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anti-Human SOX9 Antikörper:
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Human Polyclonal SOX9 Primary Antibody für ICC, IF - ABIN4355424
Vestentoft, Jelnes, Hopkinson, Vainer, Møllgård, Quistorff, Bisgaard: Three-dimensional reconstructions of intrahepatic bile duct tubulogenesis in human liver. in BMC developmental biology 2011
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Human Polyclonal SOX9 Primary Antibody für IF (p), IHC (p) - ABIN754963
Papaioannou, Mirzamohammadi, Lisse, Nishimori, Wein, Kobayashi: MicroRNA-140 provides robustness to the regulation of hypertrophic chondrocyte differentiation by the PTHrP-HDAC4 pathway. in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 2014
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Human Monoclonal SOX9 Primary Antibody für IF, IHC (p) - ABIN520382
Hodgin, Borczuk, Nasr, Markowitz, Nair, Martini, Eichinger, Vining, Berthier, Kretzler, DAgati: A molecular profile of focal segmental glomerulosclerosis from formalin-fixed, paraffin-embedded tissue. in The American journal of pathology 2010
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Polyclonal SOX9 Primary Antibody für IHC (fro), IP - ABIN541051
Pierzchalska, Grabacka, Michalik, Zyla, Pierzchalski: Prostaglandin E2 supports growth of chicken embryo intestinal organoids in Matrigel matrix. in BioTechniques 2012
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Cat (Feline) Polyclonal SOX9 Primary Antibody für IHC (p), SimWes - ABIN4355427
Antunes, Tsaryk, Gonçalves, Pereira, Landes, Brochhausen, Ghanaati, Barbosa, Kirkpatrick: Poly(γ-Glutamic Acid) as an Exogenous Promoter of Chondrogenic Differentiation of Human Mesenchymal Stem/Stromal Cells. in Tissue engineering. Part A 2015
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Human Polyclonal SOX9 Primary Antibody für IF, IHC (p) - ABIN272082
Zhang, Ding, Nie, Li-Ling, Zhang, Zhang, Chen, Li, Ding: Association of hsa-miR‑145 overexpression in human testicular cells with male infertility. in Molecular medicine reports 2015
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Human Polyclonal SOX9 Primary Antibody für IF, IHC (p) - ABIN542830
Malki, Bibeau, Notarnicola, Roques, Berta, Poulat, Boizet-Bonhoure: Expression and biological role of the prostaglandin D synthase/SOX9 pathway in human ovarian cancer cells. in Cancer letters 2007
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Human Polyclonal SOX9 Primary Antibody für ELISA, WB - ABIN543451
Passeron, Valencia, Bertolotto, Hoashi, Le Pape, Takahashi, Ballotti, Hearing: SOX9 is a key player in ultraviolet B-induced melanocyte differentiation and pigmentation. in Proceedings of the National Academy of Sciences of the United States of America 2007
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Human Monoclonal SOX9 Primary Antibody für ICC, ELISA - ABIN969568
Dupasquier, Abdel-Samad, Glazer, Bastide, Jay, Joubert, Cavaillès, Blache, Quittau-Prévostel: A new mechanism of SOX9 action to regulate PKCalpha expression in the intestine epithelium. in Journal of cell science 2009
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Polyclonal SOX9 Primary Antibody für DB, IHC (fro) - ABIN540954
Wang, McKnight, Zhang, Lu, Balk, Yuan: SOX9 is expressed in normal prostate basal cells and regulates androgen receptor expression in prostate cancer cells. in Cancer research 2007
our findings provide a mechanistic insight into SWCNT-induced carcinogenesis and the role of SOX9 in CSC regulation and metastasis.
We further confirmed absence of Sox9 expression in nuclear beta-catenin accumulating cells of adamantinomatous craniopharyngioma. Our results point to the conclusion that Sox2 and Sox9, seem to play essential roles not only in the specific formation of aCP, but also in processes involving the cerebral tumour environment, which needs to be illuminated in the future.
Results found SOX9 as a direct target of miR-613 in hepatocellular carcinoma (HCC) cells. Overexpressing miR- 613 in hepatoma cells downregulated SOX9 expression through binding to its 3'UTR. SOX9 siRNA could abolish the discrepancy of the self-renewal ability between miR-613 overexpression HCC cells and their control cells, which further confirms that SOX9 is the downstream of miR-613 in regulating liver CSCs expansion.
A sequence motif search for SOX9-responsive elements identified three motifs in the promoter region of mTOR gene. Study data demonstrate that Hedgehog signaling converges on mTOR via SOX9 and highlight the SOX9-mTOR axis as a viable additional target downstream of smoothened that could enhance tumor elimination in patients with basal cell carcinomas.
Findings identify a Sox2-Sox9 network as crucial for stem/progenitor cell maintenance in the human mammary gland. Gain and loss of function assays indicate that Sox9 is implicated in the maintenance of human breast luminal progenitor cells. SOX9 expression level is elevated in breast cancer patients after endocrine therapy failure. Its knockout reduces growth of tamoxifen-resistant breast tumors in vivo.
Increased SOX9 Expression is associated with Premalignant and Malignant Pancreatic Neoplasms.
hyperactivation of YAP unbalances the YAP-SOX9 feedback loop and confers CSC-like features in ESCC
These results unravel NEDD9 as a common target for SOX10 or high SOX9 to partly mediate their oncogenic events, and most importantly, reconcile previous discrepancies that suboptimal level of SOX9 expression is anti-metastatic whereas high level of SOX9 is metastatic in a heterogeneous population of melanoma.
Our data uncover the ZEB1/ERalpha-miR-190-SOX9 axis and suggest a mechanism by which the Wnt/beta-catenin signaling pathway is involved in breast cancer anti-estrogen therapy.
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.
These results suggest that retinoic acids produced by Aldh1a1 in the neural retina directs dorsal choroidal vascular development via Sox9 upregulation in the dorsal retinal pigment epithelial cells to enhance retinal pigment epithelial-derived VEGF secretion.
comparison of FOXL2 genome-wide occupancy in the fetal ovary with testis-determining factor SOX9 genome-wide occupancy in the fetal testis revealed extensive overlaps, implying that antagonistic signals between FOXL2 and SOX9 occur at the chromatin level.
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.
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