Use your antibodies-online credentials, if available.
Keine Produkte auf Ihrer Vergleichsliste.
Ihr Warenkorb ist leer.
Weitere Synonyme anzeigen
Wählen Sie die gewünschte Spezies
Human SOX9 Protein expressed in HEK-293 Cells - ABIN2732475
Shi, Chiang, Labhart, Zhao, Yang, Mistretta, Henning, Maity, Mori-Akiyama: Context-specific role of SOX9 in NF-Y mediated gene regulation in colorectal cancer cells. in Nucleic acids research 2015
THOR could potentiate the stemness of gastric cancer cells via directly binding to SOX9 3'UTR.
SOX9 was upregulated in breast cancer (BC) tissues and its expression was inversely correlated with that of miR511. Furthermore, SOX9 inhibition simulated the tumorsuppressive roles of miR511 overexpression in BC cells, while SOX9 reintroduction partially rescued these effects of miR511. Notably, the upregulation of miR511 targeted SOX9 to deactivate the PI3K/Akt signaling in BC in vitro and in vivo.
High SOX9 expression promotes invasion and metastasis of pancreatic ductal adenocarcinoma.
SOX9 polymorphism rs1042667 shows significant association with the occurrence of osteoarthritis (OA) in Chinese Han population, but not rs12601701. Furthermore, the interaction between the polymorphisms rs12601701 and rs1042667 is suggested to contribute to the risk of OA as well.
The present study identified Scmlike with four malignant brain tumor domains 2 (SFMBT2) as a novel regulator of SOX9 expression.
miR-30c suppressed the proliferation, migration, and invasion of GBM cells via targeting SOX9.
Isolate living subpopulations of duct cells enriched for high or low expression of HNF1beta and SOX9.
This is the first report of molecularly confirmed maternal germinal mosaicism for a SOX9 mutation. We suggest that a meticulous clinical examination of the parents, even if they are superficially healthy, is needed to avoid overlooking germinal mosaicism of SOX9 mutations.
Our study tested and verified that MALAT1 was highly expressed in colorectal cancer tissues and cells. MALAT1 regulated miR-145 expression as a competing endogenous RNA, and down-regulation of MALAT1 suppressed proliferation and invasion, promoted cell cycle G1 phase and apoptosis of cancerous cells by increasing the expression of miR-145 and decreasing SOX9 expression.
Human sex reversal is caused by duplication or deletion of core enhancers upstream of SOX9.
Results find SOX9 highly expressed in non-small cell lung cancer (NSCLC) tissues, and positively correlates with that of MALAT1. Moreover, SOX9 protein expression was higher in NSCLC tissues expressing highly especially MALAT1 mRNA.
results demonstrate that the inhibition of miR-30d attenuates the apoptosis and extracellular matrix degradation of degenerative human nucleus pulposus cells by up-regulating SOX9, suggesting a potential therapeutic target for intervertebral disc degeneration
Our study demonstrated that Reg IV positively regulates the expression of SOX9 and is involved in tumor cell invasion and migration in gastric cancer.
SOX9 may be involved in the tumorigenesis and progression of oral squamous cell carcinoma (OSCC). Furthermore, its cytoplasmic expression represents a potential predictive biomarker for tumor aggressiveness and OSCC prognosis.
This is supported by the fact that ECG correlates with the expression of SOX9 indicating that this biomarker probably plays an important role in the pathogenesis of gastric cancer and ECG formation.
role in regulation of extracellular matrix balance, the inflammatory process, and the immune response of inflamed dental pulp
Study found a positive relationship between LINC00052 and miR-101-3p, and a negative relationship between miR-101-3p and SOX9 in hepatocellular carcinoma (HCC) tissues. Besides, miR-101-3p was involved in LINC00052 inhibiting HCC cells proliferation and metastasis. At the molecular level, LINC00052 downgulated SOX9 to inhibit HCC cells proliferation and metastasis by interacting with miR-101-3p.
SOX9 expression is related to prognosis in patients with oesophageal squamous cell carcinoma, although it is not an independent prognostic factor.
the findings of this study establish the SOX9/CA9-mediated oncogenic pathway in glioma, the inhibition of which enhances the sensitivity of glioma cells to Temozolomide (TMZ) treatment, and thus highlights the value of developing small molecules or antibodies against the SOX9/CA9 pathway, for combination therapy with TMZ, in the more efficient management of glioma
Heterogeneous Expression of Embryonal Development Master Regulator SOX9 in Patients with Pancreatic Cancer
Deletion of Arid1a concomitant with Sox9 overexpression in Lgr5(+) ISCs restores self-renewal in Arid1a-deleted Lgr5(+) ISCs.
High expression of SOX9 can promote the migration and lymph node metastasis of oral squamous cell carcinoma
Irx3 is a novel chondrogenic factor of mesenchymal cells, which acts synergistically with Bmp2-mediated signaling, and regulates chondrogenesis independent of the transcriptional machinery associated with Sox9-mediated regulation.
During embryogenesis, SOX9-positive (+) cells inside hair follicles, which were previously known to give rise to hair follicle stem cells (HFSCs) and cells of the hair follicle lineage, can also give rise to Merkel Cells. Interestingly, while SOX9 is critical for HFSC specification, it is dispensable for Merkel cell formation. Conversely, FGFR2 is required for Merkel cell formation but is dispensable for HFSCs.
These results suggest that targeting SOX9 is a viable strategy to promote reparative axonal sprouting, neuroprotection and recovery after stroke.
SOX9 was over-expressed in liver after ischemia/reperfusion injury. Suppressing SOX9 markedly reduced the inflammatory response. Also, transforming growth factor (TGF)-beta1 was highly induced in liver after ischemia/reperfusion injury.
ETV5 regulates ductal morphogenesis with Sox9 and is critical for regeneration from pancreatitis
Melatonin inhibits cancer stem cell by down-regulation of SOX9-mediated signaling pathway in osteosarcoma
a novel regulatory relationship between the retinal pigmented epithelium (RPE) transcription factors Pax6 and Sox9 that controls the timing of RPE differentiation and the adjacent choroid maturation, is reported.
enhancer 13, a 557-base pair element located 565 kilobases 5' from the transcriptional start site, is essential to initiate mouse testis development; its deletion results in XY females with Sox9 transcript levels equivalent to those in XX gonads.
These results indicate that THRAP3 negatively regulates SOX9 transcriptional activity as a cofactor of a SOX9 transcriptional complex during chondrogenesis.
Sox9 is identified as important factor of VSMC function by modulation the extracellular matrix composition and calcium deposition, which are important processes in plaque development.
these findings widen our current knowledge of SOX9 targets in early chondrogenesis and call for new studies to identify the pioneer and transactivating factors that act upstream of or along with SOX9 to prompt chromatin remodeling and specific gene activation at the onset of chondrogenesis and other processes.
The data support a model of SOX9-GLI-FOXA phasic gene regulatory network in chondrocyte development. Together, SOX9-GLI auto-regulate and cooperate to activate and repress genes in proliferating chondrocytes. Upon hypertrophy, FOXA competes with SOX9, and control toward terminal differentiation passes to FOXA, RUNX, AP1 and MEF2 factors.
Ctgf is the direct target gene of SOX9 in chondrocytes and nucleus pulposus cells.
MOB1-dependent YAP1/TAZ-TEAD complex functions as a transcriptional repressor of SOX9 and thereby negatively regulates chondrogenesis.
the novel role of Tgfb2, Fbxl18, and Tle3 in formation of Sox5, Sox6, and Sox9 dependent tissues.
A critical level of endogenous active SOX9 needed to maintain colorectal tumor cell growth.
The spatiotemporal expression of Sox9 suggested its possible involvement during mouse incisor development.
Analysis of tissue maturation markers showed an increase in COLL II and a decrease in SOX9 expression in the swine tibial menisci with age.
The expression of the differentiation and stemness genes, FN1 and SOX9, is accompanied by cell proliferation.
data presented here demonstrate that the 18 bp indel in the porcine SOX9 5'-UTR is of functional importance and may therefore indeed be a causative variation in SOX9 associated traits
HIF-1alpha activates Sox9 expression and enhances Sox9-mediated transcriptional activity.
Sox9 gene transfer could significantly enhance the repair effect of bone marrow mesenchymal stem cells on the degenerated discs.
The patterns of SRY/SOX9 expression associated with the process of gonadal morphogenesis in rabbit appear similar to those of other mammals, including humans.
The protein encoded by this gene recognizes the sequence CCTTGAG along with other members of the HMG-box class DNA-binding proteins. It acts during chondrocyte differentiation and, with steroidogenic factor 1, regulates transcription of the anti-Muellerian hormone (AMH) gene. Deficiencies lead to the skeletal malformation syndrome campomelic dysplasia, frequently with sex reversal.
SRY (sex-determining region Y)-box 9 protein
, SRY-related HMG-box, gene 9
, transcription factor SOX-9
, SRY (sex determining region Y)-box 9
, SRY (sex determining region Y)-box 9 (campomelic dysplasia, autosomal sex-reversal)
, SRY-box containing gene 9
, SRY-box containing protein 9
, transcription factor SOX9
, LOW QUALITY PROTEIN: transcription factor SOX-9
, sex determining region Y-box 9
, transcription factor Sox-9-B
, transcription factor Sox9b