| 1994 |
SOX5 protein localizes to the nucleus of post-meiotic round spermatids in mouse testis. In vitro footprinting and gel retardation assays demonstrate that SOX5 binds specifically to the sequence AACAAT with ~10^-9 M affinity. Interaction of SOX5 with its target DNA induces a significant bend in the DNA, characteristic of HMG box proteins. 2D NMR analysis of the SOX5 HMG box revealed helical secondary structure and tertiary structure similar to HMG1 box 2. |
Indirect immunofluorescence (nuclear localization), in vitro footprinting, gel retardation assay, circular dichroism spectroscopy, 2D NMR |
Nucleic acids research |
High |
8078769
|
| 1998 |
A new long-form L-Sox5 (distinct from the short testis form) contains a coiled-coil domain in its N-terminal part that mediates homodimerization and heterodimerization with Sox6. Dimerization of L-Sox5/Sox6 greatly increases efficiency of binding to DNA containing adjacent HMG sites. L-Sox5, Sox6, and Sox9 cooperatively activate expression of Col2a1 via a 48 bp chondrocyte-specific enhancer containing multiple HMG-like sites, which all three proteins bind. |
Coiled-coil domain analysis, dimerization assays, DNA binding assays, reporter gene assays in 10T1/2 and MC615 cells, transgenic mouse embryo expression |
The EMBO journal |
High |
9755172
|
| 1998 |
The mouse Sox5 long-form cDNA (from 8.5-day embryo) encodes a 763-amino acid protein containing a leucine zipper motif and a glutamine-rich Q box domain, which are absent from the short testis-derived form (392 aa). These domains are conserved among type-D SOX proteins. |
cDNA cloning, sequence analysis, Southern analysis, RT-PCR |
Biochimica et biophysica acta |
Medium |
9714725
|
| 1999 |
Thermodynamic characterization of the Sox5 HMG box interaction with AACAAT-containing DNA duplexes: association constant ~4×10^7 M^-1; binding is endothermic below 17°C and exothermic above; heat capacity change on binding ~-2 kJ K^-1 mol^-1. The binding involves dehydration of polar and non-polar groups and release of counterions, with significant conformational entropy reduction. |
Fluorescence titration, isothermal titration calorimetry (ITC), differential scanning calorimetry (DSC) |
Journal of molecular biology |
High |
10588902
|
| 2001 |
Solution NMR structure of the mouse Sox5 HMG box in free solution reveals a characteristic twisted L-shape with a major wing (helices 1 and 2) and a minor wing (helix 3 in weak antiparallel association with N-terminal strand). The minor wing shows considerable backbone mobility (reduced order parameter S²) that increases toward termini, particularly C-terminal to Q62, contrasting with non-sequence-specific HMG boxes. |
Multidimensional NMR with ¹⁵N-labeled protein, ¹⁵N relaxation measurements |
Protein science |
High |
11266597
|
| 2002 |
Sox9 is required upstream of Sox5 and Sox6 expression: inactivation of Sox9 in limb bud mesenchymal cells before condensation results in complete loss of Sox5 and Sox6 expression, placing Sox9 genetically upstream of Sox5 in the chondrogenic transcription factor hierarchy. |
Conditional knockout using Cre/loxP recombination in mouse embryos, in situ hybridization for marker gene expression |
Genes & development |
High |
12414734
|
| 2003 |
Sox5 and Sox6 are expressed in the notochord cell lineage and are required for notochord extracellular matrix sheath formation and notochord cell survival. In Sox5⁻/⁻;Sox6⁻/⁻ embryos, the notochord fails to become surrounded by an ECM sheath, associated with downregulation of collagen 2, aggrecan and perlecan genes; notochord cells then undergo apoptosis. Sox5/Sox6 are thus required for nucleus pulposus formation. |
Double knockout mouse analysis, in situ hybridization, immunohistochemistry, apoptosis assays |
Development (Cambridge, England) |
High |
12571105
|
| 2004 |
The combination of SOX5, SOX6, and SOX9 (SOX trio) is sufficient to induce chondrocyte differentiation in embryonic stem cells, mesenchymal stem cells, non-chondrogenic immortalized cell lines, and primary dermal fibroblasts, while simultaneously suppressing hypertrophic and osteogenic differentiation. |
Fluorescent reporter ES cell line screen, gene transfer into multiple cell types, glycosaminoglycan assay, Safranin-O staining, marker gene expression |
Arthritis and rheumatism |
High |
15529345
|
| 2007 |
Sox9, Sox5, and Sox6 cooperatively activate COMP gene expression via a 51-bp positive regulatory element (PRE) in the COMP promoter. Sox9 binds the COMP promoter at the PRE, requiring 13 nucleotides (TGTTTACCTTGTG). Activation by Sox9 requires participation of Sox5 and Sox6 as well as coactivators CBP and p300 histone acetylase. |
EMSA (gel shift), reporter assays, siRNA knockdown, co-transfection in chondrogenic cells |
Frontiers in bioscience |
Medium |
17485346
|
| 2008 |
L-Sox5 and Sox6 promote binding of Sox9 to a far-upstream 359-bp aggrecan (Agc1) enhancer 10 kb upstream of the gene. L-Sox5/Sox6 bind three additional elements in this enhancer cooperatively, and upon binding, increase the efficiency of Sox9 binding to its own recognition site, thereby robustly potentiating Sox9-mediated transcriptional activation. A similar mechanism operates at the Col2a1 and other cartilage-specific enhancers. |
Transgenic mouse reporter assay, ChIP, EMSA, co-transfection reporter assays, site-directed mutagenesis of cis-elements |
Molecular and cellular biology |
High |
18559420
|
| 2008 |
Sox5 modulates Sox10 activity in the melanocyte lineage by binding regulatory regions of melanocytic Sox10 target genes and recruiting the corepressors CtBP2 and HDAC1, directly inhibiting Sox10-dependent promoter activation. Both binding site competition and corepressor recruitment contribute to this modulatory activity. Loss of Sox5 in Sox10 heterozygous mice partially rescues melanoblast generation. |
Sox5-deficient mouse analysis, ChIP (Sox5 binding and CtBP2/HDAC1 recruitment to target gene regulatory regions), reporter assays, genetic epistasis (Sox5⁻/⁻;Sox10⁺/⁻ compound mutants) |
Nucleic acids research |
High |
18703590
|
| 2008 |
Tip60 (a histone acetyltransferase) physically associates with Sox9 in chondrocytes (confirmed by yeast two-hybrid and endogenous co-immunoprecipitation), and forms a complex with Sox9, Tip60, and the Col2a1 enhancer DNA. Tip60 enhances Sox9 transcriptional activity and further increases Col2a1 promoter activity in the presence of both Sox9 and Sox5. ChIP confirms that Tip60, Sox9, and Sox5 all associate with the same Col2a1 enhancer region. Tip60 acetylates Sox9 mainly at K61, K253, K398. |
Yeast two-hybrid, Co-IP (endogenous complex), EMSA (ternary complex with DNA), reporter assays, ChIP, siRNA in limb-bud micromass cultures, Tip60 acetylation assays |
Nucleic acids research |
High |
18390577
|
| 2010 |
SOX5 is expressed by neural progenitors in the chick spinal cord and is turned off as differentiation proceeds. Overexpression of SOX5 in neural progenitors causes premature cell cycle exit and prevents terminal differentiation; knockdown extends the proliferative period and causes cell death in a dorsal interneuron (dI3) population. SOX5 reduces WNT-β-catenin signaling and triggers expression of the negative pathway regulator axin2. |
In ovo electroporation (overexpression and knockdown) in chick spinal cord, BrdU proliferation assay, cell death assay, luciferase reporter for WNT/β-catenin signaling, qPCR |
EMBO reports |
Medium |
20448664
|
| 2010 |
S-SOX5 (48-kDa short form expressed in tissues with motile cilia/flagella) directly binds the SPAG6 gene promoter at SOX5-binding sites and stimulates mouse and human SPAG6 promoter activity, an effect abrogated by mutation or deletion of SOX5 binding sites. S-SOX5 and FOXJ1 cooperatively activate SPAG6 promoter. Silencing of S-SOX5 by RNAi downregulates SPAG6 transcripts. ChIP and EMSA confirm direct S-SOX5 association with the SPAG6 promoter. |
Reporter assays (promoter-luciferase), site-directed mutagenesis of binding sites, siRNA knockdown, ChIP, EMSA |
The Journal of biological chemistry |
High |
20668334
|
| 2010 |
L-Sox5/Sox6 and Sox9 cooperatively bind the proximal Matn1 promoter at evolutionarily conserved elements (Pe1 and Ine), with L-Sox5/Sox6 binding to the Ine initiator element modulating Sox9 transactivation in a protein dose-dependent manner, restricting Matn1 expression to the proliferative and prehypertrophic zones of the growth plate. |
Transgenic mouse reporter assay, EMSA, ChIP, co-transfection reporter assays, binding site mutagenesis |
Molecular and cellular biology |
High |
21173167
|
| 2010 |
Sox5 and Sox6 are required for synovial joint morphogenesis. In complete Sox5⁻/⁻;Sox6⁻/⁻ mutants, joint development aborts early: Gdf5 and Wnt9a expression occurs normally in articular progenitors but joint cell differentiation fails and cavitation does not occur. Cell-specific inactivation using Col2Cre or Gdf5Cre shows that Sox5/Sox6 in chondrocytes are required for both growth plate and articular chondrocyte differentiation, with articular chondrocytes remaining undifferentiated (continued Gdf5 expression, loss of pancartilaginous gene expression) when Sox5/Sox6 are inactivated in specified joint cells. |
Complete and conditional knockout mouse analysis using Cre/loxP (Col2Cre, Gdf5Cre), in situ hybridization, immunohistochemistry |
Developmental biology |
High |
20206616
|
| 2011 |
SHOX physically interacts with SOX5 and SOX6 (identified by yeast two-hybrid and confirmed by Co-IP in human cells). The SHOX homeodomain and SOX6 HMG domain mediate this interaction. SHOX cooperates with SOX5/SOX6 and SOX9 to activate the upstream Agc1 enhancer. Disease-causing SHOX missense mutations found in Leri-Weill dyschondrosteosis disrupt this SHOX-SOX6 interaction. |
Yeast two-hybrid, Co-IP in human cells, domain mapping, immunohistochemistry (coexpression in fetal growth plates), reporter assays (Agc1 enhancer), mutant analysis |
Human molecular genetics |
High |
21262861
|
| 2012 |
L-Sox5 and Sox6 increase the efficiency of Sox9 dimeric DNA binding and boost Sox9 transactivation of the miR-140 promoter. A Sox trio response element in the proximal upstream region of pri-miR-140 is required for chondrogenic promoter activity in vivo. |
Reporter assays (miR-140 promoter-luciferase), binding site analysis, in vivo promoter activity assay in transgenic mice, EMSA |
The Journal of biological chemistry |
Medium |
22547066
|
| 2014 |
Sox5 physically associates with c-Maf via the HMG domain of Sox5 and the DNA-binding domain of c-Maf. Together, Sox5 and c-Maf directly activate the RORγt promoter in CD4⁺ T cells. A novel Th17-specific isoform Sox5t is induced by Stat3 signaling. T cell-specific Sox5-deficient mice show impaired Th17 cell differentiation. Retrovirus-mediated induction of Sox5 together with c-Maf induces Th17 differentiation even in Stat3-deficient CD4⁺ T cells but not in RORγt-deficient cells, placing Sox5/c-Maf downstream of Stat3 and upstream of RORγt. |
T cell-specific conditional KO mice, retroviral transduction, co-immunoprecipitation (Sox5 HMG domain–c-Maf DBD interaction), RORγt promoter reporter assays, genetic epistasis (Stat3⁻/⁻ and RORγt⁻/⁻ backgrounds), EAE and DTH models |
The Journal of experimental medicine |
High |
25073789
|
| 2014 |
Sox5 functions as a DNA-binding cofactor for BMP R-Smads in Xenopus ectoderm. Sox5 is expressed where BMP signaling is active; Sox5 loss causes patterning defects resembling loss of BMP signaling (loss of neural crest and epidermis, expansion of neural plate). Sox5 physically interacts with BMP R-Smads and is essential for recruitment of Smad1/4 to BMP regulatory elements in vivo. |
Xenopus embryo loss-of-function, ectoderm explant assays, co-immunoprecipitation (Sox5–BMP R-Smad interaction), ChIP (Smad1/4 recruitment to BMP target gene regulatory elements) |
Developmental cell |
High |
25453832
|
| 2014 |
Sox5 functions as a cell-autonomous fate switch in medaka neural crest: sox5 is expressed in premigratory NCCs and differentiating xanthophores, downstream of pax7a. Loss of sox5 results in excessive leucophore formation and absence of xanthophores (ml-3 mutant phenotype). Cell transplantation demonstrates a cell-autonomous role of sox5 in the xanthophore lineage. |
Forward genetic screen, positional cloning (ml-3 = sox5), cell transplantation (chimera analysis), in situ hybridization, genetic epistasis (pax7a) |
PLoS genetics |
High |
24699463
|
| 2014 |
Sox5 transactivates Twist1 expression by directly binding to the Twist1 promoter in breast cancer cells, as shown by chromatin immunoprecipitation. Depletion of Sox5 inhibits breast cancer cell proliferation, migration, and invasion, downregulates Twist1, and reverses EMT (increases E-cadherin, decreases N-cadherin, Vimentin, Fibronectin 1). |
ChIP (Sox5 binding to Twist1 promoter), siRNA knockdown, gain/loss-of-function in breast cancer cells, Western blot for EMT markers |
Biochemical and biophysical research communications |
Medium |
24607904
|
| 2015 |
SOX9 and SOX5/SOX6 cooperate genome-wide through super-enhancers to drive chondrogenesis. ChIP-seq in RCS chondrocytes reveals SOX6 binds thousands of genomic sites, frequently near SOX9 binding sites. SOX9 recognizes pairs of inverted SOX motifs; SOX6 favors pairs of tandem SOX motifs. The SOX proteins primarily target super-enhancers (SEs) linked to cartilage-specific genes including the SOX trio proteins themselves and all essential cartilage ECM components. SOX proteins are required for in vivo expression of SE-associated genes. |
ChIP-seq (SOX6 and SOX9 genome-wide binding), motif analysis, SE identification, conditional KO for validation of in vivo gene expression |
Nucleic acids research |
High |
26150426
|
| 2015 |
Sox5 and Sox6 promote migration of oligodendrocyte progenitor cells by maintaining expression of PDGFRα and responsiveness to PDGF-A. In CNS-specific Sox5/Sox6 double mutants, emigration of OPCs from the ventricular zone is delayed due to reduced PDGFRα expression. Sox5 and Sox6 cooperate with Sox9 and Sox10 to activate PDGFRα expression in OPCs (a co-activator role), contrasting with their antagonistic role on myelin genes. |
CNS-specific conditional double KO mice, in situ hybridization, immunohistochemistry, PDGF-A responsiveness assays |
Glia |
Medium |
26345464
|
| 2016 |
SOX5 binds to and transcriptionally activates the RANKL promoter in rheumatoid arthritis synovial fibroblasts (RA-SF). ChIP shows ~3-fold enrichment of RANKL-specific DNA in anti-SOX5 immunoprecipitate in IL-6-treated cells. IL-6 induces SOX5 upregulation, which mediates RANKL upregulation; SOX5 knockdown diminishes IL-6-mediated RANKL induction. In vivo silencing of SOX5 reduces RANKL-positive cells and bone erosion in CIA mice. |
ChIP (SOX5 binding to RANKL promoter), siRNA knockdown, overexpression, in vivo siRNA delivery in CIA mouse model, Western blot, luciferase reporter |
Scientific reports |
Medium |
27550416
|
| 2017 |
SOX5 directly binds the Twist1 promoter and transcriptionally activates Twist1 to drive EMT and prostate cancer metastasis. Smad3 binds the SOX5 promoter and upregulates SOX5 expression downstream of TGF-β. Knockdown of SOX5 attenuates TGF-β-induced EMT and reduces prostate cancer cell migration and mesenchymal phenotype. |
Luciferase reporter assays, ChIP (Smad3 binding to SOX5 promoter; SOX5 binding to Twist1 promoter), siRNA knockdown, xenograft mouse model |
British journal of cancer |
Medium |
29123266
|
| 2017 |
Sox5 regulates β-cell phenotype and insulin secretion: Sox5 knockdown in mouse islets induces gene expression changes similar to those in T2D and reduces depolarization-evoked Ca²⁺-influx and β-cell exocytosis. SOX5 overexpression in human T2D islets increases expression of key β-cell genes and improves glucose-stimulated insulin secretion. |
siRNA knockdown in mouse islets, electrophysiology (Ca²⁺ influx, exocytosis), gene expression profiling, SOX5 overexpression in human T2D donor islets, glucose-stimulated insulin secretion assay |
Nature communications |
High |
28585545
|
| 2017 |
SOX5 suppresses PDGFB-induced glioma development predominantly in Ink4a-deficient cells by inducing acute cellular senescence. SOX5 overexpression in glioma cells reduces Akt activation and increases p27(Kip1). Inhibition of p27(Kip1) reverses the anti-proliferative and pro-senescence effects of Sox5. This defines a pathway where Sox5 suppresses oncogenic PDGFB effects via p27(Kip1) in a p19(Arf)-dependent manner. |
Retroviral Sox5 overexpression in primary brain cells and glioma cell lines, senescence assays, proliferation assays, Western blot (Akt, p27), p27 siRNA epistasis, in vivo glioma model |
Oncogene |
Medium |
19219070
|
| 2017 |
SOX5 transactivates EZH2 in breast cancer: ChIP-seq and quantitative ChIP identify EZH2 as a direct downstream transcriptional target of SOX5. SOX5 overexpression increases EZH2 mRNA and protein; SOX5 knockdown decreases EZH2. The proliferative and invasive effects of SOX5 depend on EZH2 regulation. |
ChIP-seq (SOX5 binding at EZH2 locus), quantitative ChIP, luciferase reporter assay, siRNA knockdown, rescue experiments |
Oncology letters |
Medium |
30854049
|
| 2018 |
SOX5 promotes migration and invasion of fibroblast-like synoviocytes (FLS) in rheumatoid arthritis in part by directly binding the MMP-9 promoter at a specific SOX5-binding site and transcriptionally activating MMP-9. ChIP shows SOX5 binding to MMP-9 promoter; deletion of the putative SOX5 binding site abolishes promoter activation. In vivo knockdown of SOX5 in CIA mice reduces MMP-9 expression and pannus invasion. |
ChIP (SOX5 binding to MMP-9 promoter), luciferase reporter with site deletion mutagenesis, Transwell migration/invasion assay, siRNA knockdown, in vivo CIA mouse model with local SOX5 knockdown |
Frontiers in immunology |
High |
29706965
|
| 2018 |
In medaka and zebrafish, Sox5 represses Sox10-dependent formation of melanocytes and iridophores (Sox5 loss in Sox10-defective fish partially rescues formation of all pigment cells in zebrafish). In medaka, Sox5 promotes xanthophore specification while Sox10 loss cooperates with Sox5 loss to reduce xanthophores. Misexpression of Sox5 in xanthophore/leucophore progenitors increases xanthophores and reduces leucophores in medaka. The mode of Sox5 function (promoting vs. repressing) in xanthophore specification differs between medaka and zebrafish. |
TILLING, TALEN, CRISPR/Cas9-generated sox5 and sox10 mutants in medaka and zebrafish, compound mutant analysis, sox5 misexpression, pigment cell lineage tracing |
PLoS genetics |
High |
29621239
|
| 2019 |
SOX5 directly activates the GLUT4 promoter in ovarian cancer cells to regulate glycolysis. Apatinib suppresses SOX5 expression via the VEGFR2/AKT1/GSK3β signaling cascade, thereby reducing GLUT4-mediated glucose uptake and lactate production. SOX5 overexpression rescues apatinib-inhibited GLUT4 expression. |
Dual-luciferase reporter assay (GLUT4 promoter), SOX5 overexpression and shRNA knockdown, Western blot (VEGFR2/AKT1/GSK3β pathway proteins), glucose uptake and lactate production assays, xenograft IHC |
Cellular oncology |
Medium |
31325096
|
| 2019 |
FOX-A1 directly binds the SOX5 promoter and transcriptionally upregulates SOX5 expression in lung adenocarcinoma cells. ChIP-seq and ChIP assays confirm FOX-A1 occupancy at the SOX5 promoter. SOX5 knockdown reverses chemoresistance to docetaxel by suppressing EMT. |
ChIP-seq, ChIP assay (FOX-A1 binding to SOX5 promoter), siRNA knockdown of FOX-A1 and SOX5, Western blot for EMT markers, cell proliferation and migration assays |
EBioMedicine |
Medium |
31147293
|
| 2020 |
SOX5 interacts with YAP1 in non-small cell lung cancer cells to drive malignant potential. Co-immunoprecipitation demonstrates SOX5-YAP1 physical interaction. SOX5 promotes self-renewal, invasion and migration; knockdown of YAP1 attenuates these malignant processes, and SOX5 overexpression reverses the attenuated progression caused by YAP1 knockdown. |
Co-immunoprecipitation (SOX5-YAP1 interaction), siRNA knockdown (SOX5 and YAP1), overexpression rescue experiments, sphere formation assay, Transwell invasion/migration, xenograft mouse model |
American journal of cancer research |
Medium |
29888108
|
| 2021 |
SOX5 activates a novel RORγt enhancer (RORCE2) in Th17 cells by directly binding to it, looping RORCE2 to the RORγt promoter. Loss of the SOX5-binding site in RORCE2 abolishes RORCE2 function and affects STAT3 binding to the RORγt locus. RORCE2 deficiency suppresses RORγt expression and Th17 differentiation, reducing EAE severity. |
Enhancer identification, SOX5 binding site mutagenesis, chromosomal conformation assay (looping), STAT3 ChIP, RORCE2 knockout mouse, EAE model |
Nature communications |
High |
33473108
|
| 2023 |
SOX5 activates the HMGB2 enhancer (increasing H3K27ac and H3K4me1 marks) to upregulate HMGB2 expression, thereby promoting rejuvenation and antagonizing cellular senescence. SOX5 overexpression resets the transcription network for geroprotective genes. Lentiviral SOX5 or HMGB2 gene therapy rejuvenates cartilage and alleviates osteoarthritis in aged mice. |
Genome-wide CRISPRa screen in hMPCs, ChIP (SOX5 binding and H3K27ac/H3K4me1 at HMGB2 enhancer), RNA-seq, lentiviral gene therapy in aged mice, histological assessment of cartilage |
Cell stem cell |
High |
37832549
|
| 2011 |
Sox5⁻/⁻ mice show abnormal lung development with delayed maturation before the saccular stage (as early as E16.5). Sox5 loss is associated with decreased fibronectin expression in the lung, implicating SOX5 in regulation of fibronectin-dependent branching morphogenesis. |
Sox5⁻/⁻ mouse histology, gene expression analysis of lung development markers including fibronectin |
American journal of respiratory and critical care medicine |
Medium |
21330457
|
| 2018 |
SOX5 inhibits MITF expression in human melanoma cells. SOX5 knockdown leads to MITF upregulation; double knockdown of SOX5 and SOX10 shows a rescue effect on MITF levels, confirmed by MITF-promoter reporter assays. |
siRNA knockdown of SOX5 and SOX10 (single and double KD), MITF promoter-reporter assay, network model + experimental validation |
BMC medical genomics |
Medium |
26927636
|
| 2009 |
In medaka, Sox5 is required for germ-cell number regulation and, through exaptation of a transposable element (Rex1 within Izanagi), de novo regulates dmrt1bY transcriptional activity during primary sex determination. Sox5 mutant medaka exhibit complete female-to-male sex reversal. |
Mutant analysis, regulatory element characterization (TE insertion), transgenic reporter assays for Sox5 binding to dmrt1bY regulatory element, sex reversal phenotype scoring |
BMC biology |
Medium |
29378592
|
| 2017 |
Silencing of the Drosophila ortholog of SOX5 (Sox102F) in various neuronal subtypes causes misorientated microchaetes, shorter and less complex dendritic arbors, loss of NMJ bouton structures, impaired olfactory perception, and neurodegeneration. Silencing in the wing disrupts Wnt/wingless signaling expression pattern. In human SH-SY5Y cells, SOX5 knockdown significantly represses WNT signaling activity and alters expression of WNT-related genes. |
Drosophila RNAi in specific neuronal subtypes, OCT cardiac imaging, morphological analysis of neurons, luciferase WNT reporter assay in human cells, qPCR |
Human molecular genetics |
Medium |
28186563
|
| 2013 |
Silencing of Sox102F (Drosophila SOX5 ortholog) in cardiac tissue causes significant decrease in heart rate, heart chamber size, and cardiac wall velocities, and increased cardiac wall thickness with disrupted myofibril structure. Silencing in the wing leads to increased wingless (Wnt) signaling expression and disorganization, indicating SOX5 modulates Wnt signaling in cardiac and wing development. |
Drosophila transgenic RNAi in heart, high-speed ultrahigh-resolution OCT imaging of Drosophila heart, wing morphology analysis, wingless immunostaining |
Human molecular genetics |
Medium |
23696452
|
| 2014 |
miR-194 directly targets SOX5 (validated by luciferase assay) in human adipose-derived stem cells. Downregulation of miR-194 increases SOX5 and enhances chondrogenic differentiation of hASCs, while upregulation of miR-194 decreases SOX5 and inhibits chondrogenesis. |
Luciferase reporter assay (miR-194 targeting SOX5 3'UTR), miR-194 gain/loss-of-function, chondrogenic differentiation assays |
PloS one |
Medium |
22396742
|
| 2018 |
SOX5 overexpression in osteogenic differentiation of hMSCs inhibits alkaline phosphatase activity and osteoblast marker genes (Collagen I, Runx2, Osterix); knockdown of SOX5 enhances osteogenic differentiation. TNF-α upregulates SOX5, and SOX5 mediates TNF-α's inhibitory effect on osteogenesis through KLF4: SOX5 overexpression increases KLF4 expression, and KLF4 knockdown abrogates the inhibitory effect of SOX5 on osteogenesis. |
siRNA knockdown and plasmid overexpression, ALP activity assay, gene expression (qPCR/Western blot), KLF4 siRNA epistasis, TNF-α stimulation of hMSCs from PMOP patients |
Molecules and cells |
Medium |
29890823
|
| 2020 |
SOX5 acts as a transcriptional activator of VEGF expression in neurons: SOX5 overexpression promotes VEGF expression and activates the PI3K/AKT pathway, protecting against LPS-induced apoptosis in PC-12 cells. SOX5 binding to the VEGF promoter was confirmed by ChIP-PCR and dual-luciferase reporter assay. |
ChIP-PCR, dual-luciferase reporter assay (VEGF promoter), overexpression in PC-12 cells, TUNEL apoptosis assay, Western blot for PI3K/AKT pathway |
Gene |
Medium |
32949698
|