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SOX3 encodes a member of the SOX (SRY-related HMG-box) family of transcription factors involved in the regulation of embryonic development and in the determination of the cell fate. Additionally we are shipping SOX3 Antibodies (71) and SOX3 Proteins (5) and many more products for this protein.
Showing 10 out of 25 products:
deletion of the SOX3 gene may have a role in intellectual disability with hemophilia B
Results show that SOX3 is upregulated in human osteosarcoma (OS) tissues and provide evidence that SOX3 promotes migration, invasiveness, and EMT (show ITK ELISA Kits) in OS cells via transcriptional activation of Snail1 (show SNAI1 ELISA Kits) expression.
we provide a first map of the epigenetic landscape of SOX3 in pluripotent cells and during the early phases of neural differentiation. We found SOX3 gene to be non methylated from undifferentiated NT2/D1 to cells committed towards neural lineage.
These findings demonstrate the novel mechanism by which Sox3 contributes to endometrial cancer stem cell invasion and suggest that repression of Sox3 by microRNA-194 may have therapeutic potential to suppress endometrial carcinoma metastasis. The cancer stem cell marker, CD133, might be the surface marker of endometrial cancer stem cell.
Data indicate that SRY-box 3 transcription factor SOX-3 targets Src kinase (show CSK ELISA Kits) in epithelial ovarian cancer (EOC) cells.
SOX3 overdosage permits normal sex development in 46,XX individuals with random X inactivation.
Translocations interrupting this region may also affect the gonadal development, possibly depending on the chromatin context of the recipient chromosome. SOX3 duplications may substitute SRY (show SRY ELISA Kits) in some XX subjects
Screening for SOX3 should be advised not only for hypopituitary patients with an ectopic posterior pituitary, but also for those with a structurally normal pituitary
Our study provides additional evidence that deletion in polyalanine tracts of SOX3 is associated with hypopituitarism
SOX3 duplication is a genetic cause for XH but has incomplete penetrance. Moreover, increased SOX3 levels may be a risk factor for NTD and potentially other clinical characteristics.
CRISPR/Cas9-assisted gene swap provides strong evidence that SOX2 (show SOX2 ELISA Kits) and SOX3 proteins are functionally equivalent in developing brain and testes.
Sox3 null mice exhibit a ventral extension of the anterior pituitary that penetrates, and generates a mass beneath, the sphenoid bone
These data define Dbx1 as a direct SOX3 target gene.
Sox2 (show SOX2 ELISA Kits) and Sox3 play a role in central nervous system glia and provide mechanistic insights into their function during differentiation processes.
findings show SOX3 expression is maintained throughout telencephalic neurogenesis and is restricted to progenitor cells with neuroepithelial and radial glial morphologies; it is expressed within adult neurogenic regions; expression within the developing hypothalamus is upregulated in developing neurons and is maintained in a subset of differentiated hypoththalamic cells
Subcommissural organ function is essential for the prevention of hydrocephalus and overexpression of Sox3 in the dorsal midline alters progenitor cell differentiation in a dose-dependent manner.
It was shown that Sox2 (show SOX2 ELISA Kits) and Sox3 are dose-dependent regulators of sonic hedgehog (show SHH ELISA Kits) transcription that directly bind and activate a long-range Shh (show SHH ELISA Kits) forebrain enhancer.
In neural precursor cells , Sox3 binds genes that are later bound and activated by Sox11 in differentiating neurons (Sox2 (show SOX2 ELISA Kits))
The results indicate that Sox3 functions in an intrinsic manner to promote differentiation of spermatogonia in prepubertal mice but it is not required for ongoing spermatogenesis in adults.
in a transgenic line, Sox3 was ectopically expressed in the bipotential gonad and this led to frequent complete XX male sex reversal
these findings show that sox2 (show SOX2 ELISA Kits) and sox3 are together required for proper otic induction, but the level of expression must be tightly regulated to avoid suppression of differentiation and maintenance of pluripotency.
these data show that sox2 (show SOX2 ELISA Kits) and sox3 exhibit intrinsic differences in promoting sensory vs. neural competence, but at high levels these factors can mimic each other to enhance both states. Regional cofactors like pax2a and fgf8 (show FGF8 ELISA Kits) also modify sox2 (show SOX2 ELISA Kits)/3 functions.
significant decreases in sox3 (up to 3-fold) expression following chilling. Significant increases in expression of sox3 (up to 33-fold) during warming of chilled zebrafish embyos.
Knockdown of fgf24 or sox3 causes severe epibranchial deficiencies but has little effect on otic development
Knockdown of the four B1 sox (show PIPOX ELISA Kits) genes sox2 (show SOX2 ELISA Kits)/3/19a/19b resulted in severe developmental abnormalities.
The pro-neural effects of Sox3 can compensate for inhibition of fibroblast growth factor (Fgf) signalling in inducing neural tissue but it is not sufficient to maintain neural fate, suggesting the presence of Sox3-independent roles of Fgf at later stages.
Sox2 (show SOX2 ELISA Kits) is necessary for spinal cord regeneration and suggest a model whereby spinal cord injury activates proliferation of Sox2 (show SOX2 ELISA Kits)/3 expressing cells and their differentiation into neurons, a mechanism that is lost in non-regenerative froglets.
XSeb4R (show RBM38 ELISA Kits) protein bound specifically to the 3'UTR (show UTS2R ELISA Kits) of Sox3 mRNA. XSeb4R (show RBM38 ELISA Kits) gain-of-function in ectodermal explants revealed increased stability of the maternal Sox3 transcripts, associated with a robust Sox3 protein production.
knockdown of Oct91 inhibits neural induction driven by either Sox2 (show SOX2 ELISA Kits) or Sox3.
Animal pole localized Sox3 acts to inhibit Nodal (Xnr5 and Xnr6) expression, and induces the expression of genes (Ectodermin, Xema, and Coco) whose products repress Nodal signaling.
Results demonstrate that both sox3 and sox2 are induced in response to BMP antagonism, but by distinct mechanisms and that the activation of both genes is independent of FGF signaling; however, both require FGF for the maintenance of their expression.
Eya1 and Six1 are required for both the regulation of placodal neuronal progenitor proliferation, through their effects on SoxB1 expression, and subsequent neuronal differentiation.
This gene encodes a member of the SOX (SRY-related HMG-box) family of transcription factors involved in the regulation of embryonic development and in the determination of the cell fate. The encoded protein may act as a transcriptional regulator after forming a protein complex with other proteins. Mutations in this gene have been associated with X-linked mental retardation with growth hormone deficiency.
transcription factor SOX-3
, SRY-related protein CH3
, transcription factor SOX3
, transcription factor Sox-3
, SRY (sex determining region Y)-box 3
, transcription factor Sox-3-A
, LOW QUALITY PROTEIN: transcription factor SOX-3
, SRY-box containing gene 3