The research report should be a detailed narrative explaining the function, biological processes, and localization of the gene product. Citations should be given for all claims.
You should prioritize authoritative reviews and primary scientific literature when conducting research. You can supplement
this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.
We are specifically interested in the primary function of the gene - for enzymes, what reaction is catalyzed, and what is the substrate specificity? For transporters, what is the substrate? For structural proteins or adapters, what is the broader structural role? For signaling molecules, what is the role in the pathway.
We are interested in where in or outside the cell the gene product carries out its function.
We are also interested in the signaling or biochemical pathways in which the gene functions. We are less interested in broad pleiotropic effects, except where these elucidate the precise role.
Include evidence where possible. We are interested in both experimental evidence as well as inference from structure, evolution, or bioinformatic analysis. Precise studies should be prioritized over high-throughput, where available.
The requested identity is verified: AFAP1L2 is the human gene encoding actin filament-associated protein 1-like 2, commonly called XB130, with aliases KIAA1914 and PI3KAP. The literature consistently describes an 818-amino-acid, approximately 130-kDa AFAP-family protein encoded at chromosome 10q25.3; this matches the supplied human UniProt accession Q8N4X5 and its AFAP, AFAP_N, AFAP_C, and PH-domain annotations. No conflicting similarly named gene was used in this report. (bai2014xb130—anoveladaptor pages 2-3, bai2014xb130—anoveladaptor pages 1-2)
AFAP1L2 is not an enzyme or transporter. Its best-supported primary function is that of a multivalent intracellular adaptor/scaffold and cytoskeletal organizer. It couples activated tyrosine kinases—particularly Src-family kinases and RET/PTC—to PI3K–Akt signaling, while also associating with actin-rich membrane structures. Biochemical work indicates that XB130 can bind and crosslink F-actin through C-terminal actin binding plus N-terminal multimerization. Its clearest physiological role is at the apical membrane of thyroid follicular cells, where it organizes the actin–microtubule interface needed for epithelial polarity, follicular-lumen formation, thyroglobulin handling, iodination, and thyroid-hormone production. (shiozaki2011rolesofxb130 pages 1-2, wang2022xb130playsan pages 1-2, wang2021xb130deficiencycauses pages 1-2, yamanaka2016phosphatidylinositol3kinaseassociatedprotein pages 1-2)
Recent work has expanded this model beyond epithelial biology. A 2023 human liver-cancer proteomic study identified AFAP1L2 as a negative regulator of chronically stimulated CD8 T-cell survival and antitumor activity, while a 2024 study implicated an AFAP1L2–SRC–FUNDC1 axis in hepatocellular-carcinoma sorafenib resistance. Both findings are translationally interesting but remain preclinical, not established clinical uses. (canale2023proteomicsofimmune pages 1-3, canale2023proteomicsofimmune pages 10-12, ma2024artesunatesensitizeshuman pages 1-2, ma2024artesunatesensitizeshuman pages 5-6)
AFAP1L2/XB130 belongs to the small actin filament-associated protein family, alongside AFAP1 and AFAP1L1. The human gene reportedly contains 19 exons and produces a 3,751-bp transcript encoding an 818-residue protein. Reported aliases include XB130, KIAA1914, PI3KAP, and CTB-1144G6.4. (bai2014xb130—anoveladaptor pages 1-2, cho2019understandingtherole pages 23-28)
The protein’s modular organization explains its scaffold function:
This domain arrangement aligns with the supplied UniProt/InterPro annotations. It is important, however, to distinguish annotations from demonstrated activity: PH domains imply membrane-lipid recognition, but lipid specificity has not been defined as rigorously as the p85α and F-actin interactions. Likewise, residue numbering in the actin-crosslinking study used an approximately 843-residue PI3KAP/XB130 ortholog construct, so its reported residues 830–840 should not be transferred directly to the 818-residue human canonical sequence without sequence alignment. (yamanaka2016phosphatidylinositol3kinaseassociatedprotein pages 1-2, yamanaka2016phosphatidylinositol3kinaseassociatedprotein pages 3-6)
XB130 is phosphorylated by several protein tyrosine kinases and provides docking sites that assemble signaling complexes. Src binds XB130 through SH2/SH3-dependent interactions, phosphorylates it, and is itself driven toward the active Tyr416-phosphorylated state without a corresponding change at inhibitory Tyr527. In cell-based assays, XB130/Src signaling increased AP-1 and serum-response-element reporter activity and promoted IL-8-associated inflammatory signaling. (moodley2016physiologicalrolesof pages 46-52, rubacha2010xb130insilico pages 28-32)
In thyroid carcinoma cells, activated RET/PTC1 or RET/PTC3 phosphorylates XB130, including its Tyr54 YxxM motif. Phosphorylated XB130 then binds PI3K p85α and promotes Akt phosphorylation. AFAP1L2 knockdown reduced Akt phosphorylation while leaving MAPK phosphorylation comparatively unaffected, supporting a selective RET/PTC–XB130–PI3K–Akt branch rather than XB130 being a universal RET effector. (bai2014xb130—anoveladaptor pages 2-3, moodley2016physiologicalrolesof pages 46-52, rubacha2010xb130insilico pages 28-32)
Downstream cellular consequences documented after knockdown include impaired G1-to-S progression, reduced proliferation, and increased spontaneous or stimulus-induced apoptosis. Selected Akt-regulated nodes affected include p21^Cip1/WAF1, p27^Kip1, FOXO3a, GSK3β, and caspases 8 and 9. These data support a context-dependent survival scaffold rather than an intrinsic catalytic activity. (shiozaki2011rolesofxb130 pages 1-2, moodley2016physiologicalrolesof pages 52-58)
A 2016 mechanistic study demonstrated direct actin-related activity using recombinant protein, deletion constructs, NIH3T3 cells, and HEK293 cells. A C-terminal segment containing residues 830–840 in the tested ortholog was necessary and sufficient for F-actin localization and bound polymerized actin in pelleting assays. The N-terminal 40 residues were required for multimerization; native complexes migrated at approximately 250–1,200 kDa compared with an approximately 125-kDa monomer. Deleting either the actin-binding region or multimerization region abolished crosslinking, yielding a model in which multimeric XB130 presents several C-terminal actin-binding sites to bridge filaments. (yamanaka2016phosphatidylinositol3kinaseassociatedprotein pages 1-2, yamanaka2016phosphatidylinositol3kinaseassociatedprotein pages 3-6)
This activity has functional implications for membrane trafficking. Full-length XB130 overexpression significantly increased fluorescent-dextran uptake in HEK293 cells (p<0.01), whereas an actin-binding-region deletion behaved largely like control. In rat FRTL-5 thyroid cells, knockdown produced only a nonsignificant tendency toward reduced uptake (p=0.11), so a general endogenous requirement for endocytosis remains less certain than the biochemical crosslinking result. (yamanaka2016phosphatidylinositol3kinaseassociatedprotein pages 8-10)
Under basal conditions XB130 is predominantly cytoplasmic, with some perinuclear distribution. Following EGF, wounding, or related motility stimuli, it redistributes to F-actin-rich lamellipodia within roughly 160–200 seconds; cytochalasin D blocks this redistribution. XB130 associates with Rac1-driven lamellipodial structures rather than RhoA-driven stress fibers, and loss of XB130 reduces migration and invasion in epithelial and cancer-cell models. Thus, localization is dynamic and depends on cell type and activation state. (moodley2016physiologicalrolesof pages 52-58, cho2019understandingtherole pages 23-28)
XB130 is an intracellular protein; there is no evidence that it is secreted or an integral membrane transporter. Reported human expression is particularly high in thyroid and spleen, with protein also detected in parathyroid, brain, kidney, skin, and gastrointestinal tissues. These surveys establish distribution but not equivalent function in every tissue. (bai2014xb130—anoveladaptor pages 2-3, bai2014xb130—anoveladaptor pages 1-2)
The most mechanistically informative localization is in thyrocytes. XB130 concentrates at the apical membrane/cortical cytoskeleton of thyroid follicles, aligns with apical actin, and helps recruit or organize subapical microtubules. In motile cells it can instead concentrate at the cell periphery and lamellipodia. These observations are consistent with PH-mediated membrane recruitment plus actin and protein-partner interactions. (wang2022xb130playsan pages 1-2, wang2021xb130deficiencycauses pages 1-2)
The strongest organism-level functional evidence comes from Xb130-knockout mice. Knockout animals developed congenital hypothyroidism with reduced thyroid-hormone synthesis and secretion, low serum T4, elevated TSH, and transient postnatal growth retardation. Levothyroxine restored pituitary growth-hormone production and prevented growth retardation, showing that the growth phenotype was secondary to hypothyroidism. (wang2021xb130deficiencycauses pages 1-2, wang2021xb130deficiencycauses pages 5-7)
Mechanistically, knockout thyroids showed delayed folliculogenesis, malformed lumina, fewer or disorganized apical structures, diminished thyroglobulin release into the lumen, and reduced thyroglobulin iodination during embryonic and early postnatal development. Radioiodide experiments showed increased thyroid uptake but perchlorate-sensitive retention, indicating defective iodide organification rather than uptake. At postnatal week 2, nearly all measured thyroidal hormone pools were reduced; by week 14, intrathyroidal hormone accumulation accompanied low serum T4, consistent with compensatory synthesis but impaired secretion. (wang2021xb130deficiencycauses pages 10-12, wang2021xb130deficiencycauses pages 5-7)
A follow-up 2022 study placed XB130 between the cortical actin and microtubule systems. In three-dimensional cultures, XB130 aligned with actin at sites where apical membranes coalesced to form follicular lumina. Knockout cells had delayed lumen formation, reduced recruitment of microtubule-associated components, and disorganized acetylated-tubulin structures. Developmental imaging used approximately 4–11 mice per genotype and stage. Expression of human XB130-GFP in knockout thyrocytes supported the relevance of the human protein, although the disease phenotype itself remains demonstrated in mice rather than genetically confirmed human cases. (wang2022xb130playsan pages 8-9, wang2022xb130playsan pages 1-2)
The resulting physiological model is precise: XB130 is not part of the thyroid-hormone synthetic enzyme machinery; it constructs and maintains the polarized apical platform on which thyroglobulin secretion, iodination, retrieval, and hormone release depend. This provides an example of structural dyshormonogenesis caused by loss of a scaffold protein. (wang2021xb130deficiencycauses pages 10-12, wang2021xb130deficiencycauses pages 1-2)
Canale et al., published June 14, 2023 in Cell Genomics (DOI/URL), profiled FACS-purified CD4 and CD8 T cells, NK cells, and monocyte/macrophages from tumor, non-tumorous liver, and blood of 48 patients with HCC. They quantified 8,182 protein groups, averaging 5,209 per sample, and found AFAP1L2 elevated in tumor-infiltrating CD8 T cells in association with chronic stimulation. Human activation time courses used three to four donors. (canale2023proteomicsofimmune pages 1-3, canale2023proteomicsofimmune pages 10-12)
Genetic deletion of Afap1l2 increased CD8 T-cell viability after repeated stimulation and improved antitumor activity in mouse models, with synergy from PD-L1 blockade. The investigators interpreted AFAP1L2 as an intracellular checkpoint that limits chronically stimulated T-cell survival and effector function. This is strikingly cell-type dependent: AFAP1L2 supports survival in several cancer-cell models but restrains survival in chronically stimulated T cells. (canale2023proteomicsofimmune pages 1-3, canale2023proteomicsofimmune pages 10-12)
Proposed applications include AFAP1L2 deletion in engineered CAR-T cells or pharmacological degradation of intracellular AFAP1L2. These are expert proposals, not current clinical implementations. Because AFAP1L2 is intracellular, conventional blocking antibodies are unlikely to work; degraders, RNA-based interventions, or ex-vivo gene editing would be more plausible. The precise molecular mechanism in exhausted T cells and possible functions in NK cells remain unresolved. (canale2023proteomicsofimmune pages 10-12)
Ma et al., Autophagy volume 20, 2024, pages 541–556 (DOI/URL; accepted September 16, 2023), reported higher AFAP1L2 expression in HCC than adjacent liver (p<0.05) and an association between high expression and unfavorable overall survival (p<0.05). In HepG2-derived sorafenib-resistant cells and orthotopic xenografts, elevated AFAP1L2 interacted with SRC and promoted SRC/FUNDC1 phosphorylation, reducing LC3B recruitment to mitochondria and suppressing mitophagy. Knockdown reduced proliferation, increased apoptosis, and shifted sorafenib sensitivity in the favorable direction. (ma2024artesunatesensitizeshuman pages 1-2, ma2024artesunatesensitizeshuman pages 5-6)
Artesunate was reported to bind recombinant human AFAP1L2 in pull-down, cellular thermal-shift, and surface-plasmon-resonance experiments, with micromolar affinity; the text reports approximately K_d=28 μM, although a reproduced figure label appears to show a different fitted value, so the exact affinity should be independently verified from the original data. Sorafenib at 3.5 μM plus artesunate at 25 μM produced a combination index of 0.850, indicating in-vitro synergy. In resistant orthotopic tumors, sorafenib at 30 mg/kg every two days plus artesunate at 30 or 60 mg/kg every two days slowed tumor growth (p<0.001); groups included 6–10 mice, and the resistance-model establishment rate was approximately 70%. (ma2024artesunatesensitizeshuman pages 9-11, ma2024artesunatesensitizeshuman pages 5-6, ma2024artesunatesensitizeshuman pages 13-14)
This establishes a plausible pharmacological hypothesis but not a clinical therapy. The human evidence is observational, while causality and treatment efficacy derive from cultured cells and xenografts. Artesunate is clinically used for malaria, but it is not validated as an AFAP1L2-directed treatment for HCC or sorafenib resistance. (ma2024artesunatesensitizeshuman pages 1-2, ma2024artesunatesensitizeshuman pages 5-6)
| Functional claim | Strongest model/evidence | Key quantitative detail | Confidence and limitation |
|---|---|---|---|
| Identity and architecture: Human AFAP1L2 is XB130, KIAA1914, or PI3KAP, a modular AFAP-family adaptor rather than an enzyme. | Human-gene characterization places AFAP1L2 at chromosome 10q25.3 and identifies N-terminal phosphotyrosine and proline-rich motifs, two central PH domains, and a C-terminal coiled-coil region. (bai2014xb130—anoveladaptor pages 2-3, bai2014xb130—anoveladaptor pages 1-2) | 19 exons; 3,751-bp transcript; 818-aa, approximately 130-kDa protein. (bai2014xb130—anoveladaptor pages 1-2) | High. Identity and architecture agree with Q8N4X5 and the supplied AFAP and PH-domain annotations. Predicted motifs alone do not prove physiological interactions. |
| Src–PI3K–Akt adaptor: Tyrosine-phosphorylated XB130 couples Src-family or RET/PTC kinase activity to PI3K p85α and selected Akt outputs. | Co-immunoprecipitation, domain-binding, and knockdown experiments in human lung epithelial and thyroid or lung cancer cells show PI3K-p85α binding and effects on Akt signaling and G1–S progression. (shiozaki2011rolesofxb130 pages 1-2, bai2014xb130—anoveladaptor pages 2-3, rubacha2010xb130insilico pages 28-32) | AFAP1L2 has a YxxM motif beginning at Tyr54. Knockdown reduced Akt phosphorylation without reducing MAPK phosphorylation in TPC1 cells. (bai2014xb130—anoveladaptor pages 2-3, rubacha2010xb130insilico pages 28-32) | Moderate to high in cultured cells. Biochemical and perturbational evidence is strong, but signaling is context dependent and not established as universal in normal human tissues. |
| Direct F-actin crosslinking and endocytosis: XB130 can bind and crosslink actin filaments through multimerization. | Recombinant PI3KAP/XB130 pelleting and crosslinking assays, deletion mapping in NIH3T3 and HEK293 cells, and dextran-uptake assays. (yamanaka2016phosphatidylinositol3kinaseassociatedprotein pages 1-2, yamanaka2016phosphatidylinositol3kinaseassociatedprotein pages 3-6, yamanaka2016phosphatidylinositol3kinaseassociatedprotein pages 8-10) | In the tested ortholog, residues 830–840 supported F-actin binding and the N-terminal 40 aa supported multimerization. Complexes migrated at 250–1,200 kDa versus an approximately 125-kDa monomer. Full-length protein increased HEK293 dextran uptake with p less than 0.01; FRTL-5 knockdown produced a nonsignificant trend with p equal to 0.11. (yamanaka2016phosphatidylinositol3kinaseassociatedprotein pages 1-2, yamanaka2016phosphatidylinositol3kinaseassociatedprotein pages 8-10) | High for in-vitro crosslinking; moderate for cellular function. Ortholog and construct residue numbering cannot be transferred directly to the 818-aa human sequence without alignment. Endogenous human-cell evidence remains limited. |
| Thyrocyte polarity and folliculogenesis: XB130 organizes the apical actin–microtubule interface required for follicular-lumen formation, thyroglobulin iodination and release, and thyroid-hormone production. | Xb130-knockout mice, embryonic and postnatal thyroid analyses, hormone and radioiodide studies, primary 3D thyrocyte cultures, and rescue using human XB130-GFP. (wang2022xb130playsan pages 1-2, wang2021xb130deficiencycauses pages 1-2, wang2021xb130deficiencycauses pages 5-7) | Knockout mice had reduced serum T4, elevated TSH, impaired iodide organification despite increased uptake, and levothyroxine-rescuable growth retardation. Developmental imaging included 4–11 animals per group depending on stage. (wang2022xb130playsan pages 8-9, wang2021xb130deficiencycauses pages 5-7) | High for mouse physiology; moderate for human inference. The studies demonstrate a non-enzymatic structural cause of congenital hypothyroidism in mice, but do not establish pathogenic human AFAP1L2 variants or clinical cases. |
| Chronic CD8 T-cell checkpoint, 2023: AFAP1L2 induction restrains survival and antitumor activity in chronically stimulated T cells. | Proteomics of immune cells from human HCC tissues, liver, and blood, followed by chronic-stimulation experiments, genetic ablation, and mouse tumor models. AFAP1L2 deletion enhanced antitumor activity and cooperated with PD-L1 blockade. (canale2023proteomicsofimmune pages 1-3, canale2023proteomicsofimmune pages 10-12) | The cohort included 48 patients. Investigators quantified 8,182 protein groups, averaging 5,209 per sample; activation time-course measurements used 3–4 donors. (canale2023proteomicsofimmune pages 1-3, canale2023proteomicsofimmune pages 10-12) | Moderate translational confidence. Human proteomic association and causal experimental evidence are compelling, but the mechanism remains unresolved. Degraders and AFAP1L2-edited CAR-T cells are proposals rather than clinical implementations. |
| HCC sorafenib resistance and artesunate response, 2024: Elevated AFAP1L2 activates an SRC–FUNDC1 state that suppresses mitophagy, while artesunate can resensitize resistant experimental models. | Human HCC-tissue association, HepG2 and HepG2R gain- or loss-of-function studies, co-immunoprecipitation, direct-binding assays, and orthotopic xenograft pharmacology. (ma2024artesunatesensitizeshuman pages 9-11, ma2024artesunatesensitizeshuman pages 1-2, ma2024artesunatesensitizeshuman pages 5-6, ma2024artesunatesensitizeshuman pages 13-14) | Tumor AFAP1L2 was elevated and associated with worse survival, with p less than 0.05. Artesunate binding was micromolar; sorafenib at 3.5 μM plus artesunate at 25 μM gave a combination index of 0.850. Xenograft groups contained 6–10 mice, and combination treatment slowed resistant tumors with p less than 0.001. (ma2024artesunatesensitizeshuman pages 9-11, ma2024artesunatesensitizeshuman pages 1-2, ma2024artesunatesensitizeshuman pages 5-6) | Moderate preclinical confidence; low clinical readiness. Tissue evidence is observational and efficacy derives from cell and xenograft models. Artesunate is not validated clinically as an AFAP1L2-directed HCC therapy. |
Table: Evidence hierarchy distinguishing established AFAP1L2/XB130 functions from emerging immunotherapy and drug-resistance findings. Models, quantitative results, confidence, and limitations are identified explicitly.
At present, AFAP1L2 has three main application areas:
Most secure conclusions: AFAP1L2/XB130 is the correct human Q8N4X5 protein; it is a modular non-enzymatic adaptor; it binds kinase-signaling machinery and can crosslink actin; and mouse knockout data establish a central role in thyrocyte apical organization and folliculogenesis. (bai2014xb130—anoveladaptor pages 1-2, wang2021xb130deficiencycauses pages 1-2, yamanaka2016phosphatidylinositol3kinaseassociatedprotein pages 1-2)
Moderately secure conclusions: Src/RET-to-PI3K/Akt coupling, Rac-associated lamellipodial recruitment, and effects on proliferation or migration are well supported in cultured cells but are context dependent. AFAP1L2 should therefore not be labeled simply as an oncogene; it can support cancer-cell survival yet restrain chronically stimulated CD8 T cells. (shiozaki2011rolesofxb130 pages 1-2, canale2023proteomicsofimmune pages 1-3, canale2023proteomicsofimmune pages 10-12)
Major gaps: No high-resolution experimental structure or definitive lipid-binding specificity was identified; the normal function outside thyroid remains incompletely defined; the mechanism by which AFAP1L2 limits T-cell fitness is unknown; direct relevance to inherited human thyroid disease is unproven; and the 2024 artesunate mechanism requires independent replication and clinical testing. The apparently mild adult anatomy of knockout mice does not eliminate risks from developmental, thyroid, immune, or tissue-specific inhibition. (wang2022xb130playsan pages 1-2, canale2023proteomicsofimmune pages 10-12, ma2024artesunatesensitizeshuman pages 1-2)
A concise annotation supported by the available evidence is:
AFAP1L2/XB130 is an intracellular AFAP-family adaptor and cytoskeletal scaffold that assembles Src-family/RET–PI3K–Akt signaling complexes and can multimerize to bind and crosslink F-actin. It dynamically localizes from cytoplasm to actin-rich membrane domains; in thyroid follicular cells it operates at the apical cortex to coordinate actin, microtubules, epithelial polarity, follicular-lumen formation, and thyroglobulin-dependent thyroid-hormone production. Emerging context-specific roles include suppression of chronically stimulated CD8 T-cell fitness and regulation of SRC–FUNDC1-dependent mitophagy in sorafenib-resistant HCC.
References
(bai2014xb130—anoveladaptor pages 2-3): Xiao-Hui Bai, Hae-Ra Cho, Serisha Moodley, and Mingyao Liu. Xb130—a novel adaptor protein: gene, function, and roles in tumorigenesis. Scientifica, 2014:1-9, Jun 2014. URL: https://doi.org/10.1155/2014/903014, doi:10.1155/2014/903014. This article has 37 citations and is from a peer-reviewed journal.
(bai2014xb130—anoveladaptor pages 1-2): Xiao-Hui Bai, Hae-Ra Cho, Serisha Moodley, and Mingyao Liu. Xb130—a novel adaptor protein: gene, function, and roles in tumorigenesis. Scientifica, 2014:1-9, Jun 2014. URL: https://doi.org/10.1155/2014/903014, doi:10.1155/2014/903014. This article has 37 citations and is from a peer-reviewed journal.
(shiozaki2011rolesofxb130 pages 1-2): Atsushi Shiozaki and Mingyao Liu. Roles of xb130, a novel adaptor protein, in cancer. Journal of Clinical Bioinformatics, 1:10-10, Mar 2011. URL: https://doi.org/10.1186/2043-9113-1-10, doi:10.1186/2043-9113-1-10. This article has 45 citations.
(wang2022xb130playsan pages 1-2): Yingchun Wang, Yun-Yan Xiang, Junichi Sugihara, Wei-Yang Lu, Xiao-Hui Liao, Peter Arvan, Samuel Refetoff, and Mingyao Liu. Xb130 plays an essential role in folliculogenesis through mediating interactions between microfilament and microtubule systems in thyrocytes. Feb 2022. URL: https://doi.org/10.1089/thy.2021.0461, doi:10.1089/thy.2021.0461. This article has 11 citations and is from a peer-reviewed journal.
(wang2021xb130deficiencycauses pages 1-2): Yingchun Wang, Hiroki Shimizu, Yun-Yan Xiang, Junichi Sugihara, Wei-Yang Lu, Xiao-Hui Liao, Hae-Ra Cho, Hiroaki Toba, Xiao-Hui Bai, Sylvia L. Asa, Peter Arvan, Samuel Refetoff, and Mingyao Liu. Xb130 deficiency causes congenital hypothyroidism in mice due to disorganized apical membrane structure and function of thyrocytes. Nov 2021. URL: https://doi.org/10.1089/thy.2021.0195, doi:10.1089/thy.2021.0195. This article has 9 citations and is from a peer-reviewed journal.
(yamanaka2016phosphatidylinositol3kinaseassociatedprotein pages 1-2): Daisuke Yamanaka, Takeshi Akama, Kazuhiro Chida, Shiro Minami, Koichi Ito, Fumihiko Hakuno, and Shin-Ichiro Takahashi. 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, Jul 2016. URL: https://doi.org/10.3389/fendo.2016.00089, doi:10.3389/fendo.2016.00089. This article has 10 citations.
(canale2023proteomicsofimmune pages 1-3): Fernando P. Canale, Julia Neumann, Janusz von Renesse, Elisabetta Loggi, Matteo Pecoraro, Ian Vogel, Giada Zoppi, Gaia Antonini, Tobias Wolf, Wenjie Jin, Xiaoqin Zheng, Giuliano La Barba, Emrullah Birgin, Marianne Forkel, Tobias Nilsson, Romina Marone, Henrik Mueller, Nadege Pelletier, Lukas T. Jeker, Gianluca Civenni, Christoph Schlapbach, Carlo V. Catapano, Lena Seifert, Adrian M. Seifert, Silke Gillessen, Sara De Dosso, Alessandra Cristaudi, Nuh N. Rahbari, Giorgio Ercolani, and Roger Geiger. Proteomics of immune cells from liver tumors reveals immunotherapy targets. Jun 2023. URL: https://doi.org/10.1016/j.xgen.2023.100331, doi:10.1016/j.xgen.2023.100331. This article has 19 citations and is from a peer-reviewed journal.
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(ma2024artesunatesensitizeshuman pages 5-6): Zhaochen Ma, Wenjia Chen, Yudong Liu, Lingxiang Yu, Xia Mao, Xiaodong Guo, Funeng Jiang, Qiuyan Guo, Na Lin, and Yanqiong Zhang. Artesunate sensitizes human hepatocellular carcinoma to sorafenib via exacerbating afap1l2-src-fundc1 axis-dependent mitophagy. Oct 2024. URL: https://doi.org/10.1080/15548627.2023.2261758, doi:10.1080/15548627.2023.2261758. This article has 91 citations and is from a domain leading peer-reviewed journal.
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(yamanaka2016phosphatidylinositol3kinaseassociatedprotein pages 3-6): Daisuke Yamanaka, Takeshi Akama, Kazuhiro Chida, Shiro Minami, Koichi Ito, Fumihiko Hakuno, and Shin-Ichiro Takahashi. 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, Jul 2016. URL: https://doi.org/10.3389/fendo.2016.00089, doi:10.3389/fendo.2016.00089. This article has 10 citations.
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(yamanaka2016phosphatidylinositol3kinaseassociatedprotein pages 8-10): Daisuke Yamanaka, Takeshi Akama, Kazuhiro Chida, Shiro Minami, Koichi Ito, Fumihiko Hakuno, and Shin-Ichiro Takahashi. 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, Jul 2016. URL: https://doi.org/10.3389/fendo.2016.00089, doi:10.3389/fendo.2016.00089. This article has 10 citations.
(wang2021xb130deficiencycauses pages 5-7): Yingchun Wang, Hiroki Shimizu, Yun-Yan Xiang, Junichi Sugihara, Wei-Yang Lu, Xiao-Hui Liao, Hae-Ra Cho, Hiroaki Toba, Xiao-Hui Bai, Sylvia L. Asa, Peter Arvan, Samuel Refetoff, and Mingyao Liu. Xb130 deficiency causes congenital hypothyroidism in mice due to disorganized apical membrane structure and function of thyrocytes. Nov 2021. URL: https://doi.org/10.1089/thy.2021.0195, doi:10.1089/thy.2021.0195. This article has 9 citations and is from a peer-reviewed journal.
(wang2021xb130deficiencycauses pages 10-12): Yingchun Wang, Hiroki Shimizu, Yun-Yan Xiang, Junichi Sugihara, Wei-Yang Lu, Xiao-Hui Liao, Hae-Ra Cho, Hiroaki Toba, Xiao-Hui Bai, Sylvia L. Asa, Peter Arvan, Samuel Refetoff, and Mingyao Liu. Xb130 deficiency causes congenital hypothyroidism in mice due to disorganized apical membrane structure and function of thyrocytes. Nov 2021. URL: https://doi.org/10.1089/thy.2021.0195, doi:10.1089/thy.2021.0195. This article has 9 citations and is from a peer-reviewed journal.
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