| 2008 |
The C-terminal 33 residues of SOX11 constitute its transactivation domain (TAD). SOX11 activates transcription more efficiently than SOX4 and SOX12, owing to a more stable alpha-helical structure of its TAD. Acidic domains and the TAD itself interfere with DNA binding. |
Reporter gene transactivation assays, domain mapping, structural analysis of TAD |
Nucleic acids research |
High |
18403418
|
| 2020 |
Cryo-EM structures show that SOX11 HMG domain binds nucleosomal DNA at superhelical location 2, locally distorting DNA and facilitating detachment of terminal nucleosomal DNA from the histone octamer, thereby increasing DNA accessibility. SOX11 binding also repositions the N-terminal tail of histone H4 including K16. |
Cryo-electron microscopy structure determination |
Nature |
High |
32350470
|
| 2006 |
SOX11 is required for neuron survival and neurite outgrowth. siRNA-mediated knockdown in Neuro2a cells increased apoptosis and decreased neurite growth, upregulated pro-apoptotic BNIP3, and decreased anti-apoptotic TANK. In primary DRG neurons, SOX11 knockdown decreased neurite growth/branching and reduced Arpc3 (actin organizing protein) mRNA. |
RNAi knockdown in Neuro2a cells and primary DRG neurons, gene expression analysis |
Neuroscience |
Medium |
17055661
|
| 2008 |
In vivo siRNA-mediated knockdown of Sox11 in injured mouse saphenous nerve transiently inhibited peripheral nerve regeneration of both myelinated and unmyelinated axons. Sox11 knockdown reduced ATF3 expression at transcriptional and translational levels in injured neurons. |
In vivo siRNA injection via Penetratin conjugation, electron microscopy, immunostaining |
Brain research |
Medium |
19133245
|
| 2013 |
SOX11 promotes tumor growth in MCL xenograft models. By ChIP-microarray combined with gene expression profiling upon SOX11 knockdown, SOX11 directly targets PAX5. SOX11 silencing downregulates PAX5, induces BLIMP1, and promotes plasmacytic differentiation, blocking terminal B-cell differentiation. |
ChIP-microarray, gene expression profiling, siRNA knockdown, xenograft mouse model |
Blood |
High |
23321250
|
| 2014 |
SOX11 directly binds regulatory regions of CXCR4 and PTK2 (FAK), upregulating their expression in MCL cells. This activates PI3K/AKT and ERK1/2 FAK-downstream pathways, enhancing cell migration, stromal adhesion, endothelial transmigration, proliferation, and cell adhesion-mediated drug resistance. |
ChIP, gene expression analysis, siRNA knockdown, functional migration/adhesion assays, xenograft models, FAK/CXCR4 inhibitor treatment |
Blood |
High |
28533307
|
| 2014 |
SOX11 directly transcriptionally upregulates PDGFA in MCL cells. SOX11-positive MCL tumors had higher microvascular density and angiogenic gene signatures; conditioned media from SOX11+ cells promoted endothelial cell proliferation, migration, and tube formation. PDGFA inhibition impaired SOX11-enhanced angiogenesis. |
ChIP, gene expression profiling, conditioned media assays, endothelial cell functional assays, xenograft models with imatinib treatment |
Blood |
High |
25092176
|
| 2010 |
SOX11 directly reduces tumor growth in hematopoietic malignancies. siRNA knockdown and ectopic overexpression alter proliferation. Gene expression analysis identified Rb-E2F cell cycle regulatory pathways as associated with SOX11-induced growth reduction. SOX11 is epigenetically silenced by DNA methylation in B-cell lymphomas. |
siRNA knockdown, ectopic overexpression, GeneChip expression analysis, promoter methylation analysis |
Molecular cancer |
Medium |
20624318
|
| 2011 |
SOX11 epigenetic activation in aggressive B-cell lymphomas is mediated by a shift from inactivating histone marks (H3K9me2, H3K27me3) to activating histone marks (H3K9/14Ac, H3K4me3). SOX11 silencing in non-expressing lymphoid cells correlates with H3K27me3. HDAC inhibitor SAHA reversed SOX11 silencing but DNA methyltransferase inhibitor AZA did not. |
ChIP, bisulfite sequencing, HDAC inhibitor and DNA methyltransferase inhibitor treatment |
PloS one |
Medium |
21738649
|
| 2011 |
Sox11 knockout mice show severe reduction in sensory neuron survival in trigeminal and dorsal root ganglia, and arrest of axonal outgrowth in vivo and in vitro. This axonal growth defect could not be fully rescued by blocking cell death, indicating a cell-death-independent role in axon growth. |
Sox11 knockout mouse (knockin of LacZ replacing Sox11 coding region), histological analysis, in vitro axon growth assay |
Developmental dynamics |
High |
21117150
|
| 2010 |
In sympathetic nervous system development, Sox11 is required early for proliferation of tyrosine hydroxylase-expressing cells, while Sox4 ensures their survival at later stages. In double Sox4/Sox11 knockout mice, sympathetic ganglia remain hypoplastic due to consecutive proliferation and survival defects, leading to dysautonomia. |
Mouse mutagenesis (conditional knockouts), overexpression in chicken, histological analysis |
Development (Cambridge, England) |
High |
20147379
|
| 2013 |
Sox11 is required for both embryonic and adult neurogenesis. Sox11 null embryos develop small, disorganized brains with transient NPC proliferation deficits. Conditional Sox11 deletion in adult NPCs blunts proliferation in the SGZ. Functional genomics identified potential downstream target genes. |
Sox11 conditional knockout mice (Cre-loxP), BrdU labeling, functional genomics/transcriptomics |
Developmental dynamics |
High |
23483698
|
| 2018 |
Phosphorylation of SOX11 at serine 30 promotes nuclear over cytoplasmic localization. Mass spectrometry identified 10 putative phosphorylated serine residues in SOX11. Western blot of embryonic mouse brain lysates confirmed SOX11 is post-translationally modified by phosphorylation. |
Mass spectrometry, phospho-mutant analysis, Western blot, subcellular localization assays |
Frontiers in molecular neuroscience |
Medium |
29973868
|
| 2021 |
USP11 deubiquitinase stabilizes SOX11 protein in the developing cortex. USP11 deficiency impairs layer 6 neuron production and delays neuronal migration. Disease-associated USP11 mutant fails to stabilize SOX11. USP11 ablation reduces SOX11 protein despite induction of Sox11 mRNA, indicating post-translational regulation. |
Mouse Usp11 knockout, cortical analysis, co-immunoprecipitation, neuronal migration assays |
Science advances |
High |
33579706
|
| 2021 |
SUMOylation of SOX11 at lysine 91 (K91) regulates its nuclear localization and function. Non-SUMOylatable SOX11-K91A shows increased nuclear localization and enhanced RGC differentiation in vitro, but promotes RGC death and stronger axon regeneration after optic nerve injury in vivo. RNA-seq showed Sox11 and Sox11K91A increase axon growth gene expression but downregulate Spp1 and Opn4. |
Site-directed mutagenesis (K91A), in vitro RGC differentiation assay, optic nerve crush model in vivo, RNA-seq |
eNeuro |
High |
33441400
|
| 2012 |
Sox11 modulates BDNF transcription in an exon promoter-specific manner. Sox11 activates BDNF exon I and IV promoters via Sox binding motif 5'-AACAAAG-3'; mutation of these sites reduces activation. Sox11 overexpression in Neuro2a cells elevated exon IV and VII BDNF transcripts. |
Luciferase reporter assays, Sox binding site mutagenesis, RT-PCR expression analysis |
Journal of neuroscience research |
Medium |
22331573
|
| 2012 |
SOX11 and WT1 synergistically regulate the Wnt4 promoter in embryonic kidney mesenchyme. Sox11 and WT1 co-immunoprecipitate from embryonic kidney cells. Dominant negative WT1 mutants (P129L, F154S) that cannot interact with Sox11 cannot activate Wnt4. Morpholino knockdown of wt1 or sox11 in Xenopus inhibited Wnt4 expression in the pronephros. |
Co-immunoprecipitation, luciferase reporter assay, dominant-negative mutants, morpholino knockdown in Xenopus |
Experimental cell research |
High |
22465478
|
| 2013 |
SOX11 directly binds conserved SOX family binding sites in the 5' UTR of GDF5 and activates GDF5 expression. SOX11 overexpression in chick limb micromass cultures directly activates GDF5, and enhances Gdf5 expression in developing chick limbs. |
In vitro reporter assay, micromass cultures, RCAS virus-mediated overexpression in chick limb, binding site analysis |
BMC developmental biology |
Medium |
23356643
|
| 2018 |
SOX11 expression in MCL is regulated by CCND1 and STAT3. CCND1 increases SOX11 transcription by sequestering HDAC1 and HDAC2 from the SOX11 locus, leading to increased H3K9/14 acetylation. STAT3 activation decreases SOX11 expression; JAK1/JAK2 inhibition or STAT3 knockdown increases SOX11 expression. |
ChIP, Co-IP, RNAi knockdown, ectopic overexpression, HDAC inhibitor treatment, cytokine stimulation assays |
Blood |
High |
30530749
|
| 2018 |
SOX11 overexpression in B cells drives BCR signaling hyperactivation (pBTK and downstream molecules) and produces an oligoclonal B-cell hyperplasia with MCL-like immunophenotype (CD5+CD19+CD23-). Serial bone marrow transplant from transgenic donors produces lethal disease with decreasing latency. |
Transgenic mouse model (Eμ-SOX11-EGFP), phosphocytometric mass cytometry (CyTOF), bone marrow transplantation |
Blood |
High |
29615403
|
| 2016 |
Sox11 suppresses dendritic morphogenesis of excitatory neurons in mouse cerebral cortex. Loss-of-function causes precocious neurite branching and a neuronal migration defect; gain-of-function inhibits dendritic morphogenesis. Arrival at final cortical position induces Sox11 downregulation, which is required to permit dendritic branching. |
In utero electroporation and postnatal electroporation (loss- and gain-of-function), morphological analysis |
The Journal of neuroscience |
Medium |
27225767
|
| 2019 |
SOX11 and SOX4 regulate embryonic epidermal state and are required for wound re-epithelialization. They regulate cytoskeletal/ECM genes and directly target FSCN1 (fascin), which mediates cell migration. Sox11/Sox4 deficiency accelerates differentiation and dramatically impairs cell motility. |
Mouse knockout models, chromatin immunoprecipitation, gene expression profiling, wound healing assays |
Nature communications |
High |
31492871
|
| 2014 |
Sox11 overexpression in MSCs transcriptionally activates Runx2 and CXCR4 expression (demonstrated by dual-luciferase reporter assay) and activates the BMP/Smad signaling pathway, enhancing trilineage differentiation and migration of MSCs. |
Lentiviral overexpression, dual-luciferase reporter assay, ectopic bone formation, western blot, open fracture rat model |
FASEB journal |
Medium |
25466891
|
| 2020 |
Wnt7b induces Sox11 expression in BMSCs via a β-catenin-independent, Ca2+-dependent Nfatc1 signaling pathway. ChIP-qPCR showed Nfatc1 directly binds the Sox11 promoter. Sox11 in turn transcriptionally activates Ccnb1, Sox2 (proliferation) and Runx2, Sp7 (osteogenesis). |
ChIP-qPCR, RNA-seq, shRNA knockdown, transgenic mice, immunofluorescence, ex vivo transplantation |
Stem cells (Dayton, Ohio) |
Medium |
32346881
|
| 2021 |
SOX11 directly upregulates CD70 expression in MCL cells. CD70 overexpression in SOX11+ MCL is associated with increased Treg cell infiltration and an immunosuppressive tumor microenvironment. CD40L stimulation induces CD70 in SOX11+ but not SOX11- MCL cells in vitro. |
ChIP (binding to CD70 regulatory regions), gene expression analysis, immunohistochemistry, in vitro stimulation assays |
Blood |
Medium |
34189576
|
| 2009 |
Sox11 overexpression in glioma-initiating cells (NSC-derived) prevents tumorigenesis by inducing neuronal differentiation, accompanied by decreased plagl1 expression. Plagl1 overexpression abolishes neuronal commitment and induces tumorigenicity. Sox11 loss is found in human glioma-initiating cells, and Sox11 overexpression prevents their tumorigenesis in vivo. |
Gene expression profiling, overexpression assays, in vivo tumorigenesis, limiting dilution assays |
Cancer research |
Medium |
19808959
|
| 2017 |
Endogenous SOX11 directly binds the SDCCAG8 gene promoter in highly invasive HNSCC cells. Wild-type SOX11 but not a DNA-binding mutant activates SDCCAG8 promoter activity. Inhibitory effects of SOX11 knockdown on proliferation, migration, and invasion were partially rescued by SDCCAG8 overexpression. |
ChIP, luciferase reporter assay, mutagenesis, quantitative proteomics, rescue assay |
Journal of experimental & clinical cancer research |
Medium |
30922366
|
| 2017 |
SOX11 binds the slug (SNAI2) promoter and activates its transcription in MCF-7 tamoxifen-resistant breast cancer cells, promoting epithelial-to-mesenchymal transition and suppressing ESR1 expression. |
Chromatin immunoprecipitation, luciferase reporter assay, gene expression analysis |
Journal of cellular physiology |
Medium |
32043610
|
| 2023 |
SOX11 is a core regulatory circuitry (CRC) transcription factor in adrenergic neuroblastoma. SOX11 directly regulates 10 SWI/SNF core components (including SMARCC1, SMARCA4/BRG1, ARID1A), HDAC2, PRC1 component CBX2, KDM1A/LSD1, and c-MYB. SOX11 is regulated by multiple adrenergic-specific super-enhancers. |
ChIP-seq, enhancer analysis, gene expression dependency analysis, neuroblastoma cell line functional studies |
Nature communications |
High |
36882421
|
| 2017 |
SOX11 binds to HSP90α (HSP90AA1) in head and neck cancer cells. The interaction was identified by Co-IP/LC-MS/MS and validated by Co-IP with western blotting. |
Co-immunoprecipitation, liquid chromatography-tandem mass spectrometry (LC-MS/MS), western blotting |
Journal of proteome research |
Medium |
28915052
|
| 2018 |
SOX11 overexpression in HCC cells enhances nemo-like kinase expression and TCF4 phosphorylation, thereby inhibiting Wnt/β-catenin signaling and promoting growth inhibition and apoptosis. |
Overexpression assays, western blot, cell viability and apoptosis assays |
Biotechnology and applied biochemistry |
Low |
30517979
|
| 2013 |
Cell-type-specific deletion shows Sox11 is required for proper outflow tract development in both mesodermal cells and neural crest cells. Sox4 and Sox11 become essential after neural crest arrival in the outflow tract for differentiation and interaction through regulation of cytoskeletal, cell adhesion, and ECM molecules. |
Cell-type-specific conditional deletion in mouse (mesoderm and neural crest), phenotypic analysis |
Cellular and molecular life sciences |
High |
24310815
|
| 2018 |
Sox11 disruption in mice causes CAKUT including duplex kidney formation. SOX11 directly binds and regulates a locus control region of the protocadherin B cluster. SOX11 regulates elongation of Henle's loop. A CAKUT-associated SOX11 variant identified in patients interferes with SOX11 transactivation capacity. |
Sox11 knockout mouse, ChIP demonstrating direct binding to protocadherin B locus control region, transactivation assays |
Kidney international |
High |
29459093
|
| 2016 |
Sox11 deficiency causes cleft palate through mandibular hypoplasia; Sox11 loss reduces cell proliferation in mandibular mesenchyme via Cyclin D1. In vitro assays show Sox11 directly regulates Fgf9 expression, and FGF9 protein application to Sox11-deficient palatal shelves restores BrdU incorporation. |
Sox11 knockout mouse, BrdU proliferation assay, gene expression analysis, in vitro FGF9 rescue assay |
The Journal of biological chemistry |
Medium |
26826126
|
| 2019 |
SOX11 promotes cell migration in wounded skin by activating expression of FSCN1 (fascin actin-bundling protein 1) as a direct transcriptional target. Sox11/Sox4 deficiency impairs cell motility and re-epithelialization. |
ChIP, mouse knockout models, wound healing assays, gene expression profiling |
Nature communications |
High |
31492871
|
| 2017 |
LHX2 binds distal regulatory elements of Sox11 in cortical progenitors and interacts with NuRD complex subunits LSD1, HDAC2, and RBBP4 to maintain repressive chromatin at the Sox11 locus. Loss of LHX2 increases active histone marks at Sox11 loci and increases Sox11 expression, while LHX2 overexpression decreases it. |
ChIP, Co-IP (LHX2 with NuRD complex components), conditional knockout, overexpression, histone mark analysis |
The Journal of neuroscience |
Medium |
28053041
|
| 2022 |
LINC01296 binds nucleolin (NCL) and forms a complex that activates SOX11 gene transcription, promoting neuroblastoma tumorigenesis. Silencing LINC01296 reduces SOX11 expression; RNA pull-down validated the LINC01296-NCL interaction. |
RNA pull-down assay, Co-IP, luciferase reporter assay, siRNA knockdown, in vivo xenograft |
Molecular therapy oncolytics |
Medium |
35317520
|
| 2019 |
Sox11 in spinal cord injury promotes neuronal differentiation of endogenous neural stem cells and induces BDNF expression in the injured cord, improving locomotor recovery. |
Lentiviral Sox11 delivery to injured mouse spinal cord, immunostaining, behavioral assays |
Biochemical and biophysical research communications |
Low |
24589730
|
| 2020 |
SOX11 confers a hybrid epithelial/mesenchymal (E/M) state in ER-negative breast cancer cells, leading to alterations in metastatic tropism (increased brain and bone metastasis, decreased lung metastasis) in xenograft models. |
SOX11 overexpression in DCIS.com cells, xenograft mouse model, single-cell analysis, E/M marker analysis |
eLife |
Medium |
32909943
|
| 2015 |
SOX11 promoter in non-malignant cells shows low methylation with strong H3K27me3 enrichment. In cancer cells with low SOX11 methylation, HDAC inhibitors (vorinostat, trichostatin A) can reactivate SOX11 expression, while cells with dense methylation are resistant to re-expression. |
Bisulfite sequencing, ChIP-qPCR for H3K27me3, HDAC inhibitor treatment, methylation assays in 42 cell lines |
BMC cancer |
Medium |
25880212
|
| 2019 |
SOX11 transcriptionally activates β-catenin expression in MSCs (core promoter region -242 to -1414 identified). Sox11 also interacts with β-catenin protein (co-immunoprecipitation) suggesting post-transcriptional regulation in addition to transcriptional activation. |
Dual-luciferase reporter assay, co-immunoprecipitation, quantitative RT-PCR, in vivo cartilage defect model |
Cell and tissue research |
Medium |
30617615
|