Affinage

BAIAP2L1

BAR/IMD domain-containing adapter protein 2-like 1 · UniProt Q9UHR4

Length
511 aa
Mass
56.9 kDa
Annotated
2026-06-09
26 papers in source corpus 22 papers cited in narrative 23 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

BAIAP2L1 (IRTKS) is a membrane-deforming I-BAR/IMD scaffold protein that couples plasma-membrane curvature to actin-based protrusion formation, while moonlighting as a signaling adaptor in insulin, antiviral, p53, and chromatin pathways (PMID:17430976, PMID:30197089, PMID:23896986). Its N-terminal IMD/I-BAR domain bundles actin filaments and binds Rac (but not Cdc42), and its C-terminal WH2 extension binds actin filaments to modulate bundle length (PMID:17430976). Through the I-BAR domain it engages curvature-coupled partners including Rif GTPase and the formin FMNL2, and through its SH3 domain it recruits EPS8 and WAVE2 to drive filopodia, dorsal ruffles, and microvillar/stereociliary/microridge elongation at protrusion tips (PMID:30197089, PMID:27278019, PMID:36259517, PMID:39093051). As an insulin-receptor adaptor it sustains IR–IRS1–PI3K–AKT signaling, in part by its SH3 domain binding the SHIP2 catalytic domain to suppress PIP3 hydrolysis; IRTKS-deficient mice are insulin resistant (PMID:23896986, PMID:31212584). IRTKS also recruits the SUMO E2 ligase Ubc9 to two distinct substrates: it SUMOylates PCBP2 to drive MAVS degradation and dampen RIG-I antiviral signaling (PMID:26348439), and it SUMOylates HP1α to promote liquid-liquid phase-separated constitutive heterochromatin, whose loss derepresses repetitive elements and triggers cGAS-STING-driven senescence (PMID:39192031). Additional regulatory roles include Chk2-dependent phosphorylation at Ser331 that controls IRTKS occupancy of the p53-MDM2 complex and thereby p53 stability (PMID:28647685), Src-dependent tyrosine phosphorylation that enables pro-migratory function (PMID:21840312), OTUD4 recruitment that stabilizes SETDB1 to epigenetically silence E-cadherin and promote EMT/metastasis (PMID:37739210), and formation of lysosomal condensates that engage RRAGD to potentiate amino-acid-sensitive mTORC1 activation, driving steatosis and MASLD-to-HCC progression in mouse liver (PMID:41575860). Recurrent gene fusions in which the BAIAP2L1 dimerization (BAR/coiled-coil) domain is fused to FGFR3 or BRAF produce constitutive kinase activation and oncogenic transformation (PMID:25589496, PMID:36217175).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 2007 High

    Established the biochemical core activity of IRTKS by showing its IMD/I-BAR domain bundles actin and binds Rac, distinguishing it from the paralog IRSp53 which also engages Cdc42.

    Evidence In vitro actin bundling assays, co-IP, and domain deletion in cells

    PMID:17430976

    Open questions at the time
    • Did not define in vivo protrusion phenotypes
    • WH2 mechanism of bundle-length modulation not structurally resolved
  2. 2009 High

    Placed IRTKS as a specific host effector of enteropathogenic bacteria, showing it (not IRSp53) is recruited to Tir attachment sites via the Tir NPY451 motif during infection.

    Evidence C. rodentium mouse model and EHEC human ileal explants with tir tyrosine mutants and competitive infection

    PMID:19889090

    Open questions at the time
    • Did not resolve which IRTKS domain binds Tir
    • Downstream actin polymerization machinery not yet mapped
  3. 2011 Medium

    Connected IRTKS to migration control by mapping six Src phosphorylation sites required for its pro-migratory effect.

    Evidence In vitro/in vivo kinase assays, point mutants, wound closure in HT1080 cells

    PMID:21840312

    Open questions at the time
    • Single lab
    • How tyrosine phosphorylation alters IRTKS partner binding unresolved
  4. 2013 High

    Defined a metabolic signaling role, showing IRTKS is an insulin-receptor adaptor whose loss causes insulin resistance reversible by ectopic IRTKS.

    Evidence IRTKS-KO and diabetic mice, tolerance tests, rescue, signaling western blots

    PMID:23896986

    Open questions at the time
    • Molecular contact with IR not structurally defined at this stage
    • Tissue-specific contributions not dissected
  5. 2015 High

    Revealed an antiviral suppression mechanism via Ubc9-mediated SUMOylation of PCBP2 leading to MAVS degradation.

    Evidence IRTKS-deficient cells/mice, viral infection, SUMOylation and MAVS degradation assays, fractionation

    PMID:26348439

    Open questions at the time
    • How viral infection triggers IRTKS-Ubc9 engagement unclear
    • Relationship to its cytoskeletal roles not addressed
  6. 2015 High

    Demonstrated oncogenic fusion biology, showing the FGFR3-BAIAP2L1 fusion drives transformation through BAR-domain-mediated constitutive FGFR3 dimerization/activation.

    Evidence Stable transfection, BAR deletion mutant, in vitro/in vivo tumorigenicity, FGFR inhibitor

    PMID:25589496

    Open questions at the time
    • Does not address full-length BAIAP2L1 function
    • Tumor-type specificity of fusion not delineated
  7. 2016 Medium

    Linked the I-BAR domain to Rif GTPase signaling and SH3-domain-dependent migration, mapping EPS8/WAVE2 as effectors of dorsal protrusion formation and p38 activation.

    Evidence Reciprocal Co-IP, KO cells, dominant-negative Rif, chimeric SH3 constructs, live imaging

    PMID:27278019 PMID:27693783

    Open questions at the time
    • Single lab
    • Mechanistic basis for Tir/Rif competition on I-BAR not resolved
  8. 2017 High

    Established a DNA-damage-responsive role in p53 control, showing Chk2 phosphorylation at Ser331 evicts IRTKS from the p53-MDM2 complex to stabilize p53.

    Evidence Co-IP, ubiquitination assays, Chk2 kinase assay, IRTKS-KO MEFs/mice, tumorigenicity

    PMID:28647685

    Open questions at the time
    • How IRTKS facilitates MDM2-mediated p53 ubiquitination structurally unclear
    • Nuclear vs cytoplasmic pools not distinguished
  9. 2017 Medium

    Demonstrated genetic redundancy with IRSp53 in development, with double knockout causing embryonic lethality and placental defects.

    Evidence Single and double KO mice with developmental/histological analysis

    PMID:28067313

    Open questions at the time
    • Molecular basis of redundancy in spongiotrophoblast not defined
    • Single lab
  10. 2018 High

    Resolved tip-targeted protrusion mechanism in epithelia: I-BAR localizes IRTKS to microvillar tips, while WH2 polymerizes actin and SH3 recruits EPS8 for elongation.

    Evidence Super-resolution and live imaging, domain mutants, loss-of-function and rescue

    PMID:30197089

    Open questions at the time
    • How tip enrichment is maintained dynamically unresolved
  11. 2019 Medium

    Provided the enzymatic basis for IRTKS lipid signaling, showing its SH3 domain binds and inhibits the SHIP2 catalytic domain to preserve PIP3 and activate AKT-mTOR.

    Evidence Co-IP, domain binding, lipid phosphatase activity assay, PIP3/PI(3,4)P2 quantification in KO cells

    PMID:31212584

    Open questions at the time
    • Single lab
    • Insulin-dependent dynamics of the interaction only partially characterized
  12. 2022 Medium

    Identified FMNL2 as a curvature-coupled cofactor, with FMNL2 bending membrane to recruit IRTKS for cooperative filopodia assembly, a function specific to IRTKS over IRSp53.

    Evidence Co-IP, domain mapping, KO cell lines, filopodia quantification, rescue

    PMID:36259517

    Open questions at the time
    • Single lab
    • Order of FMNL2/IRTKS recruitment in vivo not fully resolved
  13. 2022 Medium

    Extended fusion oncogenesis to BRAF, showing BAIAP2L1 provides coiled-coil-dependent dimerization for constitutive BRAF kinase activation in thyroid cells.

    Evidence Fusion identification, kinase-dead and CC-domain mutants, 3D spheroid assays, RNAi

    PMID:36217175

    Open questions at the time
    • Single lab
    • Clinical prevalence of the fusion not established
  14. 2023 Medium

    Uncovered an epigenetic metastasis-promoting mechanism: IRTKS recruits OTUD4 to deubiquitinate and stabilize SETDB1, raising H3K9me3 to silence E-cadherin and drive EMT.

    Evidence Co-IP, ubiquitination assays, ATAC-seq, H3K9me3 ChIP, metastasis assays

    PMID:37739210

    Open questions at the time
    • Single lab
    • How IRTKS selects SETDB1/OTUD4 versus other deubiquitination substrates unclear
  15. 2024 High

    Defined a phase-separation function in heterochromatin: IRTKS condensates and Ubc9-mediated HP1α SUMOylation maintain constitutive heterochromatin, preventing repeat derepression and cGAS-STING senescence.

    Evidence LLPS reconstitution, FRAP, SUMOylation assay, ATAC-seq/RNA-seq, cGAS-STING analysis in KO cells

    PMID:39192031

    Open questions at the time
    • How nuclear IRTKS pool is regulated relative to cytoplasmic functions unclear
    • Sequence determinants of IRTKS phase separation not mapped
  16. 2024 Medium

    Showed BAIAP2L1 targets stereocilia tips dependent on EPS8/MYO15A in a calcium-independent manner, but its loss is dispensable for hearing/balance, indicating functional redundancy in this tissue.

    Evidence Immunofluorescence, KO mice, auditory brainstem response and vestibular tests

    PMID:39093051

    Open questions at the time
    • Compensating protein not identified
    • Single lab
  17. 2024 Low

    Linked IRTKS to PTEN regulation in mesenchymal stem cell osteogenesis via SH3-domain binding to the PTEN C-terminal tail.

    Evidence Co-IP, SH3 domain mapping, AKT readouts, BMSC differentiation, PTEN rescue

    PMID:38908202

    Open questions at the time
    • No in vitro phosphatase assay confirming PTEN inhibition
    • Single Co-IP, single lab
  18. 2026 High

    Defined a lysosomal mTORC1-activating role: IRTKS forms membrane-associated condensates that interact with RRAGD to heighten amino-acid sensing, with hepatic knockin driving obesity, steatosis, and MASLD-to-HCC.

    Evidence Phospho-array screening, RRAGD Co-IP, lysosomal fractionation/condensate imaging, hepatic knockin/KO mice with mTORC1 inhibition rescue

    PMID:41575860

    Open questions at the time
    • How IRTKS condensates assemble at the lysosome unresolved
    • Relationship to its other condensate (heterochromatin) behavior unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how IRTKS partitions among its cytoskeletal, plasma-membrane signaling, lysosomal, and nuclear/heterochromatin functions, and what determines context-specific recruitment of Ubc9, OTUD4, RRAGD, and SHIP2 to a single scaffold.
  • No unified model of IRTKS spatial regulation
  • Structural basis for SH3/I-BAR partner switching not solved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0008092 cytoskeletal protein binding 4 GO:0060090 molecular adaptor activity 3 GO:0098772 molecular function regulator activity 3 GO:0008289 lipid binding 2
Localization
GO:0005886 plasma membrane 4 GO:0005856 cytoskeleton 3 GO:0005634 nucleus 2 GO:0000228 nuclear chromosome 1 GO:0005764 lysosome 1
Pathway
R-HSA-392499 Metabolism of proteins 4 R-HSA-1643685 Disease 3 R-HSA-162582 Signal Transduction 2 R-HSA-4839726 Chromatin organization 2 R-HSA-168256 Immune System 1
Partners
EPS8FMNL2MYO15AOTUD4RRAGDSHIP2UBC9WAVE2

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2007 IRTKS contains an IMD (IRSp53/MIM homology domain) that bundles actin filaments and binds Rac GTPase, but unlike IRSp53, does not interact with Cdc42. Its C-terminal WH2-like extension interacts with actin filaments (not monomers) and modulates/shortens actin bundle length induced by the IMD both in vitro and in cells. In vitro actin bundling assays, co-immunoprecipitation, cell expression assays, deletion/domain mapping Journal of cell science High 17430976
2018 IRTKS localizes to the distal tips of actively growing epithelial microvilli via its N-terminal I-BAR domain, and promotes microvillar elongation through two mechanisms: (1) its C-terminal WH2 domain for actin polymerization at tips, and (2) its SH3 domain recruiting the bundling protein EPS8 to microvillar tips. Super-resolution microscopy, live imaging, domain deletion/mutation constructs, loss-of-function and rescue experiments in differentiating epithelial cells Current biology : CB High 30197089
2015 The FGFR3-BAIAP2L1 fusion protein drives oncogenic transformation through constitutive dimerization mediated by the BAR domain of BAIAP2L1, which promotes constitutive FGFR3 kinase activation. Deletion of the BAR domain decreased FGFR3 phosphorylation, dimerization, and tumorigenic activity. Stable transfection in Rat-2 cells, in vitro and in vivo tumorigenicity assays, BAR domain deletion mutant, FGFR inhibitor treatment, gene signature analysis Molecular cancer therapeutics High 25589496
2009 During C. rodentium and EHEC infection, IRTKS (but not IRSp53) is recruited to bacterial attachment sites on intestinal epithelium. IRTKS recruitment depends on Tir NPY451 motif (Y451 in Tir(CR)), establishing IRTKS as a specific downstream effector of Tir-mediated actin polymerization in vivo. C. rodentium murine infection model, human ileal explant EHEC infection, tir tyrosine mutants, immunofluorescence, competitive mixed infection Molecular microbiology High 19889090
2015 IRTKS suppresses antiviral innate immunity by recruiting the E2 SUMO ligase Ubc9 to sumoylate PCBP2 in the nucleus, causing PCBP2 cytoplasmic translocation during viral infection. Sumoylated PCBP2 then associates with MAVS to initiate its degradation, thereby downregulating RIG-I-MAVS antiviral signaling. IRTKS-deficient mouse/cell models, viral infection assays, sumoylation assays, co-immunoprecipitation, subcellular fractionation, MAVS degradation assays Nature communications High 26348439
2013 IRTKS acts as an adaptor for the insulin receptor (IR), modulating IR-IRS1-PI3K-AKT signaling by regulating IR phosphorylation. IRTKS-deficient mice exhibit insulin resistance; ectopic IRTKS can rescue insulin resistance in deficient and diabetic mice. IRTKS-knockout mice, glucose/insulin tolerance tests, ectopic IRTKS rescue, western blot of signaling components, diabetic mouse models Cell research High 23896986
2017 IRTKS overexpression promotes p53 ubiquitination and degradation via MDM2. Under DNA damage, IRTKS is phosphorylated at Ser331 by activated Chk2 kinase, causing IRTKS to dissociate from the p53-MDM2 complex, thereby attenuating p53 ubiquitination and degradation. Co-immunoprecipitation, ubiquitination assays, Chk2 kinase assay, IRTKS-deficient mice/MEFs, in vivo tumorigenicity, phospho-site identification Gut High 28647685
2016 IRTKS interacts with Rif GTPase through its I-BAR domain and signals through Eps8 and WAVE2 to generate dorsal membrane ruffles and filopodia. Eps8 regulates the size and number of dorsal filopodia downstream of Rif-IRTKS, and WAVE2 modulates dorsal membrane ruffling. The bacterial protein Tir may compete with Rif for binding to the IRTKS I-BAR domain. Co-immunoprecipitation, IRTKS-KO cells, dominant-negative Rif, live cell imaging, domain interaction mapping Journal of cell science Medium 27278019
2019 The SH3 domain of IRTKS directly binds the catalytic domain (INPP5c) of SHIP2 phosphatase, suppressing SHIP2 activity and thereby reducing conversion of PIP3 to PI(3,4)P2. IRTKS-KO increases PI(3,4)P2 and decreases PIP3; IRTKS overexpression increases PIP3 and activates AKT-mTOR signaling. The IRTKS-SHIP2 interaction is dynamically regulated by insulin. Co-immunoprecipitation, domain binding assays, lipid phosphatase activity assay, PIP3/PI(3,4)P2 measurement, IRTKS-KO cells, AKT-mTOR signaling readouts International journal of molecular sciences Medium 31212584
2011 Active Src kinase phosphorylates IRTKS at six tyrosine residues (Y37, Y156, Y163, Y274, Y293, and Y439) both in vivo and in vitro. Src-stimulated IRTKS phosphorylation is required for IRTKS-enhanced cell migration (wound closure); phosphorylation-deficient mutants abolish the pro-migratory effect. In vitro kinase assay, in vivo phosphorylation, deletion and point mutation mapping, wound closure assay with HT1080 cells FEBS letters Medium 21840312
2017 Double knockout of IRSp53 and IRTKS results in complete embryonic lethality with exacerbated placental abnormalities (particularly in spongiotrophoblast differentiation), demonstrating genetic interaction and partial functional redundancy between IRSp53 and IRTKS in placental development. Single and double KO mice, histological and developmental analysis of placentas and embryos Scientific reports Medium 28067313
2022 IRTKS is a binding partner of formin FMNL2; coexpression promotes cooperative filopodia assembly. IRTKS, but not IRSp53, is required for FMNL2-induced filopodia assembly. FMNL2 initiates filopodia assembly by bending the plasma membrane to recruit IRTKS, with FMNL2 and IRTKS acting as mutually dependent cofactors. Co-immunoprecipitation, domain mapping, KO cell lines, filopodia quantification by microscopy, rescue experiments The Journal of biological chemistry Medium 36259517
2023 IRTKS promotes accumulation of histone methyltransferase SETDB1 by recruiting deubiquitinase OTUD4 to remove Lys48-linked polyubiquitination at SETDB1 K182/K1050 sites, thereby blocking proteasomal SETDB1 degradation. Elevated SETDB1 increases H3K9me3, reduces chromatin accessibility at the CDH1 locus, suppresses E-cadherin expression, and promotes EMT and tumor metastasis. Co-immunoprecipitation, ubiquitination assays, ATAC-seq/chromatin accessibility, ChIP for H3K9me3, E-cadherin expression, metastasis assays Cancer letters Medium 37739210
2024 IRTKS is required for constitutive heterochromatin formation via liquid-liquid phase separation (LLPS). IRTKS condensates infiltrate HP1α/nucleosome heterochromatin condensates. IRTKS recruits Ubc9 to SUMOylate HP1α, enabling larger phase-separated HP1α droplets. IRTKS deficiency causes heterochromatin loss, aberrant repetitive element transcription, cGAS-STING activation, and cellular senescence/SASP. Phase separation assays, live cell imaging of condensates, FRAP, SUMOylation assay, ATAC-seq, RNA-seq, cGAS-STING pathway analysis, IRTKS-KO cells The EMBO journal High 39192031
2016 The SH3 domain of IRTKS (absent in MIM) is required for IRTKS-dependent promotion of serum-induced cell migration, cellular polarity, and p38 MAPK phosphorylation. Deletion of the SH3 domain attenuates cell motility and p38 activation; a chimeric MIM-IRTKS containing the IRTKS SH3 domain recapitulates IRTKS migratory function. Domain deletion and chimeric mutant constructs, wound migration assays, Rac1/Cdc42 activation assays, kinase phosphorylation assays, p38 inhibitor treatment Biochemical and biophysical research communications Medium 27693783
2012 IRTKS expression is specifically induced during osteoclast fusion and IRTKS interacts with the adaptor Tks5 in osteoclasts, suggesting a role in formation of fusion-competent podosome/invadopodia-like protrusions via its BAR domain. Expression analysis during osteoclastogenesis, co-immunoprecipitation of IRTKS and Tks5 Communicative & integrative biology Low 23739834
2024 BAIAP2L1 localizes to the tips of tallest-row stereocilia in inner ear hair cells in a manner dependent on row-1 complex proteins EPS8 and MYO15A. This localization is calcium-independent (unlike BAIAP2L2). Loss of BAIAP2L1 does not affect the row-1 protein complex or auditory/balance function in mice. Immunofluorescence localization, BAIAP2L1 KO mice, auditory brainstem response, vestibular function tests, co-localization with EPS8/MYO15A FASEB journal Medium 39093051
2024 IRTKS directly interacts with PTEN via its SH3 domain binding to the C-terminal tail of PTEN, and inhibits PTEN phosphorylation to promote PI3K-AKT signaling, thereby driving osteogenic differentiation of bone marrow mesenchymal stem cells. Co-immunoprecipitation, domain mapping (SH3), AKT signaling readouts, BMSC differentiation assays, PTEN rescue experiment Biomedicine & pharmacotherapy Low 38908202
2022 A novel BAIAP2L1-BRAF fusion transforms immortalized human thyroid cells in a kinase- and coiled-coil (CC) domain-dependent manner, identifying BAIAP2L1 as a fusion partner that provides dimerization activity enabling constitutive BRAF kinase activation. PCR/sequencing identification of fusion, stable transfection in thyroid cells, kinase-dead and CC-domain mutants, 3D spheroid growth assays, RNA interference Molecular cancer Medium 36217175
2026 IRTKS promotes EHEC Tir accumulation in the host plasma membrane, facilitating bacterial attachment. IRTKS gain- and loss-of-function experiments revealed that perturbing IRTKS disrupted Tir distribution/abundance, and ectopic IRTKS enhanced Tir membrane insertion in absence of other virulence factors, positioning IRTKS upstream of Tir in pedestal formation. IRTKS gain- and loss-of-function models in epithelial cells, immunofluorescence quantification of Tir distribution, ectopic Tir insertion assay bioRxivpreprint Medium 42239090
2025 In zebrafish, baiap2l1a localizes to microridges prior to actin formation, and its I-BAR domain alone is sufficient for microridge localization and partial rescue of microridge elongation. A 39-amino-acid deletion removing one α-helix impairs I-BAR microridge localization and fails to rescue elongation. Baiap2l1a genetically interacts with eps8like1a in microridge elongation. CRISPR/Cas9 knockdown in zebrafish, domain deletion constructs, AlphaFold2 structural modeling, live imaging of localization, genetic interaction analysis bioRxivpreprint Medium
2026 IRTKS forms lysosome-localized membrane-associated condensates that interact with the GTPase RRAGD, a key upstream regulator of mTORC1, thereby enhancing mTORC1 sensitivity to free amino acids. Hepatic IRTKS knockin drives mTORC1 hyperactivation, obesity, steatosis, and MASLD-to-HCC progression; genetic ablation or mTORC1 inhibition reverses these phenotypes. Phospho-antibody array screening, co-immunoprecipitation with RRAGD, lysosomal fractionation/condensate imaging, hepatic knockin and KO mice, mTORC1 activity assays, histological/metabolic phenotyping Cell reports High 41575860
2022 BAIAP2L1 interacts with ribosomal protein L3 (RPL3) via its SH3 domain (binding AA202-288 of RPL3); loss of the SH3 domain abolishes AKT signaling transduction by promoting PIK3CA degradation, identifying RPL3 as an IRTKS binding partner linking it to PI3K/AKT pathway activation in breast cancer. Co-immunoprecipitation, SH3 domain deletion mutants, AKT/PIK3CA signaling western blot, in vitro and in vivo overexpression/knockdown Cancer science Low 36308067

Source papers

Stage 0 corpus · 26 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2007 Characterisation of IRTKS, a novel IRSp53/MIM family actin regulator with distinct filament bundling properties. Journal of cell science 71 17430976
2018 IRTKS (BAIAP2L1) Elongates Epithelial Microvilli Using EPS8-Dependent and Independent Mechanisms. Current biology : CB 60 30197089
2015 Mechanism of Oncogenic Signal Activation by the Novel Fusion Kinase FGFR3-BAIAP2L1. Molecular cancer therapeutics 51 25589496
2009 Dissecting the role of the Tir:Nck and Tir:IRTKS/IRSp53 signalling pathways in vivo. Molecular microbiology 50 19889090
2015 IRTKS negatively regulates antiviral immunity through PCBP2 sumoylation-mediated MAVS degradation. Nature communications 48 26348439
2015 BAI1-Associated Protein 2-Like 1 (BAIAP2L1) Is a Potential Biomarker in Ovarian Cancer. PloS one 30 26222696
2013 Deficiency of IRTKS as an adaptor of insulin receptor leads to insulin resistance. Cell research 26 23896986
2017 IRTKS is correlated with progression and survival time of patients with gastric cancer. Gut 25 28647685
2016 The Rho GTPase Rif signals through IRTKS, Eps8 and WAVE2 to generate dorsal membrane ruffles and filopodia. Journal of cell science 24 27278019
2019 IRTKS Promotes Insulin Signaling Transduction through Inhibiting SHIP2 Phosphatase Activity. International journal of molecular sciences 18 31212584
2017 Redundant functions of I-BAR family members, IRSp53 and IRTKS, are essential for embryonic development. Scientific reports 17 28067313
2023 Cooperation between IRTKS and deubiquitinase OTUD4 enhances the SETDB1-mediated H3K9 trimethylation that promotes tumor metastasis via suppressing E-cadherin expression. Cancer letters 14 37739210
2012 Possible role of IRTKS in Tks5-driven osteoclast fusion. Communicative & integrative biology 14 23739834
2011 Src-stimulated IRTKS phosphorylation enhances cell migration. FEBS letters 13 21840312
2022 Cooperative assembly of filopodia by the formin FMNL2 and I-BAR domain protein IRTKS. The Journal of biological chemistry 12 36259517
2022 The Antitumor Activity of hAMSCs Secretome in HT-29 Colon Cancer Cells Through Downregulation of EGFR/c-Src/IRTKS Expression and p38/ERK1/2 Phosphorylation. Cell biochemistry and biophysics 11 35150389
2022 Insulin receptor tyrosine kinase substrate (IRTKS) promotes the tumorigenesis of pancreatic cancer via PI3K/AKT signaling. Human cell 11 36057038
2022 BAIAP2L1 accelerates breast cancer progression and chemoresistance by activating AKT signaling through binding with ribosomal protein L3. Cancer science 10 36308067
2016 The SH3 domain distinguishes the role of I-BAR proteins IRTKS and MIM in chemotactic response to serum. Biochemical and biophysical research communications 9 27693783
2024 Heterochromatin formation and remodeling by IRTKS condensates counteract cellular senescence. The EMBO journal 8 39192031
2022 Multiomic analysis of papillary thyroid cancers identifies BAIAP2L1-BRAF fusion and requirement of TRIM25, PDE5A and PKCδ for tumorigenesis. Molecular cancer 6 36217175
2024 IRTKS promotes osteogenic differentiation by inhibiting PTEN phosphorylation. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 3 38908202
2024 BAIAP2L1 and BAIAP2L2 differently regulate hair cell stereocilia morphology. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 3 39093051
2026 Lysosome-localized IRTKS condensates promote mTORC1 activity leading to MASLD and HCC. Cell reports 1 41575860
2024 IRTKS contributes to the malignant progression of cervical cancer cells. Medical oncology (Northwood, London, England) 1 38869721
2026 IRTKS promotes Tir membrane insertion for intimate bacterial attachment and subsequent pedestal formation. bioRxiv : the preprint server for biology 0 42239090

Missed literature

Know a paper Affinage missed for BAIAP2L1? Flag it for the maintainers and the community.

No submissions yet.