Affinage

IFT88

Intraflagellar transport protein 88 homolog · UniProt Q13099

Length
824 aa
Mass
93.2 kDa
Annotated
2026-04-28
72 papers in source corpus 25 papers cited in narrative 25 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

IFT88 is a TPR-repeat-containing core subunit of the IFT-B complex that is essential for ciliogenesis across metazoans and functions in multiple cilia-independent processes including mitotic spindle orientation, cell-cycle control, and cell migration. Within the IFT-B complex, IFT88 forms a ternary scaffold with IFT52 and IFT46, undergoes bidirectional intraflagellar transport along the axoneme, and its entry into the ciliary compartment is gated by the transition zone component TCTN2 (PMID:20435895, PMID:11290289, PMID:29866362). Outside the cilium, IFT88 localizes to the centrosome via its TPR motifs, participates in dynein1-driven transport of microtubule-nucleating factors to spindle poles, concentrates at kinetochore-fiber minus-ends to recruit NuMA for proper chromosome alignment, interacts with the Rb-regulator Che-1 to restrain G1–S progression, and maintains leading-edge microtubules during cell migration (PMID:17264151, PMID:21441926, PMID:31312011, PMID:26465598). IFT88 protein stability is regulated by competing post-translational modifications: XIAP-mediated ubiquitination (enhanced by TGF-β) targets IFT88 for proteasomal degradation promoting cilia loss and fibrosis, whereas UFL1-mediated UFMylation at Lys572 antagonizes ubiquitination by PJA2 and stabilizes IFT88 (PMID:38351372, PMID:41272290).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2000 High

    Establishing IFT88 as essential for ciliogenesis resolved the question of which IFT particle subunits are individually required for cilium assembly, showing that loss of a single IFT-B component abolishes flagella/cilia across species.

    Evidence Insertional mutagenesis in Chlamydomonas and Tg737 mutant mice with EM and light microscopy

    PMID:11062270

    Open questions at the time
    • Mechanism by which IFT88 contributes to IFT particle integrity not defined
    • Mammalian null (not hypomorphic) phenotype not yet characterized
  2. 2001 High

    Direct visualization of IFT88 (OSM-5) undergoing bidirectional transport in living cilia demonstrated that IFT88 is a bona fide cargo of the IFT machinery, not merely a structural requirement.

    Evidence OSM-5::GFP time-lapse imaging in C. elegans sensory neurons with transgenic rescue

    PMID:11290289

    Open questions at the time
    • Speed and processivity of IFT88-containing trains not quantified
    • Post-translational regulation of IFT88 transport not addressed
  3. 2002 High

    Demonstrating that IFT88 is required for photoreceptor outer segment assembly extended the ciliary requirement to a specialized sensory structure and linked IFT88 to retinal degeneration.

    Evidence Tg737 mutant mice, immunolocalization to connecting cilium, histological analysis of retinal degeneration

    PMID:11916979

    Open questions at the time
    • Specific outer segment cargoes transported by IFT88 not identified
    • Whether phenotype is developmental versus maintenance not resolved
  4. 2007 High

    Discovery of IFT88's centrosomal localization and interaction with the Rb-regulator Che-1 revealed a cilia-independent role in G1–S cell-cycle control, fundamentally expanding IFT88 function beyond ciliogenesis.

    Evidence Cell fractionation, Co-IP of IFT88–Che-1, RNAi and overexpression cell-cycle assays in human cells

    PMID:17264151

    Open questions at the time
    • Direct phosphorylation or modification linking IFT88 to Rb pathway not characterized
    • Whether Che-1 interaction is TPR-dependent not tested
  5. 2010 High

    Reconstitution of the IFT88–IFT52–IFT46 ternary complex defined the minimal interaction network within the IFT-B core, answering which subunits directly contact IFT88.

    Evidence Yeast two-hybrid, bacterial coexpression pulldown, and chemical cross-linking

    PMID:20435895

    Open questions at the time
    • Structural basis of the ternary complex not determined at atomic resolution
    • How the ternary core integrates into the full IFT-B complex not shown
  6. 2011 High

    Identification of IFT88 in a dynein1-driven complex that delivers microtubule-nucleating factors to spindle poles established a direct mitotic mechanism explaining spindle orientation defects upon IFT88 loss.

    Evidence siRNA in human cells, mouse mutant kidney cells, zebrafish embryos; live imaging and Co-IP

    PMID:21441926

    Open questions at the time
    • Identity of all cargo proteins in the IFT88–dynein1 spindle complex not exhaustive
    • Whether IFT88's ciliary and mitotic pools are independently regulated is unknown
  7. 2012 Medium

    Conditional deletion in chondrocytes revealed that IFT88-dependent cilia transduce Ihh signaling to restrain Wnt/β-catenin activity, placing IFT88 at a signaling crossroads between Hedgehog and Wnt pathways in skeletal development.

    Evidence Conditional Ift88 KO mice, gene expression profiling, nuclear β-catenin immunohistochemistry

    PMID:23034798

    Open questions at the time
    • Whether IFT88 directly modulates Wnt pathway components or only indirectly via Hh is unclear
    • Single tissue context studied
  8. 2013 High

    Maternal-zygotic IFT88 mutant zebrafish lacking all cilia still displayed oriented cell division defects without PCP phenotypes, formally separating IFT88's mitotic role from both cilia and planar cell polarity.

    Evidence MZ mutant zebrafish, live imaging, division orientation quantification during gastrulation

    PMID:24095732

    Open questions at the time
    • Molecular partners mediating the cilia-independent spindle orientation function in vivo not identified
  9. 2015 Medium

    IFT88 was shown to maintain leading-edge microtubule content during cell migration and to regulate actin cortex organization and cortical stiffness, extending its cytoskeletal roles beyond the mitotic spindle.

    Evidence siRNA/shRNA knockdown in migrating MDCK cells; LifeACT-GFP and micropipette aspiration in hypomorphic chondrocytes

    PMID:26465598 PMID:26493329

    Open questions at the time
    • Mechanism by which IFT88 stabilizes leading-edge microtubules unresolved
    • Whether actin phenotype is direct or secondary to microtubule defects unknown
  10. 2017 High

    IFT88 loss in cranial neural crest cells was shown to abolish cilia and Shh signaling, causing cleft lip/palate and mandibular defects, demonstrating tissue-specific developmental consequences of IFT88-dependent Hedgehog transduction.

    Evidence Wnt1-Cre and Osr2KI-Cre conditional Ift88 KO mice, Shh pathway analysis, comparison with Smo KO

    PMID:28069795 PMID:31657471

    Open questions at the time
    • Whether IFT88 has Hedgehog-independent roles in palatal mesenchyme not fully dissected
  11. 2018 High

    Mapping IFT70's interaction to the IFT52–IFT88 dimer and showing that TCTN2 gates IFT88 ciliary entry refined the architecture and spatial regulation of IFT-B at the transition zone.

    Evidence IFT70-KO rescue with deletion mutants, Co-IP; TCTN2 KO super-resolution imaging

    PMID:29654116 PMID:29866362

    Open questions at the time
    • Atomic-resolution structure of the IFT70–IFT52–IFT88 sub-complex not yet available
    • How the transition zone physically gates IFT88 is mechanistically unresolved
  12. 2019 High

    IFT88's localization at kinetochore-fiber minus-ends and its interaction with NuMA revealed a mechanism for k-fiber re-anchoring during mitosis, explaining chromosome alignment defects upon IFT88 depletion.

    Evidence Laser ablation of k-fibers, siRNA, Co-IP of IFT88–NuMA, immunofluorescence

    PMID:31312011

    Open questions at the time
    • Whether IFT88 is transported along k-fibers or associates statically is unknown
    • Structural basis of IFT88–NuMA interaction not defined
  13. 2022 High

    MEIG1 was identified as a spermatid-specific adaptor that recruits IFT88 to the manchette, establishing a tissue-specific IFT88 localization mechanism required for spermiogenesis.

    Evidence Co-IP from mouse testis, Meig1 KO, sucrose gradient sedimentation, immunofluorescence

    PMID:35257720

    Open questions at the time
    • Whether MEIG1 directly binds IFT88 or acts via IFT20 not resolved
    • Cargo transported by manchette-associated IFT88 not identified
  14. 2024 High

    Identification of XIAP as an E3 ubiquitin ligase for IFT88, enhanced by TGF-β, established a post-translational degradation axis linking ciliary loss to hepatic stellate cell activation and liver fibrosis.

    Evidence Co-IP, ubiquitination assays, Ift88 KO mice, liver fibrosis model, proteasome inhibition

    PMID:38351372

    Open questions at the time
    • Specific lysine residues ubiquitinated by XIAP not mapped
    • Whether XIAP-mediated degradation operates in other fibrotic tissues is untested
  15. 2025 High

    Discovery that UFL1-mediated UFMylation at K572 competes with PJA2-mediated ubiquitination to stabilize IFT88 revealed a dual post-translational switch controlling IFT88 protein levels and ciliary homeostasis.

    Evidence Site-directed K572R mutagenesis, UFL1 KO mice, UFMylation and ubiquitination assays

    PMID:41272290

    Open questions at the time
    • Whether UFMylation regulates IFT88 in specific tissues/cell types is unexplored
    • Upstream signals triggering UFMylation versus ubiquitination not characterized

Open questions

Synthesis pass · forward-looking unresolved questions
  • A high-resolution structural model of full-length IFT88 within the intact IFT-B train, the signaling inputs that toggle between UFMylation and ubiquitination, and the mechanism by which IFT88 is partitioned between ciliary and non-ciliary pools remain unresolved.
  • No atomic structure of IFT88 in the context of the full IFT train
  • Signals controlling UFMylation/ubiquitination balance unknown
  • Partitioning mechanism between ciliary and centrosomal/mitotic pools undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 3 GO:0008092 cytoskeletal protein binding 3
Localization
GO:0005929 cilium 4 GO:0005815 microtubule organizing center 3 GO:0005856 cytoskeleton 2 GO:0005783 endoplasmic reticulum 1 GO:0005794 Golgi apparatus 1
Pathway
R-HSA-1852241 Organelle biogenesis and maintenance 5 R-HSA-1640170 Cell Cycle 4 R-HSA-1266738 Developmental Biology 3 R-HSA-162582 Signal Transduction 3 R-HSA-392499 Metabolism of proteins 2
Partners
CHE-1IFT46IFT52IFT70MEIG1NUMAUFL1XIAP
Complex memberships
IFT-B complexIFT88-IFT52-IFT46 ternary complex

Evidence

Reading pass · 25 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2000 IFT88 (Chlamydomonas) and its mouse homologue Tg737 are required for assembly of cilia and flagella; loss of IFT88 in Chlamydomonas results in complete absence of flagella, and Tg737 mutant mice have shorter primary cilia in kidney tubular cells, establishing IFT88 as an essential component of intraflagellar transport for ciliogenesis. Insertional mutant characterization in Chlamydomonas, mouse mutant analysis, electron microscopy The Journal of cell biology High 11062270
2001 The C. elegans IFT88 ortholog OSM-5 localizes to the cilium base and axoneme, undergoes intraflagellar transport as visualized by time-lapse imaging of OSM-5::GFP, and is required for ciliogenesis in sensory neurons; its expression is regulated by the RFX transcription factor DAF-19. Transgenic rescue, GFP fusion live imaging, immunofluorescence Development (Cambridge, England) High 11290289
2002 IFT88/Tg737 is required for photoreceptor outer segment assembly and maintenance; IFT particle proteins localize to photoreceptor connecting cilia, and mice with Tg737/IFT88 mutation develop abnormal outer segment morphology and retinal degeneration. Mouse mutant analysis, immunolocalization, histology The Journal of cell biology High 11916979
2007 IFT88/polaris localizes to the centrosome throughout the cell cycle in a microtubule- and dynein-independent manner via its tetratricopeptide repeat (TPR) motifs; overexpression prevents G1-S transition and induces apoptosis, depletion by RNAi promotes cell-cycle progression, and IFT88 interacts with Che-1 (an Rb-binding protein), placing IFT88 in G1-S regulation in non-ciliated proliferating cells. Cell fractionation, RNAi knockdown, overexpression, Co-IP, cell cycle analysis Journal of cell science High 17264151
2010 IFT88, IFT52, and IFT46 directly interact with each other and form a ternary complex within the IFT-B core; interactions were established by yeast two-hybrid and bacterial coexpression/pulldown, and confirmed by chemical cross-linking. Yeast two-hybrid, bacterial coexpression pulldown, chemical cross-linking The Journal of biological chemistry High 20435895
2011 IFT88 depletion induces mitotic spindle orientation defects; in mitosis IFT88 is part of a dynein1-driven complex that transports peripheral microtubule clusters containing microtubule-nucleating proteins to spindle poles, ensuring proper astral microtubule array formation and spindle orientation. siRNA knockdown in human cells, mouse mutant kidney cells, zebrafish embryos; live imaging; Co-IP Nature cell biology High 21441926
2011 IFT88 localizes to the trans-Golgi network of spermatids and participates in acrosome-acroplaxome complex, head-tail coupling apparatus, and spermatid tail biogenesis; loss of Ift88 causes abnormal head shaping and tail-less spermatids, and disruption of microtubules blocks progression of IFT88-stained proacrosomal vesicles to the acrosome. Immunocytochemistry, mouse mutant analysis (Ift88 mutant), Brefeldin-A and nocodazole treatment Developmental dynamics Medium 21337470
2013 IFT88 plays a cilia- and PCP-independent role in controlling oriented cell divisions during zebrafish gastrulation and neurulation; maternal+zygotic IFT88 mutant embryos lacking all cilia show oriented cell division defects without PCP phenotypes. Maternal+zygotic zebrafish mutant analysis, live imaging, cell division orientation measurements Cell reports High 24095732
2015 IFT88 is required for cell migration independently of cilia; loss of Ift88 impairs polarization of migrating MDCK cells and reduces microtubule content at the leading edge, without affecting MT dynamics or nucleation. siRNA/shRNA knockdown, live cell imaging, fluorescence microscopy of migrating cells PloS one Medium 26465598
2015 IFT88 regulates actin organization and cortical stiffness in chondrocytes; hypomorphic IFT88(orpk) cells show increased acto-myosin stress fibers, reduced cortical tension, slower actin cortex reformation after blebbing, and altered cell mechanical properties. Confocal microscopy, micropipette aspiration, live cell actin imaging with LifeACT-GFP Osteoarthritis and cartilage Medium 26493329
2017 DGKδ (a diacylglycerol kinase resident in the ER) triggers release of IFT88-containing vesicles from ER exit sites (ERES) via interaction with IFT88; IFT88 associates with COPII-coated vesicles at ERES, and DGKδ is required for Shh signaling in vitro and in vivo. Co-IP, RNAi silencing, gene knockout, vesicle trafficking assays Scientific reports Medium 28706295
2018 IFT70 interacts with the IFT52-IFT88 dimer via its first TPR domain and terminal helix; deletion of either disrupts IFT70-IFT52-IFT88 interaction and abolishes ciliogenesis in IFT70-KO cells. Knockout cell lines, co-immunoprecipitation, deletion mutagenesis, ciliogenesis rescue assay Biology open High 29654116
2018 TCTN2 depletion causes IFT88 to leak into the basal body lumen rather than entering the cilium, demonstrating that the transition zone gates IFT88 access to the ciliary compartment. CRISPR/Cas9 knockout, super-resolution microscopy, quantitative localization analysis Biophysical journal Medium 29866362
2018 IFT88 regulates LRP-1-mediated endocytosis of extracellular proteases in chondrocytes; hypomorphic IFT88 mutation disrupts LRP-1 concentration at the ciliary base, increases receptor shedding, and reduces protease clearance, elevating aggrecanase activity independently of Hedgehog signaling. Hypomorphic mutant chondrocyte line, immunofluorescence, protease activity assays, receptor shedding assay FASEB journal Medium 29920219
2019 IFT88 concentrates at kinetochore fiber (k-fiber) minus-ends, interacts with NuMA, and is required for NuMA enrichment at newly generated k-fiber minus-ends after laser ablation; IFT88 depletion impairs k-fiber re-anchoring into spindles and chromosome alignment. MT laser ablation, siRNA depletion, Co-IP, nocodazole washout, immunofluorescence Scientific reports High 31312011
2020 WDR62 recruits CPAP to the basal body, which is required for subsequent recruitment of IFT88; WDR62 missense mutations (V66M, R439H) localize to the basal body but fail to recruit CPAP, resulting in IFT88 deficiency, ciliogenesis failure, and premature radial glia differentiation leading to microcephaly. CRISPR/Cas9 mouse models, immunofluorescence co-localization, loss-of-function analysis Human molecular genetics Medium 31816041
2020 Loss of IFT88 in endothelial cells promotes endothelial-to-mesenchymal transition (EndMT), increases Sonic Hedgehog signaling effectors, and in vivo endothelial-specific Ift88 KO exacerbates bleomycin-induced pulmonary fibrosis. siRNA knockdown in ECs, endothelial-specific Ift88 KO mice, marker expression analysis, bleomycin fibrosis model Scientific reports Medium 32161282
2022 MEIG1 is required for manchette localization of IFT88 and IFT20 in elongating spermatids; Co-IP from mouse testis confirms MEIG1-IFT88-IFT20 complex, and in Meig1 KO mice IFT88 is absent from the manchette and drifts to lighter sucrose gradient fractions, indicating MEIG1 stabilizes IFT88 in this compartment. Co-immunoprecipitation, Meig1 KO mouse, sucrose gradient sedimentation, immunofluorescence Developmental biology High 35257720
2024 XIAP functions as an E3 ubiquitin ligase for IFT88; TGF-β enhances XIAP-mediated ubiquitination of IFT88, promoting its proteasomal degradation, cilia loss, and HSC activation leading to liver fibrosis. Blocking XIAP-mediated IFT88 degradation prevents TGF-β-induced HSC activation. Co-IP, ubiquitination assay, Ift88 KO mice, liver fibrosis model, proteasome inhibition EMBO reports High 38351372
2025 UFL1-mediated UFMylation of IFT88 at lysine 572 antagonizes ubiquitination by PJA2 E3 ligase, preventing IFT88 proteasomal degradation; the K572R IFT88 mutant shows increased ubiquitination and reduced stability, and UFL1 KO mice have severe ciliary defects. Co-IP, site-directed mutagenesis, UFL1 KO mouse, proteasome inhibition, UFMylation assay Cell death and differentiation High 41272290
2025 IFT88 inhibits TRPV4-mediated calcium influx in endplate chondrocytes under excessive mechanical stress; co-immunoprecipitation shows IFT88-TRPV4 interaction, and IFT88 negatively regulates its own transcription factor C/EBPα under abnormal stress. IFT88 overexpression in vivo maintains disc height and reduces endplate ossification. Co-immunoprecipitation, dual-luciferase assay, molecular docking, siRNA knockdown, in vivo AAV overexpression, flow cytometry Journal of advanced research Medium 40441296
2012 Deletion of Ift88 from chondrocytes disrupts Hedgehog (Ihh) signaling and downregulates the Wnt antagonist Sfrp5 (a downstream Hh target), leading to increased Wnt/β-catenin signaling specifically in columnar growth plate cells. Conditional Ift88 knockout mice, gene expression profiling, pathway analysis, immunohistochemistry for nuclear β-catenin Journal of orthopaedic research Medium 23034798
2017 Loss of Tg737 in liver stem cells results in nuclear β-catenin accumulation and activation of the Wnt/β-catenin pathway, promoting EMT via a Snail-HNF4α negative feedback circuit; XAV939 (β-catenin inhibitor) rescues the malignant transformation phenotype. shRNA knockdown, pathway inhibitor rescue, β-catenin nuclear localization, Western blot Cancer letters Medium 28536011
2019 Ift88 is required in cranial neural crest cells for craniofacial/mandibular development partially through Sonic Hedgehog signaling; loss of Ift88 in mandibular mesenchyme downregulates Hh signaling, but Ift88 also affects chondrogenesis independently as Smo deletion shows distinct phenotype. Conditional Ift88 KO (Wnt1Cre), Smo conditional KO comparison, histology, in situ hybridization Journal of anatomy Medium 31657471
2017 IFT88 loss in cranial neural crest-derived palatal mesenchyme abolishes primary cilia and downregulates Shh signaling, leading to bilateral cleft lip and palate; palatal mesenchyme-specific Ift88 deletion recapitulates isolated cleft palate. Wnt1-Cre and Osr2KI-Cre conditional Ift88 KO mice, cilia immunostaining, Shh pathway analysis, proliferation assays Human molecular genetics High 28069795

Source papers

Stage 0 corpus · 72 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2000 Chlamydomonas IFT88 and its mouse homologue, polycystic kidney disease gene tg737, are required for assembly of cilia and flagella. The Journal of cell biology 912 11062270
2002 The intraflagellar transport protein, IFT88, is essential for vertebrate photoreceptor assembly and maintenance. The Journal of cell biology 407 11916979
2001 The C. elegans homolog of the murine cystic kidney disease gene Tg737 functions in a ciliogenic pathway and is disrupted in osm-5 mutant worms. Development (Cambridge, England) 196 11290289
2007 The intraflagellar transport component IFT88/polaris is a centrosomal protein regulating G1-S transition in non-ciliated cells. Journal of cell science 151 17264151
2011 The cilia protein IFT88 is required for spindle orientation in mitosis. Nature cell biology 147 21441926
2003 Loss of the Tg737 protein results in skeletal patterning defects. Developmental dynamics : an official publication of the American Association of Anatomists 115 12701101
2011 GMAP210 and IFT88 are present in the spermatid golgi apparatus and participate in the development of the acrosome-acroplaxome complex, head-tail coupling apparatus and tail. Developmental dynamics : an official publication of the American Association of Anatomists 83 21337470
2009 Early defects in photoreceptor outer segment morphogenesis in zebrafish ift57, ift88 and ift172 Intraflagellar Transport mutants. Vision research 80 19136023
2005 Disruption of IFT results in both exocrine and endocrine abnormalities in the pancreas of Tg737(orpk) mutant mice. Laboratory investigation; a journal of technical methods and pathology 80 15580285
2010 Direct interactions of intraflagellar transport complex B proteins IFT88, IFT52, and IFT46. The Journal of biological chemistry 68 20435895
2009 Zebrafish ift57, ift88, and ift172 intraflagellar transport mutants disrupt cilia but do not affect hedgehog signaling. Developmental dynamics : an official publication of the American Association of Anatomists 60 19517571
2017 Intraflagellar transport 88 (IFT88) is crucial for craniofacial development in mice and is a candidate gene for human cleft lip and palate. Human molecular genetics 52 28069795
2015 A Cilia Independent Role of Ift88/Polaris during Cell Migration. PloS one 46 26465598
2012 Ift88 regulates Hedgehog signaling, Sfrp5 expression, and β-catenin activity in post-natal growth plate. Journal of orthopaedic research : official publication of the Orthopaedic Research Society 45 23034798
2006 Altered pH(i) regulation and Na(+)/HCO3(-) transporter activity in choroid plexus of cilia-defective Tg737(orpk) mutant mouse. American journal of physiology. Cell physiology 41 17182727
2003 Delayed cystogenesis and increased ciliogenesis associated with the re-expression of polaris in Tg737 mutant mice. Kidney international 41 12631338
2013 IFT88 plays a cilia- and PCP-independent role in controlling oriented cell divisions during vertebrate embryonic development. Cell reports 40 24095732
2018 Robust interaction of IFT70 with IFT52-IFT88 in the IFT-B complex is required for ciliogenesis. Biology open 39 29654116
1995 Characterization of the human homologue of the mouse Tg737 candidate polycystic kidney disease gene. Human molecular genetics 38 7633404
2020 The association of microcephaly protein WDR62 with CPAP/IFT88 is required for cilia formation and neocortical development. Human molecular genetics 35 31816041
1996 Functional correction of renal defects in a mouse model for ARPKD through expression of the cloned wild-type Tg737 cDNA. Kidney international 35 8887283
2020 Endothelial-specific Loss of IFT88 Promotes Endothelial-to-Mesenchymal Transition and Exacerbates Bleomycin-induced Pulmonary Fibrosis. Scientific reports 33 32161282
2018 Loss-of-function of IFT88 determines metabolic phenotypes in thyroid cancer. Oncogene 29 29743590
1997 The tetratricopeptide repeat containing Tg737 gene is a liver neoplasia tumor suppressor gene. Oncogene 29 9362446
2015 IFT88 influences chondrocyte actin organization and biomechanics. Osteoarthritis and cartilage 28 26493329
2015 TGF-β Suppresses Ift88 Expression in Chondrocytic ATDC5 Cells. Journal of cellular physiology 24 25828538
2021 Decreased IFT88 expression with primary cilia shortening causes mitochondrial dysfunction in cisplatin-induced tubular injury. American journal of physiology. Renal physiology 21 34338030
2024 XIAP-mediated degradation of IFT88 disrupts HSC cilia to stimulate HSC activation and liver fibrosis. EMBO reports 20 38351372
2017 Tg737 regulates epithelial-mesenchymal transition and cancer stem cell properties via a negative feedback circuit between Snail and HNF4α during liver stem cell malignant transformation. Cancer letters 18 28536011
2021 IFT88 deficiency in proximal tubular cells exaggerates cisplatin-induced injury by suppressing autophagy. American journal of physiology. Renal physiology 17 34251272
2018 Super-Resolution Imaging Reveals TCTN2 Depletion-Induced IFT88 Lumen Leakage and Ciliary Weakening. Biophysical journal 17 29866362
2018 IFT88 mutations identified in individuals with non-syndromic recessive retinal degeneration result in abnormal ciliogenesis. Human genetics 17 29978320
2016 MicroRNA-548a-5p promotes proliferation and inhibits apoptosis in hepatocellular carcinoma cells by targeting Tg737. World journal of gastroenterology 17 27340352
2018 Cilia protein IFT88 regulates extracellular protease activity by optimizing LRP-1-mediated endocytosis. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 16 29920219
2019 Ift88 is involved in mandibular development. Journal of anatomy 15 31657471
2017 DGKδ triggers endoplasmic reticulum release of IFT88-containing vesicles destined for the assembly of primary cilia. Scientific reports 15 28706295
2012 Tg737 signaling is required for hypoxia-enhanced invasion and migration of hepatoma cells. Journal of experimental & clinical cancer research : CR 15 22974282
1995 Sequence analysis of the human hTg737 gene and its polymorphic sites in patients with autosomal recessive polycystic kidney disease. Mammalian genome : official journal of the International Mammalian Genome Society 13 8597639
2022 Ciliary IFT88 Protects Coordinated Adolescent Growth Plate Ossification From Disruptive Physiological Mechanical Forces. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 12 35038201
2017 Transcriptome profiling identifies a recurrent CRYL1-IFT88 chimeric transcript in hepatocellular carcinoma. Oncotarget 12 28489570
2011 Tg737 inhibition results in malignant transformation in fetal liver stem/progenitor cells by promoting cell-cycle progression and differentiation arrest. Molecular carcinogenesis 12 21837759
2022 MEIG1 determines the manchette localization of IFT20 and IFT88, two intraflagellar transport components in male germ cells. Developmental biology 11 35257720
1999 Structure and expression of Tg737, a putative tumor suppressor gene, in human hepatocellular carcinomas. Hepatology (Baltimore, Md.) 11 10462374
2022 Piezo1 and IFT88 synergistically regulate mandibular condylar chondrocyte differentiation under cyclic tensile strain. Tissue & cell 10 35279604
2022 Knockdown of Ift88 in fibroblasts causes extracellular matrix remodeling and decreases conduction velocity in cardiomyocyte monolayers. Frontiers in physiology 9 36467697
2019 IFT88 controls NuMA enrichment at k-fibers minus-ends to facilitate their re-anchoring into mitotic spindles. Scientific reports 9 31312011
2021 Sex-Dependent Effects of Nephron Ift88 Disruption on BP, Renal Function, and Cystogenesis. Journal of the American Society of Nephrology : JASN 8 34045314
2019 Ift88 limits bone formation in maxillary process through suppressing apoptosis. Archives of oral biology 8 30878609
2018 Role of IFT88 in icariin‑regulated maintenance of the chondrocyte phenotype. Molecular medicine reports 8 29393439
2022 Ift88 regulates enamel formation via involving Shh signaling. Oral diseases 7 35189017
2014 Normal mammary development and function in mice with Ift88 deleted in MMTV- and K14-Cre expressing cells. Cilia 7 24594320
2022 Depletion of Ift88 in thymic epithelial cells affects thymic synapse and T-cell differentiation in aged mice. Anatomical science international 5 35435578
2021 Multiomic identification of factors associated with progression to cystic kidney disease in mice with nephron Ift88 disruption. American journal of physiology. Renal physiology 5 34927449
2025 Temporal ablation of the ciliary protein IFT88 alters normal brainwave patterns. Scientific reports 4 39747370
2025 Ciliary and Non-Ciliary Roles of IFT88 in Development and Diseases. International journal of molecular sciences 4 40076734
2019 Association of IFT88 gene variants with nonsyndromic cleft lip with or without cleft palate. Birth defects research 4 30953423
2017 Basic fibroblast growth factor increases IFT88 expression in chondrocytes. Molecular medicine reports 4 28901443
2025 Ciliary IFT88 inhibits intervertebral disc degeneration under excessive mechanical stress by regulating endplate cartilage calcification. Journal of advanced research 3 40441296
2022 Profiling renal sodium transporters in mice with nephron Ift88 disruption: Association with sex, cysts, and blood pressure. Physiological reports 3 35274831
2022 Multifaceted investigation underlies diverse mechanisms contributing to the downregulation of Hedgehog pathway-associated genes INTU and IFT88 in lung adenocarcinoma and uterine corpus endometrial carcinoma. Aging 3 36084949
2025 Macrophage Accumulation and Cyst Expansion in Pkd2 , Ift88 , and Double Mutant Mouse Models. Journal of the American Society of Nephrology : JASN 2 40455584
2025 UFL1-mediated UFMylation antagonizes IFT88 ubiquitination and degradation to maintain ciliary homeostasis. Cell death and differentiation 2 41272290
2024 T cell-expressed Ift88 is required for proper thymocyte differentiation in mice. Physiological reports 2 39562155
2023 Cilia-associated wound repair mediated by IFT88 in retinal pigment epithelium. Scientific reports 2 37211572
2019 Distinct Activities of Gli1 and Gli2 in the Absence of Ift88 and the Primary Cilia. Journal of developmental biology 2 30791390
2026 Inducible Ift88-deficient mice show features consistent with mild pulmonary hypertension. Physiological reports 1 41588821
2022 The Relationship between Ultrasonographic Features of Hepatocellular Carcinoma and the Severity of Hepatocellular Carcinoma and the Expression of PTEN and Tg737. Journal of healthcare engineering 1 35368955
2021 Ift88, but not Kif3a, is required for establishment of the periciliary membrane compartment. Biochemical and biophysical research communications 1 34753064
2025 Functionally Essential and Structurally Diverse: Insights into the zebrafish Left-Right Organizer's Cilia via Optogenetic IFT88 Perturbation and Volume Electron Microscopy. bioRxiv : the preprint server for biology 0 40964258
2025 Mutations in CFAP57 disrupt the localization of MYH10 and IFT88, leading to flagellogenesis failure in humans and mice. Human genomics 0 41466333
2024 Temporal Ablation of the Ciliary Protein IFT88 Alters Normal Brainwave Patterns. bioRxiv : the preprint server for biology 0 38617207
2023 Retracted: The Relationship between Ultrasonographic Features of Hepatocellular Carcinoma and the Severity of Hepatocellular Carcinoma and the Expression of PTEN and Tg737. Journal of healthcare engineering 0 37829384