 promotes lamellipodia formation and cell migration. |
Knockout, BioID proximity labeling, Strep-Tactin pulldown, co-localization (Rab8a vesicles), migration assays |
Frontiers in cell and developmental biology |
Medium |
33748116
|
| 2022 |
MEIG1 determines the manchette localization of IFT20 and IFT88 in elongating spermatids. In Meig1 knockout mice, IFT20 and IFT88 are absent from the manchette but their localizations remain normal in earlier germ cell stages. MEIG1 forms a complex with IFT20 and IFT88 (co-immunoprecipitation from testis). IFT20 loss causes both IFT proteins to shift to lighter sucrose gradient fractions, but MEIG1 localization is unaffected in IFT20 KO, placing MEIG1 upstream of IFT complex assembly at the manchette. |
Conditional KO (Meig1 and Ift20), co-immunoprecipitation, sucrose gradient fractionation, immunofluorescence |
Developmental biology |
High |
35257720
|
| 2017 |
IFT54 C-terminal coiled-coil (CC) domain binds IFT20 and is required for its recruitment to the basal body and incorporation into IFT complexes. Complete loss of IFT54 or deletion of its CC domain destabilizes IFT20, establishing IFT54 as essential for IFT20 stability in the IFT-B complex. |
Chlamydomonas genetics (ift54 mutants + domain truncations), immunofluorescence, Western blot, IFT complex assembly assays |
Cellular and molecular life sciences : CMLS |
High |
28417161
|
| 2023 |
IFT20 interacts with TSG101, a protein that endocytoses ubiquitinated TCRs. The IFT20-TSG101 interaction promotes SMAC (supramolecular activation cluster) formation at the immune synapse, which amplifies AKT-mTOR signaling in CD4+ T cells. IFT20-deficient CD4+ T cells show SMAC malformation and reduced AKT-mTOR activity, aerobic glycolysis, and cellular respiration. |
Co-immunoprecipitation (IFT20-TSG101), IFT20 conditional KO mouse, immunofluorescence (SMAC imaging), metabolic assays, in vivo airway inflammation model |
Cellular & molecular immunology |
Medium |
37029318
|
| 2024 |
DLG1 functions upstream of SDCCAG3 and IFT20 to control ciliary targeting of polycystin-2 in kidney epithelial cells. SDCCAG3 and IFT20 form a complex (biochemical approaches + AlphaFold modelling) that associates at least indirectly with DLG1. Loss of DLG1 reduces SDCCAG3, IFT20, and polycystin-2 in cilia; a CAKUT-associated DLG1 variant p.T489R fails to rescue this phenotype. |
Conditional KO (Dlg1 in mouse kidney), proximity labeling proteomics (BioID), immunofluorescence, biochemical co-IP, AlphaFold structural modelling |
EMBO reports |
Medium |
38849673
|
| 2023 |
IFT20 triggers β-arrestin-1 to bind ASK1, promoting ubiquitination and degradation of ASK1, thereby attenuating ASK1-JNK signaling and conferring paclitaxel resistance in breast cancer cells. IFT20 knockdown enhances ASK1 signaling and apoptosis in response to paclitaxel. |
Knockdown/overexpression, co-immunoprecipitation (IFT20-β-arrestin-1-ASK1 complex), ubiquitination assays, 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. WWTR1 transcriptionally upregulates TβRII expression; IFT20 and WWTR1 deficiency in osteoblasts synergistically promotes adipogenesis and osteoclastogenesis. |
Conditional KO mouse (osteoblast-specific double KO), co-immunoprecipitation (IFT20-TβRII), ubiquitination assays, transcriptional reporter assays |
Research square (preprint) |
Low |
38562782
|
| 2025 |
IFT20 is required for MPR recycling to the trans-Golgi network in cytotoxic T lymphocytes, ensuring proper granzyme B localization to lytic granules. IFT20 deficiency impairs CTL killing capability, and defective lytic granule biogenesis is associated with TFEB-dependent upregulation of lysosomal and cytotoxic machinery gene expression. |
Conditional KO (T cell-specific), MPR trafficking assays, granzyme B localization, CTL killing assays, TFEB modulation, transcriptomic analysis |
Cell death & disease |
Medium |
40389449
|
| 2025 |
IFT20 regulates VE-cadherin localization at adherens junctions in lymphatic endothelial cells by promoting its recycling from RAB5+ endosomes back to the cell surface, thereby sequestering VEGFR-3 at the cell surface and limiting pro-lymphangiogenic signaling. IFT20 deletion causes VE-cadherin accumulation in RAB5+ endosomes, enhanced VEGFR-3 signaling, and impaired lymph drainage. |
IFT20 KD/KO (in vitro and in vivo), immunofluorescence (VE-cadherin and RAB5 co-localization), VEGFR-3 signaling assays, in vivo lymph drainage measurement |
bioRxivpreprint |
Low |
bio_10.1101_2025.01.15.631989
|