Affinage

AFAP1L2

Actin filament-associated protein 1-like 2 · UniProt Q8N4X5

Length
818 aa
Mass
91.3 kDa
Annotated
2026-06-09
42 papers in source corpus 20 papers cited in narrative 20 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

AFAP1L2 (XB130) is a cytosolic adaptor/scaffold protein that couples tyrosine-kinase signaling to PI3K/Akt activation and to actin-based remodeling of the cell cortex (PMID:17412687, PMID:19060924). It was identified as a c-Src-interacting adaptor bearing SH2/SH3-binding motifs, two PH domains, and a coiled-coil region that itself becomes tyrosine-phosphorylated and amplifies Src signal transduction (PMID:17412687). Upon phosphorylation at defined tyrosines (Y54 by the RET/PTC oncokinase; Y72 in the rodent ortholog), it recruits the p85α regulatory subunit of PI3K through p85α SH2 domains, channeling kinase input into Akt activation and downstream control of cell-cycle and survival effectors including p21, p27, FOXO3a, and GSK3β (PMID:19060924, PMID:22928011, PMID:22496359). Its phosphorylation state is set bidirectionally: receptor tyrosine phosphatase PTPRZ dephosphorylates AFAP1L2, and pleiotrophin-mediated PTPRZ inhibition raises AFAP1L2 phosphorylation to drive PI3K-AKT-mTOR signaling and oligodendrocyte precursor differentiation and remyelination (PMID:30667096). Independently of phosphorylation, AFAP1L2 directly binds and crosslinks F-actin via a C-terminal actin-binding region and N-terminal multimerization domain, translocating to lamellipodia in a Rac1-dependent manner to govern cell spreading, migration, invasion, and endocytosis (PMID:21084565, PMID:27462298). It nucleates a complex with the Tks5 scaffold and Src that sustains proliferation and survival and partitions migratory output between Rac1- and Cdc42-driven structures (PMID:26446840, PMID:27835612). In thyrocytes it links the actin cortex to the microtubule network at the apical membrane to direct folliculogenesis, and its loss causes congenital hypothyroidism rescuable by thyroxine (PMID:34652970, PMID:34470464). AFAP1L2 is broadly oncogenic and drug-resistance-associated: it drives a SRC-FUNDC1 axis that suppresses mitophagy in hepatocellular carcinoma (PMID:37733919), sustains PI3K/AKT in trastuzumab-resistant HER2+ gastric cancer (PMID:36284062), and its mRNA stability and translation are controlled by 3'UTR-binding proteins hnRNPC and hnRNPR (PMID:39800708, PMID:40268079).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2007 High

    Established AFAP1L2/XB130 as a bona fide adaptor protein physically and functionally coupled to c-Src, answering whether it participates in tyrosine-kinase signaling.

    Evidence Cloning, reciprocal Co-IP, COS-7 co-expression, siRNA knockdown and deletion mutagenesis in lung epithelial cells

    PMID:17412687

    Open questions at the time
    • Direct substrate/kinase relationship not fully resolved
    • Which domains mediate Src binding versus scaffolding not delineated
  2. 2008 High

    Identified Y54 as the kinase-targeted residue that links RET/PTC signaling to PI3K via p85α, defining the molecular route from kinase input to Akt.

    Evidence Site-directed mutagenesis (Y54), Co-IP with p85α, siRNA knockdown with Akt/ERK readout in TPC1 thyroid cancer cells

    PMID:19060924

    Open questions at the time
    • Whether other kinases phosphorylate Y54 not determined
    • Stoichiometry of the XB130-p85α-PI3K complex unknown
  3. 2010 High

    Showed AFAP1L2 translocates to the lamellipodial F-actin meshwork under Rac and growth-factor cues and is required for motility, separating its actin/migration role from its kinase-substrate role.

    Evidence Live-cell imaging, constitutively active Rac, deletion mutagenesis, wound-healing and Matrigel invasion assays in TPC1 cells

    PMID:21084565

    Open questions at the time
    • Direct actin binding not yet demonstrated at this stage
    • Mechanism of Rac-dependent recruitment unresolved
  4. 2010 Medium

    Demonstrated AFAP1L2 is required for cancer cell proliferation, survival, and tumor growth in vivo, establishing functional importance beyond signaling biochemistry.

    Evidence shRNA knockdown, cell-cycle/apoptosis assays, xenografts in nude mice, microarray profiling in WRO thyroid cancer cells

    PMID:21224076

    Open questions at the time
    • Single-lab, single-tumor-type evidence
    • Causal effectors among 246 changed genes not validated
  5. 2012 Medium

    Mapped the PI3K/Akt-dependent downstream effectors (p21, p27, FOXO3a, GSK3β) controlled by AFAP1L2 in both RET/PTC-positive and -negative cells, generalizing its proliferation/survival mechanism.

    Evidence siRNA knockdown, Western blot of Akt substrates, cell-cycle and caspase assays in WRO and A549 cells

    PMID:22928011

    Open questions at the time
    • Direct versus indirect effector regulation not separated
    • Single lab
  6. 2012 High

    Defined Y72 in the rodent ortholog as the critical p85-binding residue and placed AFAP1L2 in a cAMP/Src-driven mitogenic loop, confirming the phospho-tyrosine–p85 mechanism in a non-cancer thyroid system.

    Evidence MALDI-TOF identification, Y72F mutagenesis, PP1/PP2 inhibitors, Co-IP, PI3K activity and DNA synthesis assays in rat FRTL-5 cells

    PMID:22496359

    Open questions at the time
    • Correspondence between rodent Y72 and human Y54 not formally reconciled
    • Upstream kinase identity in this context limited to Src inference
  7. 2015 High

    Identified the Tks5 scaffold as a direct N-terminal partner forming a Tks5-XB130-Src complex required for Src/PI3K/Akt activation, revealing a higher-order scaffolding mechanism for sustained signaling.

    Evidence Yeast two-hybrid, endogenous Co-IP, interface mutagenesis (XB130 ΔN, Tks5 SH3 W1108A), proliferation/apoptosis assays

    PMID:26446840

    Open questions at the time
    • Structural basis of the SH3-polyproline interface not solved
    • Whether complex assembles constitutively or stimulus-dependently unclear
  8. 2015 Medium

    Extended the migration role to carcinogen (NNK)-induced motility in bronchial epithelium and linked AFAP1L2 to MMP-14 relocalization, connecting it to invasive machinery.

    Evidence Immunofluorescence, full-length/truncation overexpression, migration assays, MMP-14 localization in BEAS2B cells

    PMID:25980441

    Open questions at the time
    • Direct AFAP1L2-MMP-14 link not established
    • Single lab
  9. 2016 High

    Reconstituted AFAP1L2 as a direct F-actin binder and crosslinker, mapping the C-terminal actin-binding region and N-terminal multimerization domain and tying these to endocytosis, providing the biochemical basis for its cortical functions.

    Evidence In vitro F-actin binding/crosslinking with recombinant protein, deletion mutagenesis, Blue native-PAGE, dextran uptake in HEK293

    PMID:27462298

    Open questions at the time
    • In vivo contribution of crosslinking to motility not quantified
    • Regulation of actin binding by phosphorylation unknown
  10. 2016 Medium

    Showed AFAP1L2/Rac1 and Tks5/Cdc42 modules direct distinct migration modes from a shared complex, defining how the scaffold partitions cytoskeletal output.

    Evidence Immunofluorescence with WAVE2/N-WASP markers, Co-IP (XB130-Rac1; Tks5-Cdc42), co-overexpression and migration assays in airway epithelial cells

    PMID:27835612

    Open questions at the time
    • Direct versus indirect Rac1 binding not dissected
    • Single lab
  11. 2019 High

    Identified PTPRZ as the phosphatase counteracting AFAP1L2 tyrosine phosphorylation and placed AFAP1L2 in pleiotrophin-controlled PI3K-AKT-mTOR signaling for OPC differentiation and remyelination, establishing a physiological, non-cancer role and a bidirectional phospho-control axis.

    Evidence In vitro phosphatase assay, Co-IP, siRNA knockdown, PTPRZ catalytic-dead knock-in mice, pathway Western blots

    PMID:30667096

    Open questions at the time
    • Specific dephosphorylated tyrosines not mapped
    • Kinase responsible in OPCs not identified
  12. 2021 High

    Defined a developmental, kinase-independent function: AFAP1L2 links the apical actin cortex to microtubules in thyrocytes to direct folliculogenesis, and its loss causes congenital hypothyroidism rescuable by thyroxine.

    Evidence Xb130 knockout mice, 3D thyrocyte cultures, confocal imaging, histology, levothyroxine rescue

    PMID:34470464 PMID:34652970

    Open questions at the time
    • Molecular bridge to microtubule-associated proteins not identified
    • Relationship to Src/PI3K signaling in this context unclear
  13. 2023 Medium

    Linked AFAP1L2 to mitophagy control via a SRC-FUNDC1 axis driving sorafenib resistance in HCC, expanding its effector repertoire beyond PI3K/Akt.

    Evidence Co-IP, CETSA, SPR, shRNA/overexpression, TEM mitophagy readout, xenografts in HCC cells

    PMID:37733919

    Open questions at the time
    • Whether AFAP1L2 directly modulates SRC kinase activity or scaffolds FUNDC1 unclear
    • Single lab
  14. 2022 Medium

    Showed AFAP1L2 sustains PI3K/AKT in trastuzumab-resistant HER2+ gastric cancer and proposed a SRC-XB130-PTEN feedback loop, connecting it to therapy resistance.

    Evidence Co-IP (XB130-p85α), shRNA knockdown, qRT-PCR, xenografts

    PMID:36284062

    Open questions at the time
    • Mechanism of PTEN transcriptional repression not defined
    • Single lab
  15. 2025 Medium

    Identified post-transcriptional control of AFAP1L2 by 3'UTR-binding proteins hnRNPC and hnRNPR, which stabilize its mRNA against XRN1/DIS3L2 (and, for hnRNPC, enhance translation via eIF4E), explaining how AFAP1L2 levels are elevated in NSCLC.

    Evidence RNA pull-down, RIP, dual-luciferase 3'UTR reporters, Co-IP (hnRNPC-eIF4E), knockdown/overexpression, in vivo NSCLC models

    PMID:39800708 PMID:40268079

    Open questions at the time
    • Whether hnRNPC and hnRNPR act cooperatively or redundantly unclear
    • Single lab for each

Open questions

Synthesis pass · forward-looking unresolved questions
  • How AFAP1L2's two activities — phospho-dependent PI3K recruitment and phospho-independent actin crosslinking — are coordinated within a single cell and whether they share or compete for the same molecular pool remains unresolved.
  • No structural model integrating PH domains, actin-binding, and scaffolding regions
  • No high-resolution structure of any AFAP1L2 complex
  • Regulation switching between signaling and cytoskeletal modes uncharacterized

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 3 GO:0098772 molecular function regulator activity 3 GO:0008092 cytoskeletal protein binding 2
Localization
GO:0005856 cytoskeleton 3 GO:0005886 plasma membrane 2 GO:0005829 cytosol 1
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-1266738 Developmental Biology 3 R-HSA-1643685 Disease 3 R-HSA-8953854 Metabolism of RNA 2 R-HSA-9612973 Autophagy 1
Partners
FUNDC1HNRNPCPIK3R1PTPRZ1RAC1RETSRCTKS5
Complex memberships
XB130-Tks5-Src complex

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2007 XB130 (AFAP1L2) was cloned as a novel adaptor protein containing SH2- and SH3-binding motifs, two pleckstrin homology domains, a coiled-coil region, and multiple phosphorylation sites. Endogenous XB130 interacts with c-Src tyrosine kinase, and co-expression in COS-7 cells activated c-Src and elevated tyrosine phosphorylation of multiple proteins including XB130 itself. An N-terminal deletion mutant (XB130ΔN) reduced its ability to mediate Src signal transduction. Knockdown in lung epithelial cells reduced c-Src activity, IL-8 production, EGF-induced phosphorylation of Akt and GSK3β, and altered cell cycles. Co-immunoprecipitation, co-expression in COS-7 cells, siRNA knockdown, reporter assay (SRE/AP-1), deletion mutagenesis, Western blot The Journal of biological chemistry High 17412687
2008 RET/PTC oncogenic kinase phosphorylates XB130 predominantly at tyrosine 54, which promotes XB130 association with the p85α subunit of PI3-kinase via p85α SH2 domains, thereby linking RET/PTC signaling to PI3K/Akt activation. Knockdown of XB130 in TPC1 papillary thyroid cancer cells strongly reduced Akt activity without altering ERK1/2 phosphorylation, and inhibited cell-cycle progression and survival. Co-immunoprecipitation, site-directed mutagenesis (Y54), siRNA knockdown, Western blot for Akt/ERK phosphorylation, cell cycle analysis Oncogene High 19060924
2010 XB130 translocates to the cell periphery in response to EGF, wounding, and constitutively active Rac, localizing to the lamellipodial F-actin meshwork. Structure-function analysis showed that both the N-terminus (167 aa) and C-terminus (63 aa) are required for translocation to lamellipodia, while PH domains and Src-targeted tyrosines are dispensable. Silencing XB130 in TPC1 cells decreased wound closure rate, inhibited Matrigel invasion, reduced lamellipodial persistence, and slowed spreading. Live-cell imaging, constitutively active Rac expression, pharmacological inhibitors, deletion mutagenesis, siRNA knockdown, wound-healing and Matrigel invasion assays Journal of cell science High 21084565
2010 Knockdown of XB130 in WRO thyroid cancer cells inhibited G1-S phase progression, induced spontaneous apoptosis, and enhanced intrinsic and extrinsic apoptotic stimulus-induced cell death. In vivo, XB130 shRNA stably transfected WRO cells formed significantly smaller tumors in nude mice. Microarray identified 246 significantly changed genes, including 57 related to cell proliferation or survival. siRNA/shRNA knockdown, cell cycle analysis, apoptosis assays, xenograft mouse model, microarray gene expression profiling The American journal of pathology Medium 21224076
2012 XB130 mediates cancer cell proliferation and survival through PI3K/Akt downstream signals including phosphorylation of p21Cip1/WAF1, p27Kip1, FOXO3a, and GSK3β (but not FOXO1 or p53), in both RET/PTC-mutant (WRO) and RET/PTC-negative (A549) cancer cells. XB130 can be phosphorylated by multiple protein tyrosine kinases. siRNA knockdown, Western blot for phosphorylated Akt substrates, cell cycle analysis, caspase cleavage assay PloS one Medium 22928011
2012 In rat FRTL-5 thyroid cells, cAMP treatment elevated PI3KAP/XB130 mRNA and protein levels, increased its tyrosine phosphorylation by c-Src (blocked by PP1/PP2), and enhanced its interaction with p85 PI3K, leading to increased PI3K activity. PI3KAP/XB130 knockdown attenuated cAMP-dependent potentiation of IGF-I-induced DNA synthesis. A Y72F mutant incapable of binding p85 PI3K did not enhance IGF-I-induced DNA synthesis, establishing Y72 as the critical p85 PI3K-binding site. MALDI-TOF MS (protein identification), siRNA knockdown, Src kinase inhibitors (PP1/PP2), point mutagenesis (Y72F), co-immunoprecipitation, PI3K activity assay, DNA synthesis assay Molecular endocrinology (Baltimore, Md.) High 22496359
2013 XB130 suppresses expression of tumor-suppressive microRNAs (miR-33a, miR-149, miR-193a-3p) in thyroid cancer cells. These miRNAs target oncogenes MYC (miR-33a), FOSL1 (miR-149), and SLC7A5 (miR-193a-3p) at their 3' UTR, and their upregulation upon XB130 knockdown reduces cancer cell growth. miRNA array, shRNA knockdown, qRT-PCR validation, ectopic overexpression, miRNA mimic transfection, 3' UTR reporter assay PloS one Medium 23527086
2015 XB130 interacts with scaffold protein Tks5: the fifth SH3 domain of Tks5 binds to the N-terminus of XB130 (which contains polyproline-rich motifs), and both proteins form a complex with Src tyrosine kinase. Disrupting XB130/Tks5 binding (via XB130 N-terminal deletion mutant or Tks5 SH3-W1108A mutant) decreased cell proliferation and survival and inhibited serum/growth-factor-induced Src activation and downstream PI3K/Akt phosphorylation. Yeast two-hybrid screening, co-immunoprecipitation (endogenous), structure-function mutagenesis, cell proliferation and apoptosis assays, Western blot Molecular biology of the cell High 26446840
2015 XB130 translocates to lamellipodia and microfilamentous structures in BEAS2B bronchial epithelial cells after NNK stimulation, and overexpression significantly enhances NNK-induced migration. Both the N- and C-termini of XB130 are required for this migration-enhancing function. XB130 overexpression enhanced NNK-induced protein tyrosine phosphorylation and promoted matrix metalloproteinase-14 (MMP-14) translocation to cell motility-associated structures. Immunofluorescence/localization, overexpression of full-length and truncation mutants, migration assay, Western blot for tyrosine phosphorylation, MMP-14 localization Oncotarget Medium 25980441
2016 XB130 (PI3KAP) directly binds F-actin through its C-terminal region (residues 830-840), and multimerizes via its N-terminal 40 amino acids (shown by Blue native-PAGE and co-IP). Both actin-binding and multimerization are required for XB130 to crosslink F-actin in vitro. Overexpression of XB130 enhanced dextran endocytosis in HEK293 cells, dependent on its actin-binding region. In vitro F-actin binding and crosslinking assay with recombinant protein, deletion mutagenesis, Blue native-PAGE, co-immunoprecipitation, endocytosis assay (dextran uptake) Frontiers in endocrinology High 27462298
2016 In airway epithelial cells, XB130 and Tks5 translocate to the cell membrane in a stimulus-dependent manner upon EGF, PKC activator, or nicotinic acetylcholine receptor ligand stimulation. XB130 co-localizes with lamellipodial marker WAVE2 whereas Tks5 co-localizes with podosome marker N-WASP. XB130 interacts with Rac1 and Tks5 interacts with Cdc42 to promote Rho GTPase activity. Co-expression of both proteins inhibits cell migration; dissociation of the complex promotes lateral (XB130/Rac1) or vertical (Tks5/Cdc42) cell migration. Immunofluorescence localization, co-immunoprecipitation (XB130-Rac1; Tks5-Cdc42), overexpression and co-overexpression, migration assay Oncotarget Medium 27835612
2019 PTPRZ (protein tyrosine phosphatase receptor Z) dephosphorylates AFAP1L2 at tyrosine residues in vitro and in HEK293T cells. Pleiotrophin (PTN)-mediated inhibition of PTPRZ enhances tyrosine phosphorylation of AFAP1L2, which activates the PI3K-AKT-mTOR pathway to promote oligodendrocyte precursor cell (OPC) differentiation. Knockdown of AFAP1L2 or PI3K inhibition suppressed OPC differentiation and PTN-induced AKT/mTOR phosphorylation. PTPRZ catalytic-dead knock-in mice showed higher AFAP1L2, AKT, and mTOR phosphorylation and accelerated remyelination. In vitro phosphatase assay (recombinant PTPRZ on AFAP1L2), co-immunoprecipitation in HEK293T, siRNA knockdown in OPC-like cells, catalytic-dead knock-in mouse model, Western blot for PI3K-AKT-mTOR, immunofluorescence Glia High 30667096
2021 XB130 in thyrocytes critically regulates folliculogenesis by functioning as a link between the actin filament cortex and microtubule network at the apical membrane. In 3D cultures, XB130 aligns with actin filaments and participates in defining the site of apical membrane formation and lumen coalescence. Xb130-knockout thyrocytes showed delayed folliculogenesis, reduced recruitment of microtubule-associated proteins, and disorganized acetylated tubulin under the apical membrane. Xb130 knockout mouse, 3D Matrigel culture of primary thyrocytes, immunofluorescence/confocal microscopy, XB130-GFP transfection for live imaging Thyroid : official journal of the American Thyroid Association High 34652970
2021 Xb130-knockout mice develop congenital hypothyroidism due to disorganized apical membrane structure of thyrocytes, with diminished thyroglobulin iodination and release. XB130 is localized mainly on the apical membrane of thyroid follicles. Growth retardation in KO mice could be rescued by exogenous thyroxine supplementation, demonstrating that the phenotype is caused by insufficient thyroid hormone production. Xb130 knockout mouse model, histology, immunohistochemistry, immunofluorescence, Western blot, quantitative RT-PCR, levothyroxine rescue experiment Thyroid : official journal of the American Thyroid Association High 34470464
2023 AFAP1L2 activates a SRC-FUNDC1 signaling axis in HCC cells to block FUNDC1 recruitment of LC3B to mitochondria, thereby inhibiting mitophagy. AFAP1L2 overexpression in sorafenib-resistant cells leads to elevated phosphorylation of SRC and FUNDC1 and suppressed mitophagy. Artesunate reduces AFAP1L2 protein expression, suppresses SRC/FUNDC1 phosphorylation, and promotes massive FUNDC1-LC3B co-recruitment to mitochondria, overactivating mitophagy and inducing apoptosis of resistant cells. Co-immunoprecipitation (AFAP1L2-SRC interaction), CETSA (artesunate-AFAP1L2 target engagement), shRNA knockdown, overexpression, surface plasmon resonance, in vitro and xenograft in vivo models, immunofluorescence, TEM for mitophagy Autophagy Medium 37733919
2017 AFAP1L2/RET is a fusion oncogene identified in papillary thyroid cancers of young patients in Fukushima; functional analysis confirmed its transforming ability through activation of the MAPK pathway. 5' RACE identification, functional transformation assay, MAPK pathway activation analysis Thyroid : official journal of the American Thyroid Association Medium 28351223
2022 In HER2+ gastric cancer cells resistant to trastuzumab, XB130 expression is increased and p-SRC (Tyr416) facilitates binding of XB130 to PI3K p85α. XB130 knockdown reverses resistance by downregulating p-AKT. XB130 negatively regulates PTEN gene transcription, forming a positive feedback loop (SRC-XB130-PTEN) that sustains PI3K/AKT activation. Western blot, qRT-PCR, CCK8, co-immunoprecipitation (XB130-PI3K p85α), shRNA knockdown, xenograft mouse model Clinical & translational oncology Medium 36284062
2024 In bone marrow stromal cells on TiO2 nanotube surfaces, XB130 interacts with Src and activates the downstream PI3K/Akt/GSK-3β/β-catenin pathway. Filamentous actin depolymerization changes XB130 expression and distribution, thereby affecting osteogenic differentiation. XB130 overexpression promotes osteogenic differentiation while knockdown inhibits it. Co-immunoprecipitation (XB130-Src), siRNA knockdown, overexpression, Western blot for PI3K/Akt/GSK-3β/β-catenin, immunofluorescence, in vitro and in vivo osteogenesis assays Acta biomaterialia Medium 38360291
2025 hnRNPC binds to specific regions of the XB130 3'UTR, enhancing XB130 mRNA stability by inhibiting recruitment of nucleases XRN1 and DIS3L2, and simultaneously interacts with eIF4E (component of eIF4F complex) to facilitate XB130 mRNA circularization and increase translation efficiency, resulting in elevated XB130/PI3K/Akt signaling and promotion of NSCLC cell proliferation and EMT. RNA pull-down assay, RNA immunoprecipitation, dual-luciferase reporter assay, co-immunoprecipitation (hnRNPC-eIF4E), Western blot, qRT-PCR, overexpression/knockdown functional assays Cancer cell international Medium 39800708
2025 hnRNPR protects XB130 mRNA from XRN1- and DIS3L2-mediated degradation by binding to specific regions within the XB130 3'UTR, thereby elevating XB130 expression, activating the Akt signaling pathway, and promoting NSCLC cell proliferation and EMT. RNA pull-down assay, RNA immunoprecipitation, dual-luciferase reporter assay, Western blot, qRT-PCR, overexpression/knockdown, tissue microarray, in vivo experiments Cellular signalling Medium 40268079

Source papers

Stage 0 corpus · 42 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2014 XB130 promotes proliferation and invasion of gastric cancer cells. Journal of translational medicine 86 24387290
2007 XB130, a novel adaptor protein for signal transduction. The Journal of biological chemistry 74 17412687
2023 Artesunate Sensitizes human hepatocellular carcinoma to sorafenib via exacerbating AFAP1L2-SRC-FUNDC1 axis-dependent mitophagy. Autophagy 69 37733919
2008 XB130, a tissue-specific adaptor protein that couples the RET/PTC oncogenic kinase to PI 3-kinase pathway. Oncogene 57 19060924
2017 Identification of Three Novel Fusion Oncogenes, SQSTM1/NTRK3, AFAP1L2/RET, and PPFIBP2/RET, in Thyroid Cancers of Young Patients in Fukushima. Thyroid : official journal of the American Thyroid Association 44 28351223
2010 Adaptor protein XB130 is a Rac-controlled component of lamellipodia that regulates cell motility and invasion. Journal of cell science 41 21084565
2010 XB130, a novel adaptor protein, promotes thyroid tumor growth. The American journal of pathology 41 21224076
2019 The PTN-PTPRZ signal activates the AFAP1L2-dependent PI3K-AKT pathway for oligodendrocyte differentiation: Targeted inactivation of PTPRZ activity in mice. Glia 37 30667096
2012 XB130 mediates cancer cell proliferation and survival through multiple signaling events downstream of Akt. PloS one 37 22928011
2013 XB130, a new adaptor protein, regulates expression of tumor suppressive microRNAs in cancer cells. PloS one 32 23527086
2011 Roles of XB130, a novel adaptor protein, in cancer. Journal of clinical bioinformatics 27 21884627
2014 XB130-A Novel Adaptor Protein: Gene, Function, and Roles in Tumorigenesis. Scientifica 26 24995146
2016 XB130: A novel adaptor protein in cancer signal transduction. Biomedical reports 21 26998266
2012 Phosphatidylinositol 3-kinase-binding protein, PI3KAP/XB130, is required for cAMP-induced amplification of IGF mitogenic activity in FRTL-5 thyroid cells. Molecular endocrinology (Baltimore, Md.) 21 22496359
2015 XB130/Tks5 scaffold protein interaction regulates Src-mediated cell proliferation and survival. Molecular biology of the cell 18 26446840
2020 XB130, regulated by miR-203, miR-219, and miR-4782-3p, mediates the proliferation and metastasis of non-small-cell lung cancer cells. Molecular carcinogenesis 16 32159887
2019 Knockdown of XB130 restrains cancer stem cell-like phenotype through inhibition of Wnt/β-Catenin signaling in breast cancer. Molecular carcinogenesis 16 31219645
2015 XB130 translocation to microfilamentous structures mediates NNK-induced migration of human bronchial epithelial cells. Oncotarget 16 25980441
2016 XB130 is overexpressed in prostate cancer and involved in cell growth and invasion. Oncotarget 15 27509056
2019 XB130 deficiency enhances carcinogen-induced skin tumorigenesis. Carcinogenesis 13 30820526
2015 Integrated pathway and epistasis analysis reveals interactive effect of genetic variants at TERF1 and AFAP1L2 loci on melanoma risk. International journal of cancer 13 25892537
2024 TiO2 nanotube topography enhances osteogenesis through filamentous actin and XB130-protein-mediated mechanotransduction. Acta biomaterialia 12 38360291
2014 XB130 deficiency affects tracheal epithelial differentiation during airway repair. PloS one 12 25272040
2015 XB130 promotes bronchioalveolar stem cell and Club cell proliferation in airway epithelial repair and regeneration. Oncotarget 10 26360608
2021 XB130 Plays an Essential Role in Folliculogenesis Through Mediating Interactions Between Microfilament and Microtubule Systems in Thyrocytes. Thyroid : official journal of the American Thyroid Association 9 34652970
2018 XB130 Knockdown Inhibits the Proliferation, Invasiveness, and Metastasis of Hepatocellular Carcinoma Cells and Sensitizes them to TRAIL-Induced Apoptosis. Chinese medical journal 9 30246718
2016 Phosphatidylinositol 3-Kinase-Associated Protein (PI3KAP)/XB130 Crosslinks Actin Filaments through Its Actin Binding and Multimerization Properties In Vitro and Enhances Endocytosis in HEK293 Cells. Frontiers in endocrinology 9 27462298
2015 Expression of XB130 in human ductal breast cancer. International journal of clinical and experimental pathology 9 26191231
2021 XB130 Deficiency Causes Congenital Hypothyroidism in Mice due to Disorganized Apical Membrane Structure and Function of Thyrocytes. Thyroid : official journal of the American Thyroid Association 8 34470464
2021 Adaptor protein XB130 regulates the aggressiveness of cholangiocarcinoma. PloS one 8 34780466
2016 Stimulus-dependent dissociation between XB130 and Tks5 scaffold proteins promotes airway epithelial cell migration. Oncotarget 8 27835612
2015 XB130 expression in human osteosarcoma: a clinical and experimental study. International journal of clinical and experimental pathology 8 26045762
2017 XB130 enhances invasion and migration of human colorectal cancer cells by promoting epithelial‑mesenchymal transition. Molecular medicine reports 7 28849225
2016 XB130 deficiency enhances lipopolysaccharide-induced septic response and acute lung injury. Oncotarget 7 27029000
2022 Thyroidal Transcriptomic Profiles of Pathoadaptive Responses to Congenital Hypothyroidism in XB130 Knockout Mice. Cells 5 35326426
2025 Heterogeneous nuclear ribonucleoprotein C promotes non-small cell lung cancer progression by enhancing XB130 mRNA stability and translation. Cancer cell international 2 39800708
2023 The 3'‑untranslated region of XB130 regulates its mRNA stability and translational efficiency in non‑small cell lung cancer cells. Oncology letters 2 37720672
2023 XB130 inhibits healing of diabetic skin ulcers through the PI3K/Akt signalling pathway. World journal of diabetes 2 37771334
2022 Pathogenesis of Multinodular Goiter in Elderly XB130-Deficient Mice: Alteration of Thyroperoxidase Affinity with Iodide and Hydrogen Peroxide. Thyroid : official journal of the American Thyroid Association 2 34915750
2022 Molecular mechanism of XB130 adaptor protein mediates trastuzumab resistance in gastric cancer. Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico 2 36284062
2025 HnRNPR promotes non-small cell lung cancer progression by protecting XB130 mRNA from XRN1- and DIS3L2-mediated degradation. Cellular signalling 0 40268079
2015 WITHDRAWN: XB130 expression in human osteosarcoma: a clinical and experimental study. International journal of clinical pharmacology and therapeutics 0 25997546

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