Affinage

SORBS1

Sorbin and SH3 domain-containing protein 1 · UniProt Q9BX66

Length
1292 aa
Mass
142.5 kDa
Annotated
2026-06-10
39 papers in source corpus 18 papers cited in narrative 18 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SORBS1 (ponsin/CAP) is a multi-SH3-domain adaptor protein that scaffolds signaling complexes at adherens junctions, focal adhesions, and force-transducing cell-matrix contacts to couple membrane receptors to actin cytoskeletal remodeling (PMID:10085297, PMID:17462669). Its three SH3 domains engage proline-rich ligands in a domain-specific manner: l-afadin (SH3-2/3) and vinculin (SH3-1/2) bind competitively, linking ponsin to the nectin-afadin-ponsin junctional system, while paxillin (SH3-2) targets it to nascent costameres (PMID:10085297, PMID:10583506, PMID:17462669). The third SH3 domain additionally binds c-Abl upon insulin stimulation, the atypical cadherin Fat1, and ataxin-7, by which polyglutamine-expanded ataxin-7 sequesters ponsin into intranuclear inclusions (PMID:11374898, PMID:26903299, PMID:23892081). Ponsin is recruited to focal contacts by flotillins and depends on Rho-GTPase-driven actin integrity, controlling FAK/Src signaling and the Rac1/RhoA/cdc42 balance that governs endothelial migration, vascular and lymphatic sprouting, and neurite outgrowth (PMID:18722032, PMID:19029030, PMID:38414014). At the neuromuscular junction it acts downstream of MuSK/Dok-7/Crk/CrkL to drive acetylcholine receptor clustering, and MBNL-regulated inclusion of its exon 25 is required for NMJ formation and maintenance, with reduced exon 25 inclusion contributing to neuromuscular pathology in myotonic dystrophy type 1 (PMID:26527617, PMID:41250834). In cancer, SORBS1 modulates EMT, migration, and invasion through JNK/cJun, PI3K/AKT, and AHNAK-dependent pathways, acting as either suppressor or promoter depending on context (PMID:27791200, PMID:32319594, PMID:38451194).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 1999 High

    Establishing how ponsin physically integrates into adherens junctions defined its core role as a junctional adaptor; reciprocal binding to l-afadin and vinculin via distinct SH3 domains showed it links the nectin-afadin system to vinculin at cell-cell and cell-matrix junctions.

    Evidence Pulldown, co-IP, domain mapping and immunofluorescence in epithelial and nonepithelial cells; junction disruption assays in MTD-1A/MDCK cells

    PMID:10085297 PMID:10583506

    Open questions at the time
    • Competitive l-afadin/vinculin binding leaves the in vivo stoichiometry of junctional complexes undefined
    • Functional consequence of ponsin loss at junctions not tested
  2. 2001 Medium

    Linking SORBS1 to insulin signaling addressed whether it acts in receptor signaling; insulin-induced SH3C-mediated c-Abl association coupled to partial dissociation from the insulin receptor indicated a dynamic, conformation-dependent adaptor role.

    Evidence Co-IP from insulin-stimulated Hep3B hepatoma cells with deletion-construct domain mapping

    PMID:11374898

    Open questions at the time
    • Downstream metabolic output of the c-Abl interaction not established
    • Conformational change inferred rather than directly measured
  3. 2005 Medium

    Identifying teneurin-1 as a partner revealed a potential nucleus-membrane shuttling axis, showing ponsin can be relocalized between compartments depending on its binding partner.

    Evidence Yeast two-hybrid, co-IP, subcellular fractionation and colocalization with inducible teneurin-1 expression

    PMID:15777793

    Open questions at the time
    • Nuclear function of ponsin not defined
    • Physiological trigger for translocation unknown
  4. 2007 High

    High-resolution structures of the SH3-2 domain and its paxillin complex defined the atomic basis of ligand recognition and tied ponsin to force-transducing costameres in muscle differentiation.

    Evidence X-ray crystallography (0.83 A SH3, 1.63 A complex; plus powder-diffraction structure), fluorescence titration, and overexpression morphology assays

    PMID:17462669 PMID:17784760

    Open questions at the time
    • Weak paxillin affinity leaves the contribution of avidity/SH3 synergy quantitatively unresolved
    • Link between cardiac downregulation and contractile dysfunction correlative
  5. 2008 Medium

    Flotillin-dependent recruitment and Rho-GTPase-dependent localization placed ponsin functionally within actin-cytoskeleton and FAK/Rac1/cdc42 signaling at focal contacts.

    Evidence Dominant-negative flotillin, Rho-GTPase and FAK activity assays, neurite outgrowth in N2a/hippocampal neurons; microarray, fractionation and cytoskeleton-perturbation in lens epithelium

    PMID:18722032 PMID:19029030

    Open questions at the time
    • Whether ponsin directly regulates GTPase activity or acts as a passive scaffold unresolved
    • Direct flotillin-ponsin contact not mapped
  6. 2010 Medium

    Discovery of a muscle-specific isoform with an Nck-binding insertion showed alternative splicing diversifies ponsin's interactome at remodeling cell-matrix contacts.

    Evidence Isoform cloning, co-IP, colocalization and phosphorylation analysis in differentiating skeletal muscle cells

    PMID:20129698

    Open questions at the time
    • Functional role of Nck1/2 recruitment in costamere assembly not tested
    • Phosphorylation sites and regulating kinase not identified
  7. 2013 High

    NMR mapping of SH3C binding ataxin-7 explained how ponsin is sequestered into polyQ inclusions, connecting it to a neurodegenerative aggregation mechanism.

    Evidence NMR structure of SH3C and its complex with ataxin-7 PRR plus cellular sequestration imaging

    PMID:23892081

    Open questions at the time
    • Functional consequence of ponsin sequestration for SCA7 pathology not established
  8. 2016 Medium

    Fat1 was identified as another SH3-engaging partner controlling ponsin localization, extending the adhesion-receptor repertoire that positions ponsin at leading edges.

    Evidence Yeast two-hybrid, pulldown, siRNA knockdown and immunofluorescence

    PMID:26903299

    Open questions at the time
    • Downstream signaling from the Fat1-ponsin module not defined
    • Single-lab interaction without reciprocal in vivo validation
  9. 2015 High

    Placing Sorbs1 downstream of MuSK/Dok-7/Crk/CrkL with functional redundancy to Sorbs2 established its role in acetylcholine receptor clustering at the neuromuscular synapse.

    Evidence Mass spectrometry interactome, co-IP, in vitro AChR clustering and in vivo synaptic localization

    PMID:26527617

    Open questions at the time
    • Mechanism by which Sorbs1 promotes AChR clustering downstream of CrkL unresolved
  10. 2024 High

    In vivo zebrafish loss-of-function established a developmental requirement for Sorbs1 in lymphatic/venous sprouting through FAK/Src and Rac1/RhoA control of endothelial migration and adhesion, independent of Vegfc.

    Evidence Zebrafish genetic mutants, in vitro endothelial migration/adhesion and GTPase activity assays, BMP/Vegfc epistasis

    PMID:38414014

    Open questions at the time
    • Direct molecular link between Sorbs1 and the BMP pathway not defined
    • Endothelial binding partners mediating this role not identified
  11. 2024 Medium

    Cancer studies defined context-dependent roles for SORBS1 in EMT and invasion, acting through JNK/cJun, PI3K/AKT, and AHNAK, with opposing tumor-suppressive and migration-promoting outcomes across models.

    Evidence siRNA/knockout and overexpression with migration/invasion assays, pathway Western blots, AHNAK co-IP/colocalization, and macrophage co-culture

    PMID:27791200 PMID:32319594 PMID:38451194

    Open questions at the time
    • Opposing pro- and anti-tumor effects across cancer types not mechanistically reconciled
    • Direct vs indirect regulation of these pathways unresolved
  12. 2025 High

    MBNL-controlled inclusion of SORBS1 exon 25 was shown to be required for NMJ formation and maintenance and its loss contributes to neuromuscular defects in myotonic dystrophy type 1.

    Evidence Antisense exon skipping in mouse, zebrafish and hiPSC muscle; NMJ morphology, AChR clustering with agrin, locomotion, and DM1 biopsy RNA analysis

    PMID:41250834

    Open questions at the time
    • How the exon 25 segment alters ponsin's molecular interactions at the synapse not defined
    • Contribution relative to other DM1 mis-splicing events unquantified

Open questions

Synthesis pass · forward-looking unresolved questions
  • How ponsin's distinct partner repertoires and splice isoforms are coordinated to switch its function between junctional scaffolding, receptor signaling, and cytoskeletal control in specific tissues remains unresolved.
  • No integrated model linking isoform-specific interactions to tissue-specific phenotypes
  • Direct enzymatic or signaling output of ponsin scaffolding undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 4 GO:0008092 cytoskeletal protein binding 3 GO:0098772 molecular function regulator activity 2
Localization
GO:0005886 plasma membrane 3 GO:0005634 nucleus 2
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-1266738 Developmental Biology 2 R-HSA-1500931 Cell-Cell communication 2
Partners
ABL1AFDNATXN7FAT1NCK1NCK2PXNVCL
Complex memberships
MuSK/Dok-7/Crk/CrkL complexnectin-afadin-ponsin (NAP) system

Evidence

Reading pass · 18 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 Ponsin (SORBS1) directly binds l-afadin via its second and third SH3 domains interacting with the third proline-rich region of l-afadin, and directly binds vinculin via its first and second SH3 domains interacting with vinculin's proline-rich region. l-Afadin and vinculin bind ponsin in a competitive manner and these three proteins hardly form a ternary complex. Ponsin localizes at zonula adherens in epithelial cells, cell-cell adherens junctions in nonepithelial cells, and cell-matrix adherens junctions in both cell types. Pulldown assays, co-immunoprecipitation, immunofluorescence localization, domain mapping with deletion constructs The Journal of cell biology High 10085297
1999 Ponsin (SORBS1) is a component of the nectin-afadin-ponsin (NAP) system at cadherin-based cell-cell adherens junctions. During formation of polarized junctional alignment, nectin, afadin, and ponsin are simultaneously recruited to primordial spot-like junctions and subsequently to belt-like adherens junctions. Unlike cadherin, nectin and afadin (and by association ponsin) are not internalized upon low-calcium disruption of cell-cell junctions. Immunofluorescence, live-cell junction disruption assays (calcium depletion and TPA treatment) in MTD-1A and MDCK cells Genes to cells : devoted to molecular & cellular mechanisms Medium 10583506
2001 Human SORBS1 associates with c-Abl protein upon insulin stimulation in hepatoma Hep3B cells. This interaction is mediated through the third SH3 domain of SORBS1 and is accompanied by partial dissociation of SORBS1 from the insulin receptor complex, suggesting a possible conformational change induced by insulin. Co-immunoprecipitation from insulin-stimulated Hep3B cells, domain mapping using deletion constructs Genomics Medium 11374898
2005 The intracellular domain of teneurin-1 interacts with CAP/ponsin (SORBS1). This interaction recruits the soluble intracellular domain of teneurin-1 to the cell membrane enriched in CAP/ponsin, and conversely leads to translocation of CAP/ponsin to the nucleus where the intracellular domain of teneurin-1 accumulates. Yeast two-hybrid identification, co-immunoprecipitation, subcellular fractionation, immunofluorescence colocalization, hormone-inducible full-length teneurin-1 expression system Experimental cell research Medium 15777793
2007 Ponsin (SORBS1) interacts with paxillin in nascent costameres during muscle differentiation. This interaction is mediated by the second SH3 domain of ponsin binding to the proline-rich region of paxillin, with the paxillin peptide adopting a polyproline-II helix conformation in the complex. The interaction has weak binding affinity. All three SH3 domains of ponsin synergize in targeting the protein to force-transducing structures. Overexpression of ponsin alters muscle cell-matrix contact morphology, indicating a role in costamere establishment. Ponsin expression is downregulated in end-stage failing hearts and restored upon mechanical unloading. Co-immunoprecipitation, X-ray crystallography of the SH3 domain at 0.83 Å and SH3-paxillin peptide complex at 1.63 Å, fluorescence titration, transfection overexpression with morphological readout, immunoblotting Journal of molecular biology High 17462669
2007 The crystal structure of the second SH3 domain of ponsin (SORBS1) was determined to high resolution from powder diffraction data, yielding a 67-residue domain structure with resolution comparable to single-crystal techniques. Powder X-ray diffraction, structure determination and refinement Journal of the American Chemical Society High 17784760
2008 CAP/ponsin (SORBS1) is recruited to focal contacts at the plasma membrane by reggies/flotillins. Expression of a trans-negative reggie-1/flotillin-2 deletion mutant (R1EA) impaired recruitment of CAP/ponsin to focal contacts, leading to perturbed Rac1 and cdc42 GTPase activation balance and enhanced FAK activity, thereby inhibiting IGF-induced neurite outgrowth and neuronal differentiation. Dominant-negative (trans-negative) reggie-1 deletion mutant expression, immunofluorescence localization, Rho-GTPase activation assays, FAK activity assay, neurite outgrowth quantification in N2a cells and primary hippocampal neurons European journal of cell biology Medium 18722032
2008 Ponsin (SORBS1) is abundantly expressed in lens tissue and localizes predominantly to focal adhesions in lens epithelial cells, with some isoforms enriched in the Triton X-100-insoluble fraction. Constitutively active RhoA induces ponsin clustering at leading edges, while inhibition of Rho kinase or latrunculin treatment decreases ponsin protein levels, demonstrating that ponsin expression and localization depend on Rho GTPase-regulated actin cytoskeletal integrity. cDNA microarray (identifying downregulation), immunofluorescence, immunoblot, subcellular fractionation, treatment with constitutively active RhoA, Rho kinase inhibitor, and latrunculin Investigative ophthalmology & visual science Medium 19029030
2010 A skeletal muscle-specific isoform of ponsin (SORBS1) contains a large carboxy-terminal insertion that binds the adapter proteins Nck1 and Nck2. Increased co-localization of ponsin with Nck2 occurs at remodeling cell-matrix contacts of differentiating skeletal muscle cells. The novel ponsin insertion can be phosphorylated, potentially adjusting interaction affinity with Nck adapter proteins. Isoform cloning, co-immunoprecipitation, immunofluorescence colocalization, phosphorylation analysis European journal of cell biology Medium 20129698
2013 The third SH3 domain (SH3C) of R85FL/ponsin (SORBS1) specifically interacts with the second proline-rich region (PRR) of ataxin-7. NMR structural analysis revealed that SH3C contains a large negatively charged surface that binds the RRTR motif of ataxin-7. This SH3C-PRR interaction mediates the sequestration of ponsin by polyglutamine-expanded ataxin-7 into intranuclear inclusion bodies. NMR structural analysis of SH3C domain and its complex with ataxin-7 PRR, microscopy imaging of polyQ-expanded Atx7 sequestration in cells, domain mapping FEBS letters High 23892081
2015 Sorbs1 and Sorbs2 associate with the initiating MuSK/Dok-7/Crk/CrkL complex at the neuromuscular synapse, functioning downstream of MuSK and Dok-7. Sorbs1 and Sorbs2 are functionally redundant, regulate acetylcholine receptor (AChR) clustering in vitro, and are localized at synapses in vivo. Mass spectrometry identification of CrkL binding partners, co-immunoprecipitation, AChR clustering assays in vitro, in vivo synaptic localization by immunofluorescence Molecular and cellular biology High 26527617
2016 The cytoplasmic domain of atypical cadherin Fat1 interacts with SoHo adaptor proteins CAP/ponsin-1 and -2 (Sorbs1) via a proline-rich type II PXXP motif within Fat1 and the three SH3 domains within ponsin. Knockdown of Fat1 causes loss of endogenous ponsin-2 expression at cellular leading edges. Yeast two-hybrid screen, pulldown assays, cell culture expression, immunofluorescence, siRNA knockdown Biochemical and biophysical research communications Medium 26903299
2017 Depletion of SORBS1 in breast cancer cells increases filopodium-like protrusion formation and migratory/invasive ability via activation of JNK/cJun signaling. Silencing of SORBS1 also promotes epithelial-to-mesenchymal transition (EMT) and attenuates cisplatin sensitivity by inhibiting p53. siRNA knockdown, migration/invasion assays, Western blot for JNK/cJun and p53 pathway components, EMT marker analysis, drug sensitivity assays Oncotarget Medium 27791200
2018 Homocysteine increases SORBS1 promoter methylation in human umbilical vein endothelial cells, reducing SORBS1 expression. siRNA knockdown of SORBS1 increases MDA levels and reduces SOD2 expression, recapitulating the oxidative stress phenotype induced by homocysteine. Folic acid and vitamin B12 treatment attenuates Hcy-induced methylation of SORBS1 and the associated oxidative stress. Genome-wide DNA methylation assay (Infinium 450K BeadChip), bisulfite sequencing, siRNA knockdown, Western blot, RT-PCR, biochemical oxidative stress assays (MDA, SOD2) European review for medical and pharmacological sciences Medium 30402861
2020 SORBS1 forms a protein complex with AHNAK nucleoprotein in colorectal cancer cells, as demonstrated by co-immunoprecipitation and co-localization by confocal microscopy. SORBS1 knockdown reduces cancer cell migration. AHNAK functions as a tumor suppressor through inhibition of phosphorylated-ERK and ROCK1, and SORBS1 inhibits AHNAK, suggesting SORBS1 promotes cancer cell migration and growth via suppression of AHNAK. Co-immunoprecipitation, confocal microscopy colocalization, Boyden chamber migration assay, colony formation assay, vector transfection/lentivirus-mediated overexpression and knockdown, Western blot International journal of oncology Medium 32319594
2024 Sorbs1 is required for secondary sprouting and formation of lymphatic and venous vascular structures in zebrafish, particularly for precursor parachordal lymphatic structures. Mechanistically, Sorbs1 controls FAK/Src signaling and impacts cytoskeletal processes regulated by Rac1 and RhoA GTPases. Inactivation of Sorbs1 alters cell-ECM contact rearrangement and cytoskeletal dynamics, leading to defects in endothelial cell migration and adhesion. Sorbs1 interacts with the BMP pathway and functions independently of Vegfc signaling. Zebrafish genetic mutant analysis (loss-of-function), in vitro endothelial cell assays, FAK/Src signaling assays, Rac1/RhoA GTPase activity assays, cell adhesion and migration assays, epistasis with BMP and Vegfc pathways BMC biology High 38414014
2024 SORBS1 inhibits the PI3K/AKT signaling pathway and blocks EMT in breast cancer cells. High SORBS1 expression reduces breast cancer cell migration and invasion. SORBS1 expression induces macrophage polarization toward the M1 phenotype and enhances macrophage killing of breast cancer cells in co-culture. SORBS1-overexpressing and knockout cell lines, cell viability/invasion/migration assays, Western blot for PI3K/AKT pathway components and EMT markers, macrophage-cancer cell co-culture system with polarization assays Aging Medium 38451194
2025 MBNL-regulated alternative splicing of SORBS1 exon 25 is required for neuromuscular junction (NMJ) formation and maintenance. In DM1 patients, SORBS1 exon 25 inclusion is significantly reduced. Forced exclusion of Sorbs1 exon 25 in mice leads to NMJ degeneration with increased denervation and postsynaptic destabilization. In zebrafish, exon 25 misregulation impairs locomotion and disrupts AChR cluster morphology. In hiPSC-derived skeletal muscle cells, exon 25 exclusion reduces large AChR cluster formation upon agrin stimulation by 34%. Antisense oligonucleotide-mediated exon skipping in mice, zebrafish, and hiPSC-derived skeletal muscle cells; NMJ morphology analysis; AChR cluster formation assay with agrin stimulation; locomotion behavioral assay; human DM1 biopsy RNA analysis Journal of cachexia, sarcopenia and muscle High 41250834

Source papers

Stage 0 corpus · 39 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1999 Ponsin/SH3P12: an l-afadin- and vinculin-binding protein localized at cell-cell and cell-matrix adherens junctions. The Journal of cell biology 213 10085297
2002 Vinexin, CAP/ponsin, ArgBP2: a novel adaptor protein family regulating cytoskeletal organization and signal transduction. Cell structure and function 180 11937713
1999 Similar and differential behaviour between the nectin-afadin-ponsin and cadherin-catenin systems during the formation and disruption of the polarized junctional alignment in epithelial cells. Genes to cells : devoted to molecular & cellular mechanisms 85 10583506
1999 nArgBP2, a novel neural member of ponsin/ArgBP2/vinexin family that interacts with synapse-associated protein 90/postsynaptic density-95-associated protein (SAPAP). The Journal of biological chemistry 73 10521485
2001 Cloning, mapping, and characterization of the human sorbin and SH3 domain containing 1 (SORBS1) gene: a protein associated with c-Abl during insulin signaling in the hepatoma cell line Hep3B. Genomics 59 11374898
2005 The intracellular domain of teneurin-1 interacts with MBD1 and CAP/ponsin resulting in subcellular codistribution and translocation to the nuclear matrix. Experimental cell research 57 15777793
2001 Molecular scanning of the human sorbin and SH3-domain-containing-1 (SORBS1) gene: positive association of the T228A polymorphism with obesity and type 2 diabetes. Human molecular genetics 56 11532984
2008 Reggies/flotillins regulate cytoskeletal remodeling during neuronal differentiation via CAP/ponsin and Rho GTPases. European journal of cell biology 37 18722032
2007 Paxillin and ponsin interact in nascent costameres of muscle cells. Journal of molecular biology 37 17462669
2017 SORBS1 suppresses tumor metastasis and improves the sensitivity of cancer to chemotherapy drug. Oncotarget 33 27791200
2014 SORBS1 gene, a new candidate for diabetic nephropathy: results from a multi-stage genome-wide association study in patients with type 1 diabetes. Diabetologia 33 25476525
2018 Genetic variation of SORBS1 gene is associated with glucose homeostasis and age at onset of diabetes: A SAPPHIRe Cohort Study. Scientific reports 32 30002559
2019 MiR-142-5p Acts as a Significant Regulator Through Promoting Proliferation, Invasion, and Migration in Breast Cancer Modulated by Targeting SORBS1. Technology in cancer research & treatment 31 31789129
2015 Sorbs1 and -2 Interact with CrkL and Are Required for Acetylcholine Receptor Cluster Formation. Molecular and cellular biology 29 26527617
2021 Long Non-coding RNAs LOC100126784 and POM121L9P Derived From Bone Marrow Mesenchymal Stem Cells Enhance Osteogenic Differentiation via the miR-503-5p/SORBS1 Axis. Frontiers in cell and developmental biology 25 34746123
2020 SORBS1 serves a metastatic role via suppression of AHNAK in colorectal cancer cell lines. International journal of oncology 24 32319594
2007 Second SH3 domain of ponsin solved from powder diffraction. Journal of the American Chemical Society 24 17784760
2003 mRNA levels of the insulin-signaling molecule SORBS1 in the adipose depots of nondiabetic women. Obesity research 21 12690089
2024 Increased serum extrachromosomal circular DNA SORBS1circle level is associated with insulin resistance in patients with newly diagnosed type 2 diabetes mellitus. Cellular & molecular biology letters 18 38212723
2020 Integrated proteogenomic approach identifying a protein signature of COPD and a new splice variant of SORBS1. Thorax 17 31937552
2022 miR-223-3p carried by cancer-associated fibroblast microvesicles targets SORBS1 to modulate the progression of gastric cancer. Cancer cell international 16 35193596
2018 Homocysteine induced oxidative stress in human umbilical vein endothelial cells via regulating methylation of SORBS1. European review for medical and pharmacological sciences 14 30402861
2009 Association of polymorphisms of SORBS1, GCK and WISP1 with hypertension in community-dwelling Japanese individuals. Hypertension research : official journal of the Japanese Society of Hypertension 13 19282865
2003 Frequency of the T228A polymorphism in the SORBS1 gene in children with premature pubarche and in adolescent girls with hyperandrogenism. Fertility and sterility 12 12849814
2016 Genetic Variation in the Human SORBS1 Gene is Associated With Blood Pressure Regulation and Age at Onset of Hypertension: A SAPPHIRe Cohort Study. Medicine 11 26962801
2024 SORBS1 inhibits epithelial to mesenchymal transition (EMT) of breast cancer cells by regulating PI3K/AKT signaling and macrophage phenotypic polarization. Aging 10 38451194
2008 Polymorphism in the sorbin and SH3-domain-containing-1 (SORBS1) gene and the risk of brain infarction in the Japanese population: the Fukuoka Stroke Registry and the Hisayama study. European journal of neurology 10 18394047
2022 A variation in SORBS1 is associated with type 2 diabetes and high-density lipoprotein cholesterol in Chinese population. Diabetes/metabolism research and reviews 8 35107206
2021 Polymorphisms of SORBS1 Gene and Their Correlation with Milk Fat Traits of Cattleyak. Animals : an open access journal from MDPI 8 34944239
2008 Abundant expression of ponsin, a focal adhesion protein, in lens and downregulation of its expression by impaired cytoskeletal signaling. Investigative ophthalmology & visual science 8 19029030
2023 MiR-223-3p increases resistance of colorectal cancer cells to 5-fluorouracil via targeting SORBS1. Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences 5 37164919
2013 Structural basis for recognition of the third SH3 domain of full-length R85 (R85FL)/ponsin by ataxin-7. FEBS letters 5 23892081
2010 Ponsin interacts with Nck adapter proteins: implications for a role in cytoskeletal remodelling during differentiation of skeletal muscle cells. European journal of cell biology 5 20129698
2024 The cytoskeleton adaptor protein Sorbs1 controls the development of lymphatic and venous vessels in zebrafish. BMC biology 4 38414014
2016 Interaction of atypical cadherin Fat1 with SoHo adaptor proteins CAP/ponsin and ArgBP2. Biochemical and biophysical research communications 4 26903299
2008 A single nucleotide polymorphism in exon 7 of sorbin and SH3-domain-containing-1 (SORBS1) in Korean PCOS patients. Molecular medicine reports 4 21479384
2025 Alternative Splicing of SORBS1 Affects Neuromuscular Junction Integrity in Myotonic Dystrophy Type 1. Journal of cachexia, sarcopenia and muscle 2 41250834
2025 SORBS1 Knockdown Resists S/G2 Arrest and Apoptosis Caused by Polyphyllin H-Induced DNA Damage in Pancreatic Cancer. Oncology research 0 40918460
2007 Polymorphisms in promoter regions of PDHB, SORBS1, and EDG1 genes showing marbling-associated expression changes. Research communications in molecular pathology and pharmacology 0 21469508

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